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Surgery > Vascular surgery > Flashcards

Vascular surgery Flashcards

1
Q

Risk factors for PVD

A

Male, age 60-70, smoking, DM, HTN, high cholesterol, obesity, sedentary

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2
Q

Intermittent claudication

A

Chronic LL arterial insufficiency - pain on walking a reproducible distance, worse uphill, forced to stop then pain stops, recurs at same walking distance
Usually worse in one limb
Leriche syndrome - impotence (may be ass)
Peripheral pulses reduced/absent on affected side, trophic skin changes rare
Majority stay same/improve, some need surgery, some need amputation
Marker of CAD

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3
Q

Chronic ischaemic rest pain

A

Severe arterial obstruction, usually v severe and burning, worse at night, relieved by hanging foot off bed
May also have tissue loss

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4
Q

How does acute critical ischaemia present?

A

Pain - sudden onset
Pallor - white, then mottled due to stagnated deoxygenated blood, if doesn’t blanch on pressure is not viable
Pulseless - foot pulses absent, femoral/popliteal may also be gone
Perishing coldness
Paraesthesia - severe sign
Paralysis - of calf muscles, severe

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5
Q

What skin changes may be seen in PVD?

A

Trophic changes - esp gaiter area. Like atrophic red skin
Chronic venous disease - venous eczema, haemosiderin deposits (red cells extravasate into tissue due to raised pressure), lipodermatosclerosis, ‘champagne bottle leg’
Colour - blue toes (pre-gangrene), black toes (necrosis-dry gangrene, if infected wet gangrene), redness (implies oxygenated blood in caps)
Ulceration

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6
Q

What may cause leg swelling?

A

Local - sluggish venous return (immobile, pregnant), lymphatic obstruction tropical disease, chronic venous insufficiency (causing superficial venous reflux), congenital e.g. Milroy’s, acute obstruction of venous return

Regional - LVF, venous obstruction by pelvic mass, radiation destruction, IVCO

Systemic - CCF, low albumin, fluid overload

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7
Q

What is the relevance of u/l and b/l leg swelling?

A

B/l more likely central cause

U/l more likely surgical

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8
Q

Upper limb swelling

A

Axillary vein thrombosis - from excess use or cervical rib obstructing
May also be blue, heavy, prominent collateral veins
Usually goes away

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9
Q

Upper limb acute white/blue colour

A

Embolism/trauma to brachial a

May also have the 6 Ps

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10
Q

White fingers

A

Raynaud’s disease (white - blue - red from vasospasm), or secondary Raynaud’s phenomenon e.g. to SLE, Sjogren’s

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11
Q

Red painful fingers

A

Reflex sympathetic dystrophy after trauma

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12
Q

Vascular pain upper limb

A

Subclavian a narrowing (usually asymptomatic, may get muscle pain on exercise)
Or acute ischaemia from a cardiac thrombus

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13
Q

Upper limb neurovascular pain

A

Thoracic outlet syndrome - C8/T1

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14
Q

Severe LL ischaemia (chronic)

A

Usually w/o IC, usually older less active patients
Rest pain, trophic skin changes, ischaemic ulcers between toes/pressure areas, positive Buerger’s test
Most progress to necrosis - infection + wet gangrene - sepsis so do surgery before this

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15
Q

How does spinal stenosis present?

A

Pain relieved by sitting not standing, worse going downhill as more pressure on nerve roots
Pain goes down lateral leg in the TFL

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16
Q

What is Buerger’s test?

A

Raise leg, goes pale at <20 degrees is positive, then hang legs over bed again it becomes very red

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17
Q

What is critical limb ischaemia?

A

Arterial insufficiency so bad that it threatens limb viability. Persistently recurring rest pain needing analgesia for >2w, or ulceration/gangrene with ABPI <0.5. Limb pale, cold, pulseless, hair loss, skin change, thickening of nails

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18
Q

Interpretation of the ankle brachial pressure index

A

Ankle/brachial systolic pressure (ankle usually slightly above arm).
Normal: 0.9-1.2
>1.2: calcification in diabetics prevents cuff compression
0.8-0.9: mild disease
0.8-0.5: moderate, severe IC
<0.5: critical ischaemia, rest pain
<0.2: gangrene + ulceration

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19
Q

What are the commonest sites for peripheral arterial disease?

A

Superficial femoral a
Common iliac arteries
Patchy disease beyond the popliteal trifurcation

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20
Q

How would you manage a patient with chronic LL ischaemia?

