Vascular Surgery Flashcards
(131 cards)
1
Q
define ulcers
A
abnormal breaks in the skin or mucous membranes
2
Q
what are the common causes of lower limb ulcers?
A
venous origin (80%)
arterial insufficiency
diabetic related neuropathy
immobilisation - pressure over bony prominence
rare - infection, trauma, vasculitis or malignancy
3
Q
what is a venous ulcer caused by?
A
venous insuffiency…due to valvular incompetence or venous outflow obstruction…impaired venous return…venous hypertension causes trapping of white blood cells in capillaries and forms fibrin cuff hindering oxygen transportation into the tissue..activating white cells to release inflammatory mediators
4
Q
what are the clinical features of a venous ulcer?
A
shallow and irregular borders and a granulating base
usually over medial malleolus
painful (worse at end of day)
aching
itching
bursting sensation
may be varscose veins and oedema, and other signs of venous insuffiency - varicose eczema, thrombophlebitis, haemosiderin skin staining, lipodermatosclerosis, atrophie blanche
5
Q
what is a common complication of a venous ulcer?
A
prone to infection and can present with associated cellulitis
6
Q
what are the risk factors for developing a venous ulcer?
A
increasing age
pre existing venous incompetence or history of venous embolism
pregnancy
obesity
severe leg injury/trauma
7
Q
which investigations are required for venous ulcers?
A
duplex USS
insuffiency usually at sapheno-femoral or sapheno-popliteal junctions
Ankle brachial pressure index - arterial component to the ulcers
swabs - infection
thrombophilia and vasculitic screening in young patients
8
Q
how do you manage venous ulcers?
A
conservative - leg elevation, increased exercise (aids venous return due to calf muscle), weight reduction and better nutrition
if infection - abx
multicomponent compression bandaging
if varicose veins too - surgery
9
Q
what is an arterial ulcer caused by?
A
reduction in arterial blood flow…decreased perfusion of tissues and poor healing
10
Q
what are the clinical features of arterial ulcers?
A
small deep lesions, well defined borders and necrotic base
occur distally at sites of trauma and in pressure areas like a heel
intermittent claudication
pain at night - limb ischaemia
long period of time
no granulation tissue as no healing
cold limbs
thickened nails
necrotic toes
hair loss
absent pulses
11
Q
what are the risk factors for arterial ulcers?
A
same risk factors for peripheral arterial disease - smoking, DM, hypertension, hyperlipidaemia, increasing age, family history, obesity, physical inactivity
12
Q
which investigations are required for arterial ulcers?
A
ankle brachial pressure index
if low - more severe (less than 0.5- severe, >0.9 normal)
location of arterial disease - imaging such as duplex uss
13
Q
how are arterial ulcers managed?
A
critical limb ischaemia
so
conservative - smoking cessation, weight loss, increased exercise
medical - CV risk so statin, antiplatelet such as aspirin
surgical - angioplasty or bypass grafting
14
Q
what are neuropathic ulcers caused by?
A
peripheral neuropathy…loss of protective sensation which leads to repetitive stress and unnoticed injury forming…painless ulcers forming on pressure points…usually DM and B12 defiency
15
Q
what are the clinical features of neuropathic ulcers?
A
burning/tingling in legs
single nerve involvement
amotrophic neuropathy (painful wasting of proximal quadriceps)
variable size
punched out appearance
sites of pressure - metatarsal head or heel
peripheral neuropathy
warm feet and good pulses
16
Q
which investigations are required for neuropathic ulcers?
A
blood glucose levels and serum b12 level
concurrent arterial disease checked- ABPI and maybe duplex
swab - infection
x ray - osteomyelitis
test of peripheral neuropathy
17
Q
how do you manage neuropathic ulcers?
A
diabetic foot clinic
hba1c less than 7%
improved diet and exercise
chiropody - foot hygeine and footwear
abx if infection
ischaemic or necrotic tissue - surgical debridement
18
Q
what can be seen alongside neuropathic ulcers?
A
charcot’s foot - loss of joint sensation results in continual unnoticed trauma and deformity…predisposes to ulceration
charcots - swelling, distortion, pain, loss of function, rocker bottom sole
19
Q
a patient presents with an acutely painful limb that is cold and pale, what is your top diagnosis?
