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Flashcards in General Vascular Surgery Deck (94)
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1
Q

Define a normal ABPI measurement

A

0.9-1.3

2
Q

A ptnt has IC, experiencing a cramping pain in his calf muscles on walking, what else might he suffer from if the arterial occlusion is located at the bifurcation of the aorta?

A

erectile dysfunction (impotence)

3
Q

why might a ptnt with IC also notice a numbness and paraesthesia in the skin of the foot at the same time as muscle pain begins?

A

muscle pain due to inadequate blood supply so blood shunted from skin to muscle.

4
Q

why in some ptnts with IC does following a decrease in the walking distance before becoming static, the walking distance actually increases with symptom remission?

A

development of a collateral circulation

5
Q

differentials for IC?

A

osteoarthritis
spinal stenosis
venous claudication
prolapsed IV disc

6
Q

define varicose veins

A

saccular dilatations of veins that are often tortuous

7
Q

why does pregnancy predispose to varicose vein?

A

elevated progesterone leads to smooth muscle relaxation and venous distension
also, iliac veins compressed by gravid uterus

8
Q

causes of secondary varicose veins?

A

post-thrombotic damage
pelvic tumours
acquired AV fistulae
congenital venous anomalies e.g. CG valvular agenesis

9
Q

how does varicose process progress?

A

starts in distal veins and ascends proximally

10
Q

commonest symptoms of varicose veins?

A

unsightliness
aching
mild ankle oedema

11
Q

complications of varicose veins?

A

venous ulceration, calf pump failure syndrome- pigmentation, eczema, lipodermatosclerosis
haemorrhage
superficial thrombophlebitis

12
Q

test useful for demonstrating origin of a varicose vein?

A

percussion test
system of origin of varicose veins can be demonstrated with tourniquet test, but insensitive compared to duplex scanning.

13
Q

how is presence of valvular incompetence in vein being examined demonstrated?

A

cough impulse test

14
Q

investigation required for varicose veins?

A

duplex USS

15
Q

tment of varicose veins in ptnts unsuitable for surgery and pregnant women?

A

compression stocking

16
Q

why is long saphenous vein not stripped much below the knee in saphenofemoral ligation?

A

to reduce risk of damaging saphenous nerve

17
Q

where is thrombosis frequently initiated?

A

in vein valve sinuses of the soleal plexuses

18
Q

clinical features of DVT?

A
limb swelling
pain
tenderness
erythema
dilated superficial veins
19
Q

how might leg appear following an extensive iliofemoral thrombosis?

A

swollen white leg= phlegmasia alba dolens, or blue leg= phlegmasia cerulea dolens

20
Q

differentials for DVT?

A
cellulitis
lymphoedema
torn calf musscles
calf haematoma
ruptured baker's cyst
21
Q

DVT investigations?

A

ascending venography

colour duplex USS- but relatively insensitive in detecting below knee thromboses

22
Q

what can be used to detect reduced venous capacitance after a thrombosis?

A

plethysmography

23
Q

PE clinical features?

A

dyspnoea
haemoptysis
pleuritic chest pain
sudden death as interruption of venous return to L heart

24
Q

gold standard investigation for PE?

A

CTPA: CT pulmonary angiogram

contraindicated in significant renal disease due to use of IV contrast, and in pregnancy due to risk of radiation exposure- in these circumstances consider V/Q perfusion scan- this is NOT useful if preexisting lung disease.

25
Q

evidence of PE on chest radiograph?

A

hilar enlargement
consolidation
pleural effusion- homogenous white opacification with meniscus sign
oligaemia-reduction in b.volume in peripheral circulation

26
Q

what tment may be given if recurrent PE in face of adequate anticoagulation?

A

filter insertion

27
Q

below or above knee amputations preferable?

A

below- so knee intact, making subsequent mobility and prosthetic limb use much better.

28
Q

indications for amputations?

A
end-stage unreconstructable atherosclerotic disease
diabetic microangiopathy and infection
emboli
trauma
infection e.g. NF, gas gangrene. septic arthritis-S.aureus, osteomyelitis
bony malignancy
malformations
intractable ulceration
painful paralysed limbs
29
Q

amputation complications?

A
wound infection
too long or too short
bony spurs
stump neuroma
phantom pain
muscle herniation
DVT
30
Q

type of foot amputation often necessary in diabetic infection?

A

ad hoc foot amputation= non-viable tissue excised and deep infection drained
heel and other weight-bearing areas retained if possible
wound may be closed with primary suture or skin grafting

31
Q

define an aneurysm

A

a localised permanent dilatation of an artery of >50% of the normal diameter or 1.5 times normal diameter.