A

Medical - lifestyle, statins for all, anti platelet (clopidogrel), optimise DM control

Surgical - when exercise hasn’t improved symptoms or in critical limb ischaemia. For single regions angioplasty + stenting, for diffuse disease bypass grafting, if incurable/sepsis amputation

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21
Q

What is acute LL ischaemia?

A

Sudden reduction in limb perfusion that threatens its viability

Common sites are aortic bifurcation (saddle embolus), CFA bifurcation + popliteal trifurcation

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22
Q

What is the cause of acute LL ischaemia?

A

Thrombosis - most common. Atheroma plaque ruptures, acute or acute-on-chornic. E.g. popliteal aneurysms

Embolism - thrombus from a proximal source occludes a more distal artery, ischaemia worse as fewer collaterals distally. Causes include mitral stenosis, AF, post-MI, AAA, prosthetic valve.

Less common - trauma e.g. compartment syndrome, hyper coagulable states

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23
Q

Describe the Rutherford classification for acute limb ischaemia

A

I - viable, no sensory/motor loss, Dopplers audible

IIA - marginally threatened prompt treatment, minimal sensory loss, no motor loss, arterial doppler inaudible

IIB - immediately threatened. more sensory loss, rest pain, mild-moderate motor deficit, inaudible arterial doppler

III - irreversible. Major tissue loss, profound sensory + motor deficits, both arterial + venous dopplers inaudible

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24
Q

Outline the management of acute limb ischaemia

A

High flow O2, heparin bolus + infusion
Rutherford I and IIa - prolonged course of heparin and r/v
IIb and beyond - surgical. E.g. embolectomy, thrombolysis, angioplasty, bypass. If irreversible urgent amputation or palliative (mottled, non-blanching, woody muscles)

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25
Q

How do diabetic foot ulcers develop?

A

Neuropathy - microangiopathy affecting sensation, motor (distorted weight bearing) + autonomic (less sweating + vascular control)
Arteriovenous communications beneath skin
Glucose-rich tissue allows bacterial growth
Obliterative atherosclerosis - DM predisposed to this and occurs younger

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26
Q

How might a foot ulcer in a diabetic patient present?

A

Neuropathic - painless, red, warm, strong pulses
Atherosclerotic - pale, painful, cold, pulseless
Or both together e.g. can be v ischaemic but painless
Ulcers often between toes, infection with S aureus, spreads along tendon sheaths, painless necrosis of individual toes
Pressure points

Osteomyelitis is a complication

27
Q

How are diabetic foot ulcers managed?

A

Infection - AB, dressing, IV AB if systemic, excise necrotic tissue, blood glucose control
Debridement/revascularisation/amputation

28
Q

Describe the venous system of the LL

A

Deep - within muscles, muscle contraction pumps blood up against gravity, valves stop retrograde flow
Superficial - drain above the deep fascia. Great saphenous (antero-medial, goes into FV) and small saphenous (posterior, goes into popliteal). No muscle pump, valves at SPJ + SFJ usually enough
Interconnecting superficial veins
Perforating veins drain superficial into deep

29
Q

Why does thrombosis develop?

A 
Venous stagnation (less arterial replenishment of caps)
AV shunts direct blood away from dermal caps
Venous HTN - plasma proteins leak - interference in metabolic exchange
30
Q

What is chronic deep venous insufficiency?

A

After a DVT, clot undergoes inflammation, organisation + recanalisation of the vein - valves damaged - reflux downwards

31
Q

What clinical signs are there in a post-thrombotic limb?

A

Chronic LL oedema
Varicose veins
Haemosiderin deposition in gaiter area - venous eczema
Ulceration
Lipodermatosclerosis - collagenous scar tissue instead of soft SC fat - champagne bottle leg
Venous HTN

32
Q

Superficial vein thrombosis

A

Spontaneous thrombosis, usually in VVs, causes inflammation, more in pregnancy, thrombophlebitis migrans (cancer).
Rapid onset acute pain, varicose veins, erythematous/oedematous skin, hard veins
Tx: NSAIDs, may need ligation at junction with deep vein to prevent spread

33
Q

Deep vein thrombosis

A

Pain, swelling in calf/ankle, pain on DF (Homan’s sign), warm leg, pulses may be impalpable from oedema, swollen thigh in iliofemoral veins
Often asymptomatic

34
Q

Axillary vein thrombosis

A

Uncommon

Sudden onset limb swelling, aching pain, bluish tinge, normal sensation, may be ass w thrombophlebitis migrans, TPN …

35
Q

Why do varicose veins develop?

