Case 21: Limb Problems Flashcards

1
Q

what is an aneurysm

A

a dilation of an artery which is bound by all 3 walls of the vessel

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2
Q

what is a pseudoaneurysm

A

bleed from an artery which pools in an enclosed space next to the vessel

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3
Q

what is a dissection

A

the intima tears and blood enters, separating it from the media and creates a false lumen which can become aneurysmal and/or lead to reduction of distal blood flow

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4
Q

most common artery affected by aneurysm

A

AA

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5
Q

most common artery of the leg to be affected

A

popliteal

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6
Q

typical presentation of popliteal aneurysm

A

easy palpable popliteal
may have co-morbid abdominal aneurysm

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7
Q

complications of popliteal aneurysm

A

more likely to cause thrombosis rather than rupture- leads to acute limb ischaemia

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8
Q

management of popliteal aneurysm

A

for acute ischaemia- femoropopliteal bypass

is discovered before thrombosis- graft

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9
Q

what is an ulcer

A

a discontinuity of skin with complete break in the epidermis and possibly dermis and subcutaneous tissue

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10
Q

what is an erosion

A

a partial break in epidermis, appears bright red and weepy

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11
Q

causes of ulcers

A

trauma and/or internal pathology

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12
Q

types of ulcers

A

arterial
venous
vasculitis
neuropathic

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13
Q

what is the most common cause of neuropathic ulcers

A

diabetic foot

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14
Q

how to investigate causes of ulcers

A

ABPI for arterial disease
urine glucose for diabetes
test skin sensation and vibration is suspected neuropathic ulcer
doppler US for venous insufficiency
FBC, Us and Es and ESR may show signs of vasculitis, infection or arterial disease

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15
Q

management of ulcers

A

treat underlying cause- PVD, diabetes, vasculitis

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16
Q

are venous or arterial ulcers more common

A

venous
venous= 2/3
arterial= 1/3

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17
Q

pathophysiology of venous ulcers

A

venous insufficiency can cause fluid to leak from veins and capillaries leading to oedema and deposition of plasma proteins, including fibrinogen and inflammatory mediators

this leads to hypoxia, damage to local tissues and eventually ulceration

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18
Q

commonest cause of venous ulcers

A

incompetence of perforator veins

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19
Q

what does a venous ulcer look like

A

rough edge
redness

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20
Q

typical location of venous ulcer

A

medial leg along great saphenous vein

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21
Q

what may you see on surrounding skin of venous ulcer

A

purple/blue skin (blood) and/or brown (hemosiderin)

varicose veins

lipodermatosclerosis (inflammation of the subcutenaous fat causing pain and constriction of the soft tissue)

venous eczema (crust and weepy)

hot

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22
Q

management of venous ulcer

A

if slough is affecting healing can use desloughing dressing (iodine dressing)

usually use non-adherent dressing

surround with compression bandaging to squeeze fluid out over days, then compression stockings long term

elevation helps fluid drainage

antibiotics if signs of infection

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23
Q

management for venous ulcer with superficial vein incompetence

A

surgery (junction disconnection, stripping and avulsion) or endogenous ablation

this is not suitable post-DVT

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24
Q

how to manage venous eczema

A

betnovate (betamethasone)

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25
Q

pathophysiology of arterial ulcers

A

caused by chronic peripheral vascular disease

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26
Q

risk factors for arterial ulcers

A

diabetes
smoking

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27
Q

what do arterial ulcers look like

A

punched out appearance
Clear edge

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28
Q

common places for arterial ulcers

A

distal pressure points- toes, pads, heels, maelloli

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29
Q

what may be surrounding skin of arterial ulcers be like

A

pale
painful
cool
shiny
hairless
weak/absent pulse
signs of infection

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30
Q

appearance of vasculitis ulcers

A

vessel destruction initially leads to purpura then necrosis (black/green/yellow areas)

ulcers with a blue/purple edge then appear after a few days

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31
Q

what bacteria causes gangrene

A

Clostridium perfringens (releases alpha toxin)

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32
Q

how do you typically get gangrene

A

the bacteria inhabit the soil or normal gut flora

enters in major trauma/GI surgery

rarely is non-traumatic due to colorectal carcinoma or immunosupression

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33
Q

gangrene signs and symptoms

A

pain (may be sudden onset and out of proportion to symptoms)

skin crepitus crackly on palpation

skin becomes dark purple, swollen and bullae form

septic shock

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34
Q

gangrene management

A

surgical debridement

Iv antibiotics

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35
Q

what causes PVD

A

atherosclerosis of peripheral arteries

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36
Q

what limbs are most commonly affected by PVD

A

legs most commonly but can also affect arms

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37
Q

when does acute limb ischaemia progress to necrosis

A

within 6 hrs if untreated

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38
Q

commonest site affected by chronic PVD

A

the upper 2/3 of calf due to superficial femoral artery

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39
Q

2nd commonest site affected by chronic PVD

A

buttock and hip due to aortic and iliac artery

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40
Q

other sites affected by chronic PVD

A

thigh (iliac or common femoral artery)
lower 1/3rd of calf (popliteal artery)
foot (tibial or perineal artery)

