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vascular Sara Flashcards

1
Q

what is chronic limb ischaemia? (include pathophysiology)

A

A gradual reduction in the blood supply to a limb caused by atherosclerosis of vessels supplying the limb.
Atheroma builds up within the intima of the vessel resulting in stenosis of the vessel. This reduces blood flow. During times of exercise this blood flow is not enough and results in ischaemia and thus anaerobic respiration. lactate and K build up causing the individual cramping pain.

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2
Q

what are the risk factors for chronic limb ischaemia?

A

smoking - massive risk factor - increases platelet activation, fibrinogen levels, reduces HDLs and increases lipids

diabetes, HTN, hyperlipidaemia

FHx

associated with ischaemic heart disease and cerebrovascular disease

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3
Q

how does chronic limb ischaemia present?

A

intermittent claudication: pain/cramping gradually comes with activity and reduces rapidly with rest.
usually calf pain but can also be buttocks and thigh.

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4
Q

what are important differential diagnosis when considering chronic limb ischaemia?

A

spinal stenosis
acute limb ischaemia
muscle sprain
DVT

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5
Q

what do you expect to find on examination of someone with chronic limb ischaemia?

A

inspection: pale, poor skin condition (ulcers)
palpation: cool temp, weak foot pulses, slow cap refil . include palpation of abdo for AAA and popliteal fossa for popliteal aneurysm
listen for carotid bruits (associated)

always compare both legs

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6
Q

how can you investigate chronic limb ischaemia?

A

bloods: FBC (anaemia can aggrevate it), lipids and glucose (risk factors) , clotting.
ABPI
tredmill testing - walking brings on pain. Ask them to go uphill and if better consider spinal stenosis
feel calves for tenderness at rest - sprain/DVT
duplex USS - view stenosis
BP and ECG for risk factor
angiography - CTA or MRA
check for thrombophilia/homocysteine if young (<50)

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7
Q

where can atheromas be located to cause chronic limb ischaemia?

A

superficial femoral arteries - majority
calf arteries - mainly in diabetics
aorto-iliac arteries

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8
Q

what is leriches syndrome?

A

bilateral intermittent claudication
buttock claudication
erectile dysfunction

due to atheroma in the aortic bifurcation therefore affecting both internal and external iliac arteries.

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9
Q

what are the complications of chronic limb ischaemia?

A

necrosis /gangrene and sepsis and the need for amputation

this risk is higher for diabetics or those who continue to smoke.

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10
Q

how do we treat chronic limb ischaemia?

A

conservative: manage risk factors (stop smoking), exercise rehab
pharm: statins, aspirin, clopidogrel
percutaneous transluminal angioplasty
surgical bypass

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11
Q

how does exercise rehab help chronic limb ischaemia?

A

helps walking technique
improves collateral supply
improves capillary perfusion

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12
Q

what is percutaneous transluminal angioplasty?

A

helps chronic limb ischaemia
catheter put into vessel and balloon dilated to help reduce the stenosis +/- stenting.
patient has to be willing to change lifestyle otherwise disease will reoccur

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13
Q

how does surgical bypass work in chronic limb ischaemia?

A

use duplex USS to find a suitable vein for bypass. e.g. common femoral to popliteal. follow up and check with duplex.

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14
Q

what is ABPI? How is it performed?

A

ankle brachial pressure index. compares blood pressure at ankle to that in the arm to give a value about the degree of PVD.

put BP cuff around ankle. using Doppler find the foot pulse. inflate cuff till pulse has gone. slowly deflate and record the pressure which the pulse returns. this is the ankle systolic pressure.
find systolic pressure in arm

ABPI= ankle/brachial.

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15
Q

what do different values for ABPI mean?

A 
>0.9 normal
0.8 - 0.9 mild
0.5-0.8 - moderate
<0,5 = severe 
<0.4 = critical

chronic limb ischaemia

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16
Q

how can we make the ABPI more sensitive?

A

record after exercise. if the value drops it is more likely there is PVD

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17
Q

what does an ABPI of >1.4 suggest?