A
acute limb ischaemia
20
Q
what are the clinical features of acute limb ischaemia?
A
pain
pallor
pulseless
perishingly cold
paraesthesia
paralysis
21
Q
how do you examine a patient with suspected acute limb ischaemia?
A
both limbs - if full pulses in one leg and none in other…urgent intervention
22
Q
what risk factors should be asked about for acute limb ischaemia?
A
a fib
hypertension
smoking
DM
recent MI
23
Q
which investigation is required for acute limb ischaemia?
A
CT angiogram
urgent vascular review
24
Q
what initial management is required for acute limb ischaemia?
A
emergency - irreversible tissue damage occurs within 6 hours
fluid resuscitated
IV heparin
25
what is the top differential for a hot and swollen limb?
DVT
localised to calf with tenderness or firmness
or cellulitis
26
how is a DVT diagnosed?
history of pro thrombotic disease
well's score calculation, >1 = USS doppler
27
how is a DVT initially managed?
therapeutic doses of LMWH and then swapped to DOAC for 3-6 months
if iliofemoral DVT with severe sx- urgent vascular review
28
what are some neurological causes of acutely painful limb?
radiculopathies - back pain that radiates to affected area and worse on movement, muscle weakness,paraesthesia, altered reflexes
central causes -MS
spinal causes - disc herniation
peripheral - infective or trauma
29
what is an abdominal aortic aneurysm?
permanent localised dilation of the abdominal aorta of more than 50% of the artery..more than 3cm in diameter
30
what are the risk factors for AAA?
hypertension
hyperlipidaemia
family history
male
increasing age
DM is a negative risk factor
31
what is the aetiology of AAA?
unknown...
atherosclerosis
trauma
infection
CT diseases - marfans, ehler's danlos
inflammatory disease
32
what are the clinical features of AAA?
abdo pain
back or loin pain
general malaise
distal emboli producing limb ischaemia - 6P's
pulsatile mass in abdomen
shock/syncope
33
what is the screening programme for AAA?
national abdominal aortic aneurysm - when 65, men have uss...50% reduction in mortality
34
what is the main differentials for AAA?
main one - renal colic - back pain with no other sx
others - diverticulitis, IBD, IBS, GI haemorrhage, appendicitis, ovarian torsion or rupture
35
which investigations are required for AAA?
USS - to confirm diagnosis
then CT with contrast
36
how do you manage AAA?
medical - if less than 5.5cm monitored with duplex USS, either yearly or 3 monthly. Also conservative tx to reduce CV risk factors - smoking cessation, improved BP control, aspirin and statin, weight loss and increased exercise
surgery - if more than 5.5cm or expanding >1cm/year or symptomatic AAA (if patient unfit left until 6cm before surgery)
--open repair: midline laparotomy or long transverse incision, exposing aorta, clamp proximally and iliac arteries distally, remove segment and replace with graft
--- endovascular repair: introduce graft via femoral arteries and fix stent across the aneurysm
37
what is a complication of endovascular repair of AAA?
endovascular leaking - an incomplete seal forms around aneurysm resulting in blood leaking around graft
38
what are the complications of AAA?
rupture (top)
retroperitoneal leak
embolism
aortoduodenal fistula
39
what are the risk factors for a ruptured AAA?
increased risk exponentially with diameter of aneurysm
smoking
hypertension
female
40
what are the clinical features of a ruptured AAA?
sudden onset of abdo pain and back pain associated with collapse...or mild abdo sx and tenderness over aneurysm - indicate contained retroperitoneal rupture
syncope
vomit
haemodynamically compromised
pulsatile abdo mass and tender
classic triad - flank/back pain,hypotension and pulsatile abdo mass
41
how do you manage a ruptured AAA?
high flow oxygen
IV access (2 large bore cannulae)
urgent bloods - FBC, U and E, clotting, crossmatch for minimum 6U units
BP should be kept below 100mmHg systolic to prevent dislodging the clot and precipitating further bleeding
transferred to local vascular unit
medical (if small AAA) - treat risk fx - smoking, hypertension, hypercholesteraemia, doxycycline (matrix metalloproteinase inhibitor) ans stains can reduce expansion
42
what us the pathway of the femoral catheter for an endovascular repair?