32
Q

types of true aneurysms?

A

fusiform

saccular

33
Q

RFs for aneurysms?

A

same as for atherosclerosis- smoking, hyperlipidaemia, hypertension, male, older age, FH BUT NOT DM.
smoking, male, FH= most important

34
Q

causes of aneurysms other than atherosclerosis?

A

trauma- pseudoaneurysm/false aneurysm e.g. stab wound
infection e.g. mycotic in endocarditis, syphilis
CT disorders e.g. Marfans, Ehlers-Danlos
inflammatory

35
Q

common surgery now for AAAs of a diameter of 5.5cm or more?

A

endovascular aneurysm repair- stent inserted via femoral artery
appropriate for aneurysms below origin of renal arteries so adequate length of normal aorta for endograft attachment without blood leakage.

36
Q

advantages of EVAR?

A

no abdominal incision
no aortic cross clamping
improved CR, renal and GI function
reduced hospital stay

37
Q

disadvantages of EVAR?

A

endoleaks- continued perfusion of aneurysm sac
movment of stent- this can cause limb ischaemia
failure of stent
thromboembolic complications

38
Q

diameter of aorta defined as an aneurysm?

A

> 3cm

39
Q

define a false aneurysm

A

collection of blood around an artery, communicating with the lumen, but lacking the normal 3 arterial layers

40
Q

how are patients with aneurysms detected with a diameter of less than 5.5 cm monitored?

A

USS- yrly if between 3 and 4.4cm

3 mnthly if 4.5-5.4 cm

41
Q

how do >50% of ptnts with popliteal artery aneurysms present?

A

distal leg ischaemia caused by thrombosis or embolism

can treat with thrombolysis, followed by aneurysm ligation and bypass.

42
Q

investigation with 100% sensitivity for AAAs?

A

abdominal USS

43
Q

% of strokes and TIAs carotid artery disease is responsible for?

A

20%

44
Q

indication for ptnt to have a carotid endarterectomy?

A

symptomatic ptnts with an ipsilateral stenosis of 70% or more (NASCET)
or 50-99% stenosis?
symptoms= transient neurological events

asymptomatic= 70-99% stenosis in Leicester

45
Q

ptnt on aspirin and is having a carotid endarterectomy, what do they do with aspirin?

A

still take it

46
Q

how is carotid artery disease examined for?

A

carotid pulse on palpation?

bruit on auscultation

47
Q

all ptnts presenting with TIAs should have what investigation for their carotids?

A

duplex USS
this will establish degree and site of stenosis, indicate level of bifurcation and determine heterogeneous nature of plaque- potentially unstable and more likely to give rise to symptoms.
significant stenosis indicated by peak systolic velocity of 1.25m/s, with marked spectoral broadening.

48
Q

how can cerebral b.flow be monitored in carotid endarterectomy under GA?

A

transcranial doppler of middle cerebral artery

must use a shunt if evidence of cerebral dysfunction

49
Q

problems with carotid angioplasty?

A

high stroke rate
considerable amount of particulate microembolization
disregard of ECA

50
Q

nerves to look out for in carotid endarterectomy on cutting into neck anterior to SCM?

A

vagus nerve- in carotid sheath, dysphagia and hoarse voice
hypoglossal nerve- damage would result in loss of VC function and dysphagia, tongue would deviate towards side of op
ansa cervicalis= loop in cervical plexus, innervates most of infrahyoid muscles.

51
Q

clinical presentation of calf pump failure?

A
aching
venous claudication
swelling
varicose veins
pigmentation
eczema
lipodermatosclerosis
ankle stiffness
ulceration= end-point
52
Q

calf pump failure tment?

A

compression and elevation
elevation reduces venous pressure at rest
graduated compression reduces transmural venous pressure by increasing surrounding tissue pressure. graduated compression stocking used in VV tment if no venous ulceration, graduated from high pressure distally.

53
Q

conservative tment of varicose veins when ulceration developed?

A

4-layer compression bandaging

54
Q

lab screening tests for preoperative vascular ptnts?

A
Hb
platelets
clotting
urea and creatinine
electrolytes
group and screen, with or without crossmatch of packed rbc
55
Q

how can a vascular ptnt be optimised before an operation?