A

sometimes atherosclerosis results in calcification and hardening of the arteries. therefore they become less compressible with pressure and this will give an abnormally high ABPI. in this case the result is an inaccurate measure of limb ischaemia/ PVD

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18
Q

what is acute limb ischaemia?

A

sudden decrease in limb perfusion that threatens the viability of the limb

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19
Q

what are the clinical features of acute limb ischaemia?

A

sudden onset of 6Ps - pain, pallor, paresthesia, paralysis, perishingly cold and pulseless.

Colour is variable:
at first there may be pallor due to arterial spasm. Then the anaerobic respiration leads to release of vasoactive substances and vasodilation and so the limb can appear paradoxically red/ purple and mottling

unilateral

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20
Q

how can you tell the limb is still salvageable in acute limb ischaemia?

A

if the mottling blanches under pressure

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21
Q

what are the causes of acute limb ischaemia?

A

chronic limb ischaemia - i.e. atheroma which has progressed
embolism from MI, AF, prosthetic valve or aneurysm
thrombotic condition
trauma - compartment syndrome

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22
Q

what are the complications of acute limb ischaemia?

A

irreversible muscle necrosis and paralysis
need for amputation
repurfusion injury and compartment syndrome
electrolyte disturbances (release of K+ ) effects heart/gut
rhabdomyolysis - AKI

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23
Q

what is the Buergers test?

A

test for chronic limb ischaemia

raise leg and look for pallor - if pallor at 20 degree the ischaemia is severe. compare to the other leg

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24
Q

how can we examine for acute limb ischaemia?

A

look for sign of 6Ps

investigate cause e.g. AAA

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25
Q

what investigations should we do in someone presenting with acute limb ischaemia?

A

FBC, clotting, U and Es
serum lactate - assess level of ischaemia
thrombophilia screen if <50yrs and no risk factors
ECG - AF?
Doppler US
CT angiography

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26
Q

how does CT angiography work?

A

inject dye and this dye should flow through circulation

CT dye appears white and thus can see areas where there is stenosis or circulation is blocked.

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27
Q

how can you manage acute limb ischaemia?

A

high flow O2 - increase oxygenation to tissue
analgesia
IV heparin
emergency angioplasty, bypass surgery or amputation or embolectomy for emboli

monitor K+ and myoglobin levels

advice on risk factors

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28
Q

how does embolectomy work?

A

use a fogarty catheter and insert balloon through vessel and then dilate behind the clot and pull the clot out with the catheter and balloon.
requires general or local anaesthetic.

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29
Q

how does duplex Doppler and spectral Doppler USS work

A

duplex - red for arterial, blue for venous. allows you to observe flow

spectral shows speed and quality of flow

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30
Q

what is critical limb ischaemia?

A

chronic limb ischaemia has advanced to critical staged

defined by: rest pain >2 weeks, requiring opiates, ulcer/gangrene, ABPI <0.4

rest pain includes pain in foot at night that can be relieved by dangling foot out of bed (gravity)

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31
Q

what is an aneurysm?

A

A permanent dilation of a vessel more than 1.5x its normal size

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32
Q

what are the different types of aneurysms?

A

true - pathological degeneration involving all layers of vessel wall e.g. due to atherosclerosis

false/pseudoaneurysm - leakage of blood out of an artery into a cavity supported by connective tissue that is expansible and pulsatile.

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33
Q

what are the causes of aneurysms?

A

congenital - berry aneurysms of circle of willis
degenerative - atherosclerosis
connective tissue disorders - marfans and ehlers danlos
infective - mycotic aneurysms in infective endocarditis and syphilis
dissection
trauma

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34
Q

what is the pathophysiology behind an aneurysm?

A

loss of elastin and smooth muscle from medial wall and so artery can stretch and doesn’t recoil as much.

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35
Q

where is the body do aneurysms occur?

A

most common = aorta
then popliteal
also common femoral, intra-abdominal sphlanchnic, subclavian and carotid

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36
Q

what is Ectasia

A

Localised area of enlargement of a vessel but <1.5x normal size

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37
Q

what is arteriomegaly?

A

generalised enlargement of arterial tree

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38
Q

how do popliteal aneurysms present?