femoral, external, common, abdo aorta, aortic arch
43
what are the differentials for a ruptured aaa?
massive MI or acute pancreatitis - ecg and serum amylase
44
which two factors are considered in treating a ruptured aaa?
size of aneurysm and the general health of patient
45
which two factors are considered in treating a ruptured aaa?
size of aneurysm and the general health of patient
if more than 5.5cm or with an expansion of 1cm/year
46
what is involved in the pre operative assessment of patients with asymptomatic AAA?
- CT or MRI
- haematological and bichemical tests
- chest radiograph and ECG (if ischaemic HD)
- renal assessment if have impairment
- anaesthetic assessment
47
what is the aetiology of peripheral vascular disease?
about 20% of the middle aged population (65-75), only a quarter have sx (intermittent claudication)
48
what do people with severe peripheral vascular disease present with?
critical limb ischaemia
49
what is the pathophysiology of peripheral vascular disease?
atheromatous plaques - atherosclerosis...causes development of atheroma that produces area of narrowig or leads to occlusion of the affected artery
50
what are the risk factors of peripheral vascular disease?
smoking
hypercholesteraemia
hypertension
DM
family history
cardiac disease, cerebrovascular disease - caused by atherosclerosis
51
what is intermittent claudication?
pain in the muscles of lower limbs elicited by walking
affects men over age of 50 the msot
52
what artery is most likely to be affected by intermittent claudication?
superficial femoral artery in adductor canal region
53
how is intermittent claudication relieved?
rapidly relieved by rest for a few mins
54
what is intermittent claudication caused by?
pain is brought on by build up of anaerobic metabolites and pain producing chemicals such as substance P in muscle due to inadequate arterial supply
55
what are the differential diagnosis of intermittent claudication?
- spinal stenosis - cauda equina compression - pain radiates down legs which is made worse by walking and prolonged stading and NOT relieved by rest
- sciatica - lumbosacral root compression
- lower limb arthritis
- musculoligamentous strain
56
what are some complications of intermittent claudication?
if progression (unlikely) ... can lead to amputation ...risk higher in diabetics
57
how do you take a history in a patient with intermittent claudication?
1. where in leg does patient experience pain/cramp?
2.when start?
3. it is relieved by rest
4. what distance can they manage before stop
5. how much does interfere with ADL
6. what risk factors does patient have - smoking, cholesterol, BP, diabetes, IHD, CVD family history)
7. does the patient have any relevant past medical history?
58
how do you examine a patient with lower limb PVD?
inspection - colour of feet/toes, skin breakdown, ulceration, gangrene (inspect inbetween toes and heel)
palpation - temp, assess capillary refill, palpate pulses and check if irregular (afib), rule out abdo aorta aneurysm
auscultation - listen for bruis (aorta,iliac, femoral, adductor canal region), cartoid
59
which investigations are required for pvd?
blood test - anaemia (may precipiate sx of pvd), check glucose(DM), lipids, renal function
ankle brachial pressure index - normal>1.1, arterial disease<0.9 (can be falsely high if have co morbidities)
exercise test - if claudication, measure ABPI pre and post exercise. if a drop in ABP post exercise indicates PVD
arterial duplex scan - areas of stenosis and occlusion
60
how is intermittent claudication treated?
- risk factor modification- smoking cessation, reduce cholesterol with statins, DM, BP
- regular exercise
- antiplatelet therapy - aspirin or clopidorgel....reduces CV mortality
- angioplasty -if claudication bad
- surgical bypass - if angiplasty non successful
- pharmacological - vasoactive type drugs like naftidofuryl (not v beneficial)
61
define critical limb ischaemia
arterial insuffiency results in significant risk of limb loss without intervention..results in nocturnal rest pain...relieved by dangling leg out of bed
may have skin breakdown and gangrene
62
what is the difference between critical limb ischaemia and claudication?
claudication affects single segment disease, but CLI is multi level in arterial tree
63
which treatments are required for critical limb ischaemia?
