Ciculation and lymphatic systems Flashcards
Signs of chronic venous insufficiency
L - lipodermatosclerosis
E - eczema
G - gaps in the skin (ulceration)
S - swelling
Indications for preoperative Duplex USS of varicose veins?
- DVT history
- signs of chronic venous insufficiency
- recurrent varicose veins
- to clarify SSV or LSV incompetency
Varicose veins treatment
Conservative
- education (avoid prolonged standing and elevate legs)
- grade II graduated elastic compression stockings
- weight loss, regular exercise
Endovascular
- sclerotherapy - 1% sodium tetradecyl sulphate (liquid or foam)
- radiofrequency ablation (catheter in vein and heated to 120C)
- Endovascular ablation
Surgical
- Trendelenburg procedure (saphenofemoral ligation)
- multiple avulsons
- strippling from groin to upper calf
(post op - bandage tightly and elevate for 24 hours)
Syndrome associated with varicose veins
Kippel-Trenaunay-Weber syndrome - varicose veins - port wine stains - bony + soft tissue hypertrophy of limbs - significant oedema Parkes-Weber syndrome - multiple AV fistulae - limb hypertrophy - can lead to high output cardiac failure
Venous ulcer causes
Deep venous insufficiency
- Valvular disease: varicose veins, deep vein reflux, communicating vein reflux
- Outflow tract obstruction: post-DVT
- Muscle pump failure: primary (stroke, neuromuscular disease), secondary (musculoskeletal pathology/ankle injury)
Venous ulcer treatment
Non-surgical: 50-70% healed at 3mths, 80-90% at 12mths
- avoid trauma
- four-layer compression bandaging
- rest and leg elevation
- once healed, grade II compression stockings for life
Surgical
- if ulcer fails to heal, exclude other causes +/- biopsy
- debridement + split skin graft
- if due to primary varicose veins, treat them
Four-layer compression bandaging layers
- non-adherent dressing over ulcer plus wool bandage
- crepe bandage
- blue-line bandage
- adhesive bandage to prevent other layers slipping
How to measure ABPI
- inflate cuff over upper arm, measure systolic pressure with doppler at brachial artery
- inflate cuff over calf, measure systolic pressure with doppler at dorsalis pedis
- find doppler sound, inflate cuff till disappears, slowly deflate till sound restarts = sys pressure
- ankle/brachial = ABPI
Significance of ABPI
normal = 1
claudication 0.6-0.9
rest pain 0.3-0.6
impending gangrene 0.3 or less
What foot pathology are diabetics prone to?
- diabetic neuropathy
- peripheral occlusive arterial disease
- Charcot neuroarthropathy
- osteomyelitis
- foot ulceration
Can lead to amputation
Aetiology of diabetic foot ulcers
- neuropathic (45-60%)
- ischaemic (10%)
- mixed neuroischaemic (25-45%)
Diabetic neuropathy is due to (1) microvascular disease leading to nerve hypoxia, and/or (2) direct effects of hyperglycaemia on neuronal metabolism
Why might ABPI be normal/higher in diabetics?
Calcification of the walls of the vessels - prevents cuff compressing vessels = abnormally high ABPI.
Also seen in CRF
Differences in peripheral vascular disease in diabetics?
- Intra-arterial digital subtraction angiography indicated earlier.
- Aggressive treatment of infections
- Meticulous foot care + chiropodist
- Sepsis treated with surgical debridement
Are their any problems with diabetics undergoing angiography?
- if renal impairment, can be dramatically worsened by intra-arterial contrast
- well-hydrate patients with IV fluids peri-procedure
- stop metformin
Indications for amputation
4 D’s
- Dead (ischaemic): PVD, thromboangitis obliterans, AV fistulae
- Damaged (trauma): unsalvageable limb, burns, frostbite
- Dangerous (malignancy): bone, soft tissue
- Damn nuisance (infection/neuropathy): osteomyelitis, nec fasc, charcot neuropathy
Complications of amputations
Patients often have other medical problems which increases risk. Operative mortality 20%, 1 year 50% Early - psychological + social - haematoma + infection - DVT + PE - phatom limb pain - skin necrosis Late - osteomyelitis - stump ulceration - stump neuroma - fixed flexion deformity - difficulty mobilising - spurs + osteophyte formation
Intermittent claudication differential
Leg pain can be dividied into:
- Musculoskeletal: specific joint pathology e.g. OA
- Neurological: spinal stenosis (leading to spinal claudication)
- Vascular: intermittent claudication, DVT
Why do patients with rest pain typically get more severe pain at night?
Reduction in perfusion due to:
- reduced effect of gravity lying down
- reduced cardiac output at night
- dilation of skin vessels due to warm bedding
In which patients are AAA most common
- men
- > 60
- smokers
- hypertensives
- family history
Who should have AAA’s repaired?
- symptomatic aneurysms (back pain, tenderness, distal embolic events, rupture/leak)
- asymptomatic (>5.5 cm diameter, increase >1 cm per year)
- 10% risk of rupture per year for aneurysm >5.5cm
Alternative to open AAA repair?
Endovascular repair is equivalent to