A

mainly asymptomatic
50% are bilateral
can get symptoms of complications:
- acute limb ischaemia if embolization occurs
- symptoms associated with rupture (rare)

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39
Q

how do you examine for a popliteal aneurysm?

A

flex knees and feel for popliteal pulse usually quite weak. IF you can feel a pulse an aneurysm should be suspected. feel for a pulsatile mass.

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40
Q

How can we investigate a popliteal aneurysm?

A

CT angiography - gold standard
USS duplex - differentiates between this and bakers cyst
should examine for AAA because often associated

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41
Q

what are the complications of a popliteal aneurysm?

A

main risk is embolization

Rupture is rare

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42
Q

how do you manage a popliteal aneurysm?

A

if >2cm or symptomatic, it should be treated due to risk of embolization

Hunterian ligation of popliteal aneurysm and bypass surgery - open surgery where the vessels is ligated and replaced with bypass graft
OR
endovascular stenting - can be done under local and thus preferred for unfit patients.

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43
Q

what is the risk of endovascular stenting in popliteal aneurysms?

A

stent thrombosis

aneurysm sac can fill through collateral vessels.

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44
Q

what causes femoral artery aneurysms?

A

percutaneous endovascular interventions

IV drug users who inject into groin

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45
Q

what are the symptoms of femoral artery aneurysm?

A

claudication / acute limb ischaemia
swelling in the groin
fever if infection occurs

46
Q

how do we investigate femoral artery aneurysms?

A

USS duplex scan

CT angiography

47
Q

how can we treat a femoral artery aneurysm?

A

open surgical repair

48
Q

what are the two different ways an aortic aneurysm can rupture? how do these compare to one another

A

anteriorly /intraperitoneal - less common
posteriorly/ retroperitoneal - more common

intraperitoneal rupture has no supporting tissue and thus bleed is massive and die quickly.
Retroperitoneal rupture - tissues behind aorta support the bleed giving time for treatment

49
Q

how does a ruptured aortic aneurysm present?

A

abdo pain and vomiting
severe back pain
collapse
patient looks weak, cold, sweaty, clammy, tready pulse

classic triad: abdo/back pain, low BP and pulsatile mass

50
Q

how do you manage a ruptured aortic aneurysm?

A

oxygen
IV access - take bloods (X match), give fluids
catheterise
surgery - open or stent.

51
Q

what causes death in those with ruptured aortic aneurysms?

A

haemorrhage and multiorgan failure

52
Q

what are the differentials for an ruptured AA?

A

MI
P.E
pancreatitis
Renal colic

53
Q

what diameter of the aorta is normal and what is classed as an aneurysm?

A

normal for men = 2.5, women = 2cm

so anything about 3cm is an aneurysm

54
Q

what are the common sites for aortic aneurysms?

A

infra renal is most common

can also be thoracoabdominal

55
Q

what is the difference between A and B aortic disections? what is more life threatening an A or B aortic dissection

A

Aortic A dissection involve the ascending aorta and arch and can propagate to descending aorta
aortic B dissection do not involve ascending aorta

A - requires surgery

56
Q

what are the complications of aortic aneurysms

A

most common complication is retroperitoneal rupture

can also cause embolization and acute limb ischaemia , thrombosis , aortoduodenal fistula and pressure on other structures.

57
Q

what are the symptoms of aortic aneurysms?

A

mainly asymptomatic
sometimes abdominal pain, back or loin pain
sometimes generalised malaise and weight loss
pulsatile abdominal mass

symptoms of any complications:

  • rupture - severe back pain, iliac fossa and groin and haemodynamic instability
  • embolization - symptoms of limb ischaemia
58
Q

how would you investigate an AAA?

A

Palpate abdomen and feel for pulsatile mass
USS/ CT angiography
if ruptured look for signs of shock
look for other aneurysms e.g popliteal - associated

59
Q

when is non-operative and operative treatment of AAA required?

A

<5.5cm = non operative and just requires surveillance if between 3 and 5.4.
>5.5cm/ symptomatic or rapidly expanding - surgery

60
Q

what conservative management/advice of AAA is given?