- angioplasty - can be in conjunction with endarterectomy
- surgical bypass - femoropopliteal, femorodistal, aortobifemoral, axillobifemoral
- amputation - if others have failed, or relieve pain
64
define varicose veins
tortuous, twisted or lengthened veins...trunk veins are most common, affect long and short saphenous veins or their major tributaries
65
how does venous dysfunction usually manifest in the population?
reticular veins (permanently dilated bluish intradermal veins, 1-3mm) or telangiectasias (confluence of permanently dilated intradermal venules of less than 1mm, spider veins)
66
what are the risk factors for varicose veins?
obesity
sitting or standing still for long periods
pregnancy
genetic predisposition
67
what is the aetiology of varicose veins (3)?
1. primary - valvular failure...distended superficial veins (most common)
2. secondary - superficial veins carry reversed flow as a collateral mechanism compensating for obstructed neighbouring deep vein...enlargement and tortuosity
3. arteriovenous fistula - increased high pressure..engorgement and tortuosity of superficial veins
68
what are the symptoms of varicose veins?
cosmetic appearance
discomfort - aching, tension, heaviness and itching..esp after long periods
nocturnal cramps
69
what are the most common complications of varicose veins?
from veins - haemorrhage (due to skin erosion or trauma to varicosity) and thrombophlebitis (thrombosis of varicose veins)
from venous hypertension - oedema, skin pigmentation (increased haemosiderin), eczema, atrophie blanche (white scarring), lipodermatosclerosis (fibrosis of subcutaneous fat), ulceration (necrosis of skin by failing nutritional exchange with capillaries)
70
how do you take a history from someone with suspected varicose veins?
1. what sx
2. any complications - haemorrhage, thrombophlebitis, swelling, discolouration, eczema
3. any concerns (may just need reassurance)
4. hisotry of fracture/surgery or DVT
5. any previous treatment for VV
6. OCP or HRT? (increase risk of VTE post VV surgery)
71
how do you examine a patient with varicose veins?
inspect legs with hip and knee flexed while standing (venous filling)...note the distribution, ie along saphenous system
trendelenburg/tourniquet test (look up)
72
how are varicose veins treated?
open surgery - saphenofemoral disconnection, long saphenous stripping and avulsions
endovenous laser ablation - long or short saphenous
73
what are the 9 types of leg ulcers?
location is important for which type:
1. venous disease - majority
2. arterial - atherosclerosis and arteriovenous malformations
3. vasculitis - SLE, RA, scleroderma, polyarteritis nodosa, wegener's granulomatosis
4. lymphatic insuffiency
5. neuropatic - DM, feet
6. haematological - sickle cell
7.traumatic - burns, pressure sore, radiation
8. neoplastic - basal or squamous cell carcinoma, melanoma
9. others - sarcoidosis, gangrenosum
74
describe the pathophysiology of venous ulcers
chronic venous obstruction or DVT - develop oedema...impaired tissue perfusion as oxygen and metabolites have diffuse over greater distance...tissues around ankle becomes ischaemia and suffer reperfusion injury on walking or elevation of leg...leads to inflammatory process...further oedema and tissue fibrosis
75
how do you perform clinical exams on suspected venous ulcers?
inspect lying and standinh
document size, appearance and site
surrounding skin for signs of venous hypertension
assess pulses and measure ABPI (if more than 0.9 =normal)
76
which investigations are required for suspected venous ulcers?
blood tests - exclude DM and any blood disorders
venous duplex scan
arterial duplex scan in reduced ABPI
swabs for evidence of infection/cellulitis
leg biopsy - skin malignancy
77
how do you effectively manage venous ulcers?
compression bandaging if arterial circulation ok
leg elevation
improved mobility
reduced obesity
improved nutrition
varicose vein surgery
skin grafting
78
what is the most common cause of ischaemic stroke?
thromboembolism due to disease in ICA or MCA
most common site - ICA
79
what is the aetiology of carotid infarction?