A

Dilated tortuous prominent segments of superficial veins due to failure at SFJ - uninterrupted column of blood dilates superficial veins - most in long saphenous

Majority idiopathic. Rarer causes - DVT, pelvic mass (preg, fibroids, ovarian mass)

RFs: women + pregnancy (progesterone changes collagen smooth muscle + pressure on pelvic veins by the foetus), obesity, prolonged standing

36
Q

Clinical features of varicose veins

A

Aching legs after standing, heaviness, tension, cosmetic issues, ankle oedema, recurrent superficial thrombophlebitis, skin changes, saphena varix (dilatation of SV @ SFJ, cough impulse so mistaken for FH)

37
Q

Management of varicose veins

A

Cons: avoid prolonged standing, lose weight, exercise to improve muscle pump, compression stockings, if have venous ulcers need graduated compression banding

Surgery: if symptomatic, have LL skin changes, superficial vein thrombosis (hard and painful). E.g. vein ligation stripping + avulsion, thermal ablation

38
Q

How are venous ulcers caused?

A

Venous insufficiency - retrograde flow in superficial system - distal pooling of blood - less O2 delivered

This may be due to calf muscle failure, DV incompetence, volume overload from superficial incompetence

39
Q

How do venous ulcers present?

A

Shallow, irregular borders, granulating base, often in gaiter area, dry itchy skin, distended veins, less painful than arterial (usually not), occur over m-y, more likely to be friable

40
Q

How are venous ulcers managed?

A

Elevate legs, exercise, emollients for dry skin, 4-layered compression banding (ABPI must be >0.7), radio frequency ablation

41
Q

How do arterial ulcers present?

A

Small deep lesions, well-defined borders, necrotic base, often distally at sites of pressure/trauma, likely to have IC/CLI, develop over a long time without healing so no granulation tissue, may have signs of CLI. If purely arterial sensation is maintained

42
Q

What are the clinical features of neuropathic ulcers?

A

Burning/tingling, variable size, punched out appearance, hyper-keratinised edges, necrotic crater, may have glove + stocking sensory losses, warm feet + good pulses (unless also arterial!)

43
Q

Charcot’s foot?

A

Loss of joint sensation in DM - unnoticed trauma + deformity - predisposes - swelling, distortion, distortion, pain, loss of function, loss of transverse arch (‘rocker bottom’)

44
Q

Non-vascular causes of leg ulcers

A

Haem - polycythaemia rubra vera, sickle cell anaemia
Trauma - burns, cold, pressure, radiation
Neoplastic - BCC, SCC, Marjolin’s ulcer, Bowen’s disease
Sarcoidosis, tropical ulcers, pyoderma gangrenosum

45
Q

True vs false aneurysm?

A

True aneurysm - pathological degeneration of vessel wall

False - leakage of blood out of an artery into a cavity surrounded by CT, expansile + pulsatile

46
Q

Causes of aneurysms?

A 
Congenital - berry aneurysm on CoW (can cause SAH)
Degenerative - atheroma
CT disease - Marfan's, EDS
Infective - syphyllis
Dissection
Trauma
Inflammation e.g. Takayasu's aortitis
47
Q

What is a AAA?

A

Dilatation of abdominal aorta >3cm

48
Q

How do AAAs present?

A

Most asymptomatic
CF include abdominal/back/loin pain, distal embolisation causing limb ischaemia, malaise, WL
Complications: rupture, retroperitoneal leak, embolisation, aorta-duodenal fistula

49
Q

What is the AAA screening programme?

A

A one off abdominal USS for men aged 65
If 3-4.4cm monitor yearly
If 5-5.4cm monitor 3 monthly
If >5.5cm/symptomatic/expanding more than 1cm per year surgery

50
Q

Possible CF of thoracic aortic aneurysms

A

CF of Marfan’s/EDS (degradation of tunica media) as commonest cause, or bicuspid aortic valve

Pain (anterior-ascending, neck-aortic arch, between scapulae-descending), back pain from compression, hoarse voice (arch-damage to LRLN), distended neck veins (SVC compression), symptoms of HF, dyspnoea/cough from tracheal/bronchial compression

51
Q

Aneurysms in peripheral arteries

A

Popliteal-commonest, high risk of embolus. Acute limb ischaemia or IC, rupturing rare, pulsatile mass in PF. Need treating if >2cm/symptomatic

Femoral-due to percutaneous vascular interventions + IVDU, may have infection/thrombosis/rupture/embolus. Open surgical repair

Splenic-commonest visceral, RF if female portal HTN multiparous pancreas issues. Vague epigastric/LUQ pain, if ruptures severe. Endovascular repair + embolisation/stent graphs

Hepatic-percutaneous instrumentation, trauma, post-transplant (false aneurysm around vessel anastomoses). RUQ/E pain, jaundice if biliary obstruction. Repair

Renal-often asymptomatic, may cause haematuria/resistant HTN/loin pain

52
Q

Aortic dissection?