A 
stop smoking 
BP control
statins
weight loss 
exercise
61
Q

what are the two options for repairing an AAA?

A

open repair: midline laparotomy to expose aorta. clamp proximally and distally. remove the segment of aorta and replace with a graft

endovascular aneurysm repair (EVAR) - stenting. Radiographically guided intraluminal stent graft via femoral artery.

62
Q

how do we manage AAA post op?

A

advice: stop smoking, control BP, statins, weight loss

surviellence - to assess for complications.

63
Q

how does open repair compare to endovascular repair of AAA ? (i.e. advantages and disadvantages)

A

open repair has a longer op time and more complications associated with operation (haemorrhage, colonic ischaemia from clamping, renal failure, embolism, cardiac and resp failure)
However less long term complications and better long term outcome.

EVAR has a reduced op time, reduced time for occlusion of aorta, less pain and less hospital stay. However longer term complication e.g. endoleak, endotension.

64
Q

what are the complications of EVAR?

A

stent will narrow the artery and increase pressure which adds strain on heart

stent may block branches of aorta - ischaemia

endoleak: blood leaks into space outside stent and aneurysm can continue to expand
endotension: aneurysmal sac continues to expand with no identifiable leak.

65
Q

what is aortic dissection?

A

Tear in intimal layer of aorta and blood flows between layers tearing them apart. The dissection can progress anterograde (towards iliac arteries) or retrograde (towards aortic valves)

66
Q

what are the risks for aortic dissection?

A 
HTN
atherosclerosis
male 
Caucasian 
marfans, ehler danlos, bicuspid aortic valves.
67
Q

what are the clinical features of an aortic dissection?

A

tearing/ stabbing chest pain that radiates to back.

Patient may feel in shock if hypovolaemic:

- if blood loss to dissection
- cardiogenic shock due to aortic valve involvement and tamponade

tachycardia

aortic regurg murmur

68
Q

how can an aortic dissection be diagnosed? what other investigations are important?

A

CT angiogram for definitive diagnosis

ECG, troponin - rule out MI

69
Q

what are the complications of aortic dissection?

A

the dissection creates a flap which can flap back and block other braches or the lumen resulting in ischaemia

70
Q

how is aortic dissection managed?

A

often medically with HTN medication to prevent progression

if high risk i.e. about to rupture, type A etc. Then surgically treated

71
Q

what are varicose veins?

A

torturous, twisted and lengthened veins with valvular incompetence.
The valves no longer meet in the middle and thus you get a reflux of blood from the deep system to the superficial system

72
Q

where do varicose veins occur?

A

small or great saphenous veins

73
Q

what causes varicose veins?

A

majority are primary and caused by genetics, COCP, pregnancy, obesity, standing a lot, (NOT HTN, lipids, smoking like in PVD)
IV drug users - when using deep veins of legs (also risk of DVT with this

can also be secondary to DVT, pelvic tumour and arterio-venous fistulae

74
Q

how can varicose veins be classified?

A

trunk - big bulging
reticular - smaller ones
Telangiectasia

can be classified using CEAP classification: 
C1 = telangiectasia/reticular
C2 = varicose veins
C3= oedema 
C4a = pigmentation or eczema
C4b = lipodermatosclerosis or athrophie blanche 
C5 = healed venous ulcer
C6= active venous ulcer
75
Q

what type of varicose veins are most common?

A

reticular and telangiectasia

these are both more of a cosmetic problem.

76
Q

what is a saphena varix?

A

Dilation of the saphenous vein at the saphenofemoral junction in the groin.
displays with coughing so can be mistaken for a femoral hernia but on closer inspection has a blueish tinge.

77
Q

what are the symptoms associated with varicose veins?

A 
visible vein
heaviness, tension, aching 
itching is associated with trunk ones.
venous eczema 
skin changes - haemosiderin 
ulceration 
phlebitis
78
Q

State some questions that would be relevant to a varicose veins history

A

Ask about previous DVT, COCP/ HRT
Ask about skin changes
FHx?

79
Q

how are varicose veins examined?