A

stop smoking
address co-morbid conditions e.g. coronary disease
continue antiplatelets, don’t want post op MI
continue with beta blockers, sudden withdrawl can result in adrenergic hypersensitivity
must be on statin, and continued periop
stabilise blood sugars in diabetics, know HbA1c
maximise BP control
preop chest wall exercises if resp disease
dietary support
lose weight if obese
counsel about what to expect post op
arrangements early for future discharge planning, espec. in elderly

56
Q

post op comps with carotid endarterectomy?

A

stroke- usually embolic in surgery
cranial nerve damage
hyperperfusion syndrome

57
Q

what is ‘trashing’ of the foot?

A

also known as blue toe syndrome, result of blockage of small blood vessels in foot causing ischaemia and necrosis.
can occur as complication of surgery e.g. angioplasty due to embolisation. distal emboli lodge which may cause whole foot infarction.
can occur as complication of medical tment e.g. alteplase, or anti-thrombotic tment
or occur spontaneously, with break off from an atheromatous plaque or with a popliteal artery aneurysm
often pt over 50, with palpable foot pulses, but presence of livedo reticularis-blue/purple skin discolouration, and severe pain in foot and possibly up leg.

58
Q

why is life long monitoring needed post EVAR?

A

stents may leak and aneurysm progress

risk can be reduced by coiling the internal iliac arteries

59
Q

ptnt with DM, has PVD and is having angiography. why must his metformin be stopped beforehand?

A

avoid metabolic acidosis

60
Q

define chronic critical leg ischaemia

A

persisitently recurring rest pain requiring adequate analgesia for 2 or more wks, with ankle systolic pressure of 50 mmHg or less and/or toe systolic pressure of 30mmHg or less.

ulceration or gangrene (visible necrosis, putrefaction) of foot or toes, with an ankle systolic pressure of 50mmHg or less and/or a toe systolic pressure of 30mmHg or less.

critical: defines that the arterial flow is a limb-threatening impairment requiring surgical intervention.

61
Q

use of thrombolysis/angioplasty in critical leg ischaemia?

A

intra-arterial catheter infusion of streptokinase, urokinase or TPA can clear arterial segments and is useful in distal occlusions e.g. embolisation from popliteal artery aneurysms.

62
Q

what may be given LT in ptnts with PVD to reduce risk of fatal CVS events?

A

aspirin

63
Q

3 classifications of varicose veins?

A

trunk- dilated, tortuous veins arising from the long or short saphenous vein and their branches
reticular- permanently dilated bluish intradermal veins usually from 1-3mm in diameter
telangiectasia- a confluence of permanently dilated intradermal venules of less than 1mm in diameter (also known as thread veins or spider veins)

64
Q

in which 3 situations do varicose veins arise?

A

primary (or simple)
secondary
AV fistula

65
Q

when do primary ( or simple) VVs arise?

A

occur as a result of valvular failure resulting in distended superficial veins in the lower limb. They are the commonest type of varicose vein.

66
Q

when do secondary VVs arise?

A

occur when superficial veins carry reversed flow as a collateral mechanism compensating for obstructed neighbouring deep vein. The enforced reverse flow causes enlargement and tortuosity in previously normal veins.

67
Q

how do VVs occur with AV fistulae?

A

increased high pressure flow causes engorgement and tortuosity of superficial veins in the vicinity of an arteriovenous fistula.

68
Q

a common symptom of VVs in the elderly?

A

nocturnal cramps

69
Q

ptnts with VVs may complain of leg discomfort, how might this be described?

A

aching, tension, itching and heaviness, particularly after standing for prolonged periods or in hot weather.

70
Q

VV complications?

A

those from the varicose veins= haemorrhage and thrombophlebitis, and those from venous hypertension= skin pigmentation, skin eczema, lipodermatosclerosis, ulceration, atrophe blanche.
Haemorrhage– due to skin erosion or from minor trauma at site of superficial varicosity. Can be arrested by direct pressure and leg elevation
Thrombophlebitis – results from thrombosis of the varicose veins, and presents with painful, inflamed, and tender varicose veins
Skin pigmentation – due to accumulation of haemosiderin in the skin. from extravasated red cells
Ulceration – occurs due necrosis of skin by failing nutritional exchange with capillaries and is always accompanied by skin pigmentation.
Atrophe blanche – white scarring in the lower leg caused by venous hypertension
Lipodermatosclerosis – inflammatory process leading to skin induration and fibrosis of the subcutaneous fat.

71
Q

what test can be used to define level of superficial venous incompetence in varicose veins, after examining legs to see if distribution is in long or short saphenous systems?