A

Tear in intimal layer of aortic wall - blood gets between the layers - splits them. Acute or chronic, may progress towards iliac arteries (distal) or towards aortic valve (retrograde)

RF: HTN, atherosclerosis, CT disease like margans, bicuspid aortic valve

53
Q

How does aortic dissection present?

A

Tearing/stabbing CP, may radiate to back
Tachycardia, hypotension, new AR murmur (decrescendo diastolic), signs of end-organ hypoperfusion
Neuro sequelae

Complications: aortic rupture, AR, myocardial ischaemia, cardiac tamponade, stroke/paraplegia from cerebral/spinal artery involvement

54
Q

Management of aortic dissection

A

o Type A: involve ascending aorta, aortic arch and can propagate to descending aorta, includes DeBakey types I and II. Worst prognosis. Surgery to remove ascending aorta, replace w synthetic graft, may need to repair aortic valve, reimplantation of aortic arch branches into the graft
o Type B: dissections don’t involve ascending aorta, include DeBakey type III. If uncomplicated best to manage medically (manage HTN with beta blockers, CCB second line), endovascular repair with stent graft maybe, can become chronic with continued leakage
o Long term: lifelong anti-HTN therapy and surveillance imaging

55
Q

What are the causes of acute mesenteric ischaemia?

A

Embolism - AF, post-MI, prosthetic valve, AAA, TAA
Thrombus in situ - atherosclerosis
Non-occlusive - hypovolaemia or cariogenic shock
Venous occlusion - coagulopathy, cancer, inflammation

56
Q

How does acute mesenteric ischaemia present?

A

Abdominal pain - diffuse
N+V
Later stage may have bowel necrosis - perforation
Acidosis, raised amylase

57
Q

Management of acute mesenteric ischaemia?

A

IV fluid resus, catheter fluid balance, broad spec ABs

Excision of necrotic/non viable bowel, or revascularisation of bowel

58
Q

Chronic mesenteric ischaemia?

A

Atherosclerosis in CT/SMA/IMA (usually at least 2 are affected for symptoms) - ischaemic bowel - increased demand to supply

CF: postprandial pain, WL, concurrent vascular issues, diarrhoea, N&V

M: medical (anti platelet, statin, stop smoking, exercise), endovascular mesenteric angioplasty if bad

59
Q

Ruptured AAA?

A

Risk increased with smoking, female, HTN + diameter.
Most rupture retroperitoneally, 20% go intraperitoneal which is really bad
CF: abdo/back/flank pain, syncope, hypotension, pulsatile abdo mass
M: high flow O2, 2 large bore cannulae, bloods inc XM for minimum 6 units, permissive hypotension (keep BP <100 as too high will dislodge clots), if unstable open repair, if stable CT angiogram to see if can do endovascular

60
Q

Vascular trauma to limb

A

C: penetrating wounds, blunt trauma, iatrogenic, # e.g. supracondylar, knee dislocation

Signs: external arterial bleeding, rapidly-expanding haematoma, palpable thrill, audible bruit, obvious acute limb ischaemia, weak u/l pulse, neurogenic defect

Fluid resus, preserve saphenous + cephalic veins for repair, most need surgery

61
Q

Acutely painful limb

A

The 6Ps - acute limb ischaemia
Hot + swollen - DVT, cellulitis, other MSK infections
Traumatic
Neuro - radiculopathies, central e.g. MS, spinal e.g. infection

62
Q

Thoracic outlet syndrome

A

Compression of NV bundle within thoracic outlet in middle aged, usually due to rib anomalies/muscular anomalies/hyperextension/repetitive stress/#clavicle

Thoracic outlet is apex of axilla, NV contents here are axillary artery (claudication, ALI), axillary vein (AV thrombosis, swelling-Paget Schrotter syndrome), brachial plexus (parenthesis, motor weakness)

CXR for bony abnormalities (aTOS), duplex USS (vTOS/aTOS), n conduction studies

Most conservative e.g. physio, botulinum injections (neurogenic), anti-coag in aTOS

In urgent e.g. ALI obv need surgery

63
Q

Chest vascular trauma

A

Most damage descending thoracic aorta @ isthmus
May cause tension pneumothorax or cardiac tamponade - both can cause cardiac arrest
Stent graft

64
Q

Retroperitoneal bleeds

A

E.g. pelvic #, iatrogenic, spontaneous

Hypotension, fall in Hb, lower back pain, iliac fossa mass/tenderness

Surgery (5 decks)

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