A

find out if long or short saphenous vein
inspect skin for ulcers, skin changes, tenderness (phlebitis) and hardness (thrombosis).
if there are ulcers palpate for pulses to rule out PVD

Tap test
auscultate over the varices for a bruit - indicates arteriovenous malformation
Trendelenburg test

CVS examination if time .

80
Q

what is the tap test for varicose veins?

A

tap varicose veins and palpate the saphenofemoral junction to feel the transmitted tap (if valves are competent they will interrupt the transmission of the tap

81
Q

what is the Trendelenburg test for varicose veins?

A

lie them on a couch and lift legs to drain the vein and make sure it is empty.
cut of vein using a tourniquet
stand and see if vein fills up
move tourniquet up/down to find where the problem starts

82
Q

what investigations are required for varicose veins?

A

gold standard = Doppler USS - listen for flow in incompetent valves e.g saphenofemoral junction in groin or short saphenous behind the knee.

83
Q

how are varicose veins managed?

A

reassurance that they aren’t a problem and more a cosmetic issue
education - avoid standing for long periods, weight loss, compression hosiery to help venous return.

last resort is surgery
- when there are skin changes (include ulcers, eczema) or superficial vein thrombosis

84
Q

what are the surgical options for varicose veins?

A
  1. vein ligation, stripping and avulsion
    • incision made in groin/popliteal fossa and incompetent vein is tied and stripped away. general anesthetic
  2. foam sclerotherapy:
    • injecting a sclerosing/irritating agent into a varicosed vein and causing inflammation to close the vein off. USS guidance to ensure the foam doesn’t enter the deep system. requires local anaesthetic only
  3. thermal ablation or endovascular laser obliteration (EVLT)
    • heat vein from inside out using radiotherapy and later catheters - destroys endothelium and closes vein off. USS guidance. general or local anaesthetic. risk of nerve damage and DVT.
85
Q

when surgically stripping varicose veins what do you need to be careful of?

A

saphenous and sural nerves.

will lead to changes in sensation

86
Q

what are the complications of varicose veins?

A

cosmetic issue
thrombophlebitis (only trunk ones)
bleeding

complications from venous hypertension

  • leg ulcers
  • oedema
  • eczema
  • haemosiderin stain - due to bilirubin leak and iron stain
  • lipodermatosclerosis - inflammation of fat under epidermis
  • atrophic blanche - white areas of skin

reticular and spider ones never cause many problem. Trunk ones can lead to complications

87
Q

what are post -surgical complications of varicose veins?

A

haemorrhage
thrombophlebitis - foam or ablation treatments
DVT - endovenous treatment s
reoccurance
nerve damage - saphenous/sural
stroke/ visual symptoms - foam sclerotherapy

88
Q

what are the causes of an acute peripheral vascular trauma?

A

stab wounds
bone fractures
- supracondylar humerus and brachial artery
dislocation:
- posterior shoulder dislocation and axillary artery
- dislocation of knee and popliteal artery

iatrogenic - cardiac catheterisation, balloon and angioplasty

89
Q

what are the hard and soft signs of acute arterial injury?

A

hard signs:

  • external arterial bleed
  • rapidly expanding haematoma
  • palpable thrill, audible bruit
  • obvious acute limb ischaemia

soft:
- history of bleed at scene
- diminished unilateral pulse
- small non-pulsatile haematoma
- neurogenic deficit

90
Q

how do we manage acute vascular damage?

A

IV lines into uninjured areas and give IV fluids - avoid giving fluids distal to injured area. try to preserve saphenous and cephalic veins as these may be required for surgical repair

emergency surgery to repair - may need repair or amputation

91
Q

When is the aorta likely to be transected acutely?

A

high energy RTA
the descending aorta is very fixed in chest so in a RTA can become completely/partially transected.
majority die before reaching hospital

92
Q

how is acute transection of aorta managed?

A

if not treated within 24 hours, patient will die
stent graft - similar to aneurysmal repair
may need to consider management for tension pneumothorax of cardiac tamponade too from the blood leakage.

93
Q

what are the causes of retroperitoneal bleeds?

A

pelvic fractures
surgery in pelvis
warfarin
angiogram/plasty

94
Q

what are the signs of a retroperitoneal bleed?