1. thromboembolism of ICA/MCA
2. small vessel disease - lacunar infarcts
3. cardiogenic thromboembolism - afib or vegetations or endocarditis
4. haematological - myeloma, sickle cell
5. others - SLE, giant cell arteritis
80
how would carotid disease present?
asymptomatic - detected from bruit
symptomatic = TIA or CVA
81
what is TIA versus CVA?
TIA - acute loss of focal cerebral or monocular visual loss (amaurosis fugax) with symptoms lasting less than 24 hours and no apparent cause other than vascular origin- requires scan within 24 hrs
CVA - ICA disease...anterior circulation infarcts...hemisensory/motor defect affecting face, arm and leg and higher cortical dysfunction (dysphagia, visuspatial neglect)
82
how is carotid disease investigated?
carotid artery duplex scan =portable and non invasive
CT or MRI angiogram
83
how is symptomatic carotid artery disease managed?
treat risk fx - hypertension, smoking,DM, IHD, antiplatelet and statin therapy
carotid endarterectomy ( not always required)
84
how do diabetic arteries appear on USS?
calcified vessels - thickened walls, narrow vessels, poor colour flow definition
85
define ABPI
measure of BP in ankle in comparison to BP in arm...presence and severity of vascular disease in lower limb
1. apply BP cuff to ankle
2. find vessel with doppler
3. inflate cuff to 20mmHg above pressure where pulse no longer heard
4. slowly deflate until pulse returns,
5. measure arm systolic
6. ankle systolic/brachial systolic
<0.3 - CRITICAL LIMB ISCHAEMIA, <0.5 - SEVERE DISEASE, 0.8-0.5 = MODERATE DISEASE, 0.81-1.0 = MILD DISEASE
waveform analysis - triphasic normal, biphasic abnormal, monophasic v bad
86
define cartoid artery disease and its clinical features
build up of atherosclerotic plaque in ICA (dont worry about ECA) or common carotid...stenosis and occlusion
majority asymptomatic, can result in ischaemic stroke (TIA or stroke)
turbulent flow at bifurcation of common carotid predisposes
87
what are the risk fx of carotid artery disease
over 65, smoking, hypertension, hypercholesterolaemia, obesity, DM, history of CVD
88
why might carotid artery disease may be asymptomatic?
supply from contralteral ICA and vertebral arteries via circle of willis
89
what might be found on examination for carotid artery disease?
cartoid bruit in neck
90
give 3 differentials of carotid artery disease
cartoid dissection
vasculitis
thrombotic occulsion of Carotid
91
which initial investigations are required for carotid artery disease?
CT head or CT angiography
bloods - FBC, U and E, clotting, lipid profile, glucose
ECG - afib
duplex USS - degree of stenosis
92
how should stroke be managed?
both - high flow oxygen, blood glucose optimised, swallowing screen assessment
ischaemic - IV atelplase and aspirin
haemorrhagic - correction of any coagulopathy and refer to neurosurgery
93
what does cartoid endarterectomy involve and the main complications?
removing atheroma and associated damaged intima
stroke, nerve damage to hypoglossal or vagus, infection
94
what are the long term complications of cartoid artery disease-> stroke?
dysphagia
seizures
incontience
depression
cognitive decline
95
define aortic dissection
tear in the intimal layer of the aortic wall causing blood to flow between and splitting apart the tunica intima and media
96
what are the two types of aortic dissection?
acute (diagnosed within 14 days)
chronic (diagnosed beyond 14 days)
97
what are the risk factors for aortic dissection?
men
connective tissue disorders
50-70 yrs
atherosclerotic
hypertension
bicuspid aortic valve
98
define anterograde and retrograde dissections
anterograde - progagate towards iliac arteries
retrograde - propagate towards aortic valve
99
how are aortic dissections classified?
stanford and debakey
100
what are the clinical features of aortic dissection?
tearing chest pain..radiate to back
tachycardia
hypotension
aortic regurg murmur
101
what investigations are required for suspected aortic dissection?
baseline bloods- FBC, u and e, LFT, troponin, coagulation, cross match, ABG, ECG
CT angiogram
102
how do you manage aortic dissection?