A

trendelenburg’s or tourniquet test
ptnt supine on examination couch and elevate the affected leg to 90° until the venous blood has drained from the great saphenous vein (distended veins may need to be massaged to facilitate this). place tourniquet around the upper thigh of the patient’s leg tightly enough to occlude the long saphenous vein but not to compromised arterial supply. The patient is then asked to stand and venous filling is observed. Rapid filling in the presence of the tourniquet suggests perforator incompetence. If there is no significant filling with the tourniquet in place but rapid filling occurs on release, this implies saphenofemoral junction incompetence. Tourniquet can be applied at distal levels to further define perforator incompetence if necessary.

72
Q

average prevalence of AAA in elderly men?

A

5%

73
Q

classical symptom triad in ruptured AAA?

A

collapse
abdominal distension
abdominal pulsatile mass

74
Q

recommended threshold for treating asymptomatic AAA?

A

> 5.5cm, based on level 1 evidence from randomised trials

75
Q

average mortality for elective AAA repair?

A

5-7%

76
Q

average operative mortality for a ruptured AAA?

A

50%

77
Q

commonest mortality cause in ptnts undergoing elective AAA surgery?

A

cardiac disease

78
Q

% of ischaemic strokes due to carotid artery disease?

A

50%

79
Q

comment location of carotid stenosis?

A

origin of ICA due to haemodynamic phenomenon in this region

80
Q

features of an unstable carotid plaque?

A

intra-plaque haemorrhage
adherent thrombus
rupture
ulceration

81
Q

trial originally providing evidence for CE in symptomatic carotid artery disease ptnts?

A

european carotid surgery trial

82
Q

most dangerous consequence of a bleed following carotid artery op?

A

airway obstruction

83
Q

risk of stroke in carotid endarterectomy?

A

2-5%

84
Q

drug management TIA?

A

initial aspirin 75-300mg
then long-term treatment with modified-release dipyridamole 200 mg twice daily in combination with aspirin 75 mg once daily is recommended

85
Q

LT drug tment following ischaemic stroke?

A

75mg clopidogrel once daily

86
Q

initial drug tment in ischaemic stroke?

A

Alteplase if cane be given within 4.5 hrs of symptom onset.
Treatment with aspirin 300 mg once daily for 14 days should be initiated 24 hours after thrombolysis (or as soon as possible within 48 hours of symptom onset in patients not receiving thrombolysis)

87
Q

most common cause of anterior circulation stroke?

A

AF

88
Q

ABPI denoting critical ischaemia?

A

less than 0.4

89
Q

causes of leg ulcers?

A

Venous disease – 80-85% of all leg ulcers
Arterial – atherosclerosis and arteriovenous malformations
Vasculitis– systemic lupus erythematosus, rheumatoid arthritis, scleroderma, polyarteritis nodosa, Wegener’s granulomatosis
Lymphatic insufficiency
Neuropathic – diabetics often get them on the feet due to peripheral neuropathy
Haematological – polycythaemia rubra vera, sickle cell anaemia
Traumatic – burns, cold injury, pressure sore, radiation, factitious
Neoplastic – basal or squamous cell carcinoma, melanoma, Marjolin’s ulcer, Bowen’s disesae
Others – Sarcoidosis, pyoderma, gangrenosum

90
Q

how do venous ulcers develop?

A

occur in ptnts with chronic venous hypertension due to VVs or prev. DVT causing deep vein obstruction or thrombosis, producing an oedematous lower limb. this impairs tissue perfusion, as lengthened diffusion distance for O2 and metabolites to cross to reach tissue cells. so ankle tissues ischaemic in times of dependence and suffer reperfusion injury on walking or leg elevation, causing an inflammatory process which causes further tissue oedema and fibrosis.

91
Q

scan used to look for superficial or deep venous incompetence/obstruction?

A

venous duplex scan

92
Q

7 aspects to effective leg venous ulcer management?

A
compression bandaging, 3 or 4 layer, if arterial circulation ok
leg elevation
improve mobility
reduce obesity
improve nutrition
varicose vein surgery
skin grafting
93
Q

complications of acute limb ischaemia?

A
irreversible necrosis and gangrene
tissue loss and ulceration
ischaemic neuropathy
painful ischaemic neuritis
high rate of amputation
septicaemia and AKI
94
Q

why can AKI occur as complication of ALI?

A

sudden deterioration in blood supply may lead to septicaemia with mass vasodilation, drop in BP and inadequate perfusion to the kidneys, causing AKI

also as complication following reperfusion: may get myoglobinuria and AKI.