A

pale, clammy, hypotensive
complaining of back back pain
haematoma at groin puncture site
may have iliac fossa mass/tenderness

suspected if low BP and drop in Hb following femoral artery catheterisation

95
Q

How are acute retroperitoneal bleeds managed?

A

resuscitation
urgent CT to diagnose
surgical repair

96
Q

what is carotid disease?

A

The stenosis of carotid arteries caused by the build up of atherosclerotic plaques. Usually asymptomatic but can lead to stroke/TIA if plaque ruptures and embolises.

The carotid bifurcation is prone to atheroma due to turbulent flow

97
Q

what are the risk factors for carotid disease?

A

age, FHx
HTN, smoking, diabetes, hypercholesterolemia
obesity
CVS disease history

98
Q

how does carotid disease present?

A

stenosis usually is asymptomatic because there is good collateral blood supply.
TIA / stroke symptoms:
- visual changes - amaurosis fugax , hemianopia
- slurred speech
- hemimotor/hemisensory - e.g. face drop of body dropping to one side (loss of strength)

99
Q

how can you differentiate between a TIA and stroke?

A

TIA <24 hours of symptoms

100
Q

what is amaurosis fugax?

A

monocular vision loss. described as a curtain coming down over vision.
lasts few seconds/mins
due to embolus in central retinal artery.

101
Q

what is hemianopia?

A

loss of one half of visual field in both eyes.

caused by blockage of vertebrobasilar circulation.

102
Q

how can you investigate carotid disease?

A

risk factors: ECG, CXR, glucose, lipids, FBC, clotting
duplex USS of carotid artery - assess blood flow
CT angiography gives more accurate % of stenosis

103
Q

what predicts the likelihood of a stroke occurring after a TIA?

A 
ABCD2
A= age >60 - 1 point
B = blood pressure >140/90 = 1 point
C = clinical presentation:
     unilateral weakness - 2 points
     speech deficit - 1 point 
D = 
    duration: >60mins =2 points; 10-59 mins = 1 point
    Diabetes - 1 point

higher the score higher the risk of stroke in next 48hrs to 7 days. more reason to operate.

104
Q

how Is carotid disease classified?

A 
degree of stenosis
mild - <50%
moderate: 50-69%
severe: 70-79%
critical: 80-99%
occlusion - 100%
105
Q

how do we manage carotid stenosis?

A

conservative / supportive therapy
- blood pressure control, diabetes control, statin, aspirin, stop smoking, stop alcohol, exercise.
Carotid endartectomy
carotid angioplasty

106
Q

how is carotid endartectomy performed?

A

expose carotid bifurcation
clamp and open vessel
use a shunt because collateral supply isn’t sufficient
using Doppler of middle cerebral artery assess blood flow to brain is adequate throughout surgery.
unclamp
remove plaque and vessel walls up to adventitia. replace with a graft.
reverse the shunt and close up.

after monitor BP and neurological state

107
Q

what are the indications to carotid endartectomy?

A

fit patient - <75 men/ <70 women and life expectancy of >5yrs
symptomatic for 6 months and >50% occlusion
patient has agreed despite knowing risks (e.g. stroke)

108
Q

what are the risks of carotid endartectomy (CEA)?

A 
stroke 
hypoglossal nerve damage - weak tongue
glossopharyngeal nerve damage  - difficulty swallowing
MI
local bleed
infection
109
Q

how does carotid angioplasty compare to CEA?

A

less invasive and no risk of cranial nerve damage

but more likely to restenose and increased rate of stroke

110
Q

how is a stroke managed?

A

first rule out haemorrhagic

Ischaemic :

  • IV alteplase if admitted within 4.5 hours of symptom onset
    - 300 mg aspirin for 14days

haemorrhagic - neuro surgery

long term:

  • manage CVS risk - includes statins
  • clopidogrel/aspirin long term
  • CEA to prevent reoccurance
  • speech/language and physiotherapy
111
Q

how can we find the saphenofemoral junction?

A

pubic tubercle
4cm across
4cm below

Surgery sara (10 decks)

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