41
Q

what is claudication

A

predictable, reproducible pain on exertion causes by ischaemia of the muscle which is relieved by rest

42
Q

predictable, reproducible pain on exertion causes by ischaemia of the muscle which is relieved by rest

A

30%

43
Q

Qs to ask to assess claudication severity

A

how many yards can walk before having to stop due to pain, on flat at normal pace on their best day

44
Q

definition of critical limb ischaemia

A

rest pain, unrelieved by medication for 2 or more weeks and/or evidence of tissue loss (ulcer/gangrene)

45
Q

other features of critical limb ischaemia

A

pain may be absent due to neuropathy

pain in feet and toes

pain worse at night due to reduced gravitational pull

swollen leg (may also be red from metabolite-triggered capillary dilation)

46
Q

fontaine classification

A

is for chronic limb ischaemia

1= asymptomatic
2= intermittent claudication (2a if stops over 200m, 2b if less than 200m)
3= rest/nocturnal pain
4= necrosis/gangrene

47
Q

acute limb ischaemia 6 Ps

A

pain at rest
pulseless
pale
paraesthesia
perishingly cold
paralysis (late feature suggesting irreversible damage)

48
Q

ABPI results

A

<0.9 is claudication
<0.6 is rest pain
<0.3 is gangrene

49
Q

management of PVD

A

active- rehabilitation programmes

CVD prevention

clopidogrel= 1st line antiplatelet

naftidrofuryl (vasodilator) can increase walking distance

50
Q

management of acute limb ischaemia

A

heparin IV then embolectomy with Fogarty catheter

thrombolysis with alteplase if not surgically fit

51
Q

when would you consider amputation

A

ulceration and gangrene

52
Q

what are varicose veins

A

tortuous dilated superficial veins usually in the legs

53
Q

what is the usually cause of varicose veins

A

incompetent valves

54
Q

vein affected when there are varicose veins along medial leg

A

sapheno-femoral function of the long saphenous vein

55
Q

vein affected when there are varicose veins along lateral calf

A

sapheno-popliteal junction of the short saphenous vein

56
Q

vein affected when there are varicose veins along medial calf

A

perforator veins

57
Q

RFs for varicose veins

A

family history
prolonged standing
abdominal or pelvic masses compressing IVC or iliac veins (pregnancy, obesity)

58
Q

investigation for varicose veins

A

doppler US

59
Q

conservative management of varicose veins

A

compression therapy (stockings or graded compression bandaging)

weight loss

avoid prolonged standing

simple analgesia if pain

60
Q

surgical management of varicose veins

A

indicated if pain or ulceration

SFJ ligation and vein stripping, stab avulsions, radiofrequency or laser ablation, injection of sclerosing foam

61
Q

what medication must you stop before varicose vein surgery

A

must stop oral contraceptive pill 4-6 weeks pre-op due to DVT risk

62
Q

modifiable risk factors for atherosclerosis

A

T2D
obesity
hypertension
hypercholesterolaemia
physical inactivity
smoking

63
Q

non-modifiable risk factors for atherosclerosis

A

T1D
family history
age
sex

64
Q

renal effects of atherosclerosis

A

hypertensive nephropathy
hypertension resistant to medical treatment

65
Q

cerebrovascular effects of atherosclerosis

A

TIA
stroke
amaurosis fugax
drop attacks

66
Q

peripheral vascular effects of atherosclerosis

A

intermittent claudication
gangrene
arterial foot ulcer
ischaemia rest pain

67
Q

coronary artery of atherosclerosis

A

angina
ACS

68
Q

mesenteric artery effects of atherosclerosis

A

post-prandial abdominal pain
weight loss
hypertension resistant to medical management

69
Q

what is amaurosis fugax

A

transient unilateral loss of vision

often described as ‘a curtain falling’ over their vision

due to emboli passing into the ophthalmic artery, which is usually from a stenosis in the ipsilateral carotid artery