high flow oxygen
gain IV access
fluid resuscitation
may require surgery - removal of ascending aorta and replacmenet with synthetic graft
hypertension management - IV beta blockers
103
what are the complications of aortic dissection?
aortic rupture
aortic regurg
MI
cardiac tamponade
stroke
104
define aneurysm
persistent, abnormal dilation of an artery to 1.5 times its normal diameter
105
what is a thoracic aortic aneurysm?
involves ascending aorta or root (majority)
aortic arch
descending aorta
thoracoabdominal aorta segments
106
what is the aetiology of thoracic aortic aneurysm?
degradation of the tunica media...artery loses structural integrity and dilates
107
what are the main causes of thoracic aneurysm?
connective tissue disorders
bicuspid aortic valve
107
what are the main causes of thoracic aneurysm?
connective tissue disorders
bicuspid aortic valve
108
what are the main risk factors for thoracic aneurysm?
family history
hypertension
atherosclerosis
smoking
high BMI
male
increased age
109
what are the clinical features of thoracic aneurysm?
can be asymptomatic
if in ascending aorta - anterior chest
aortic arch - neck
descending aorta - between scapula
other sx - hoarse voice, distented neck veins, sx of HF, dyspnoea
110
what is the amin investigation performed for thoracic aneurysm?
CT chest scan with contrast
111
how is thoracic aneurysm managed?
statin and anti platelet therapy - decrease risk of MI
blood pressure control
smoking cessation
112
what is the prognosis of thoracic aneurysm?
developed second aneurysm
113
how do you initially manage acute limb ischaemia?
high flow o2
therapeutic dose heparin
monitor APPT
114
what surgical management is available for ALI?
embolectomy
thrombolysis
bypass surgery
angioplasty
if irreversible - mottled non blanching appearance with hardy woody muscles
115
what are the complications of acute limb ischaemia?
compartment syndrome
release of substances from damaged muscle cells - causing hyperkalaemia and acidosis and myoglobin causing AKI
116
define chronic limb ischaemia
peripheral arterial disease that results in symptomatic reduced blood flow to the limbs
caused usually by atherosflerosis
117
how can chronic limb ischaemia present?
asymptomatic...intermittent claudication...ischaemic rest pain...ulceration or gangrene (increased severity)
118
ABPI for critical limb ischaemia
<0.5
119
what is a differential for acute limb ischaemia?
spinal stenosis - neurogenic claudication
120
what are soem complications of critical limb ischaemia?
acute on chronic ischaemia
amputation
reduced mobility and quality of life
121
mesenteric ischaemia
generalised abdo pain out of proportion to findings, N+V, non specific tenderness
ABG, routine blood tests, CT scan with contrast (oedematous bowel)
urgent rescuscitation, abx, excision of necrotic bowel, revascularisation of bowel, can result in necrosis
122
what are the common site for peripheral aneurysms?
popliteal artery
123
define deep venous insuffiency
occurs as a result of failure of venous system (DVT or valvular insuffiency), characterised by valvular reflux, venous hypertension, and obstruction (Plus varicose veins)
124
define deep venous insuffiency
occurs as a result of failure of venous system (DVT or valvular insuffiency), characterised by valvular reflux, venous hypertension, and obstruction (Plus varicose veins)
124
define deep venous insuffiency
occurs as a result of failure of venous system (DVT or valvular insuffiency), characterised by valvular reflux, venous hypertension, and obstruction (Plus varicose veins)
124
define deep venous insuffiency
occurs as a result of failure of venous system (DVT or valvular insuffiency), characterised by valvular reflux, venous hypertension, and obstruction (Plus varicose veins)
125
what are the risk factors for deep venous insuffiency?
age, female, pregnancy, prevous DVT, obesity, smoking
126
what are the clinical features of deep venous insuffiency?
chronically swollen limb, aching, pruritic, painful, venous claducation (bursting pain and tightness on walking),
physically = varicose eczema, thrombophlebitis, haemosiderin etc
127
how is DVI managed?
compression stocks
analgesia
no point in valvuloplasty
128
what are some complications of DVI?
swelling
recurrent cellulitis
chronic pain and ulceration
DVT
varicose veins