70
Q

what are drop attacks

A

sudden episodes of dizziness or syncope

71
Q

what is sunset foot

A

do buergers test

affected leg is raised and held up for a while

turns white and cold- may indicate chronic arterial stenosis of the lower extremity

putting the leg down would resume blood flow to the foot under the effect of gravity, therefore the leg would regain its red discoloration

this is called sunset foot sign

72
Q

features of neuropathic ulcers

A

deep in depth
pink wound bed
small in size
thickened/raised edge

73
Q

features of arterial ulcers

A

sunset foot
small sized
punched out
distal location
black tissue

74
Q

features of venous ulcers

A

thickened skin
pink wound bed
irregular edge
shallow wound
gaiter
varicose veins

75
Q

potential changes to the appearance of the limbs in chronic venous insufficiency

A

erythema
ulceration
oedema
rash
brown skin (due to haemosiderin deposition)
thickened skin

76
Q

potential symptoms of chronic venous insufficiency

A

night cramps
itching
aching
restless legs
pain
heaviness

77
Q

pathophysiology of varicose veins

A

venous insufficiency can be due to failing of the valves in the veins of the legs

this means the veins aren’t able to stop blood falling down the leg

this means blood pools at the bottom of the legs, and the veins dilate to accommodate

more common in standing occupations and pregnancy

78
Q

pain in leg when walking differentials

A

musculoskeletal= knee oestoarthritis

neurological= spinal canal stenosis

peripheral arterial= intermittent claudication

venous= chronic venous insufficiency

79
Q

RFs for intermittent claudication

A

smoking
hypertension
male
family history of CVD
older age

80
Q

red flag symptoms for the leg pain

A

rest pain- ischaemic rest pain warrants urgent referral to vascular

night pain

tissue loss

sudden onset symptoms associated with sensorimotor deficit- indicative of acute limb ischaemia and is a medical emergency

leg swelling- suggests DVT and needs duplex US to rule out

81
Q

typical findings of intermittent claudication in right leg

A

right foot paler and cooler than the left
with a delayed capillary refill

on left femoral, popliteal, posterior tibial and dorsalis pedis pulses were palpable, but on the right only femoral

no evidence of tissue loss

82
Q

what actually causes the pain in intermittent claudication

A

the muscles have increased O2 demands during exercise which cannot be delivered due to the muscles compromised blood supply

muscles most commonly affected are in calf due to femoral-popliteal vessels being affected

83
Q

which exercise most commonly brings on intermittent claudication pain

A

walking (especially uphill)

84
Q

what is atherosclerosis

A

hardening and narrowing of the arteries due to plaque (most commonly lipid)

85
Q

symptoms of atherosclerosis in the coronary arteries

A

vomting
anxiety
angina
coughing
syncope/pre-syncope
(can lead to MI)

86
Q

symptoms of atherosclerosis in the carotid arteries

A

weakness
headaches
facial numbness
paralysis
(can lead to stroke)

87
Q

symptoms of atherosclerosis in the kidneys

A

reduced appetite
hand/feet swelling
increased BP

88
Q

how can atherosclerosis cause a thrombus

A

the plaque ruptures
causes coagulation to stop the contents spilling out into he blood
this creates a thrombus (this can go on to impede blood flow)

89
Q

there is increase in which type of cholesterol in atherosclerosis

A

LDL

90
Q

what investigation would you do to distinguish between intermittent claudication and spinal canal stenosis

A

MRI

91
Q

how is an ankle brachial pressure index (ABPI) performed

A

doppler auscultates the brachial
BP cuff is inflated until signal disappears

doppler then placed at posterior tibial/dorsalis pedis
BP cuff inflated (at ankle) until signal disappears

92
Q

results of ABPI

A

the results are expressed as ratio (ankle:brachial)

if 1- leg and arm are the same so normal

if below 0.8- may have intermittent claudication (or no symptoms at all)

if below 0.4- might have pain at rest and/or at night and tissue loss (suggests chronic limb-threatening ischaemia)

93
Q

when would you offer angioplasty and stenting for intermittent claudication

A

after modifiable risk factors have been reinforced

when supervised exercise programme has not lead to satisfactory improvement in symptoms

imaging has proved that angioplasty is suitable

94
Q

which 2 medications should be commenced with intermittent claudication

A

an antiplatelet- aspirin/clopidogrel

statin (regardless of serum cholesterol levels)

95
Q

how is angioplasty performed

A

needle punctures common femoral artery at groin level

contrast dye is injected into artery to visualise stenosis/occlusion

wire passed through diseased artery and ballon is passed over wire

it is inflated in the diseased segment with widen blood flow

96
Q

what to do if angioplasty doesn’t work

A

can do bypass

incisions are made over the arteries above and below the disease

usually great saphenous vein is removed from the leg, reversed and stitched to the artery as an alternative conduct

97
Q

does intermittent claudication progress to worse

A

1/3= symptoms resolve and unaffected
1/3= symptoms remain stable and do not progress
1/3= symptoms worsen (claudication distance decreases, lifestyle more impacted), can progress to critical limb ischaemia (rest and/or night pain)

98
Q

what % of those with intermittent claudication have amputation

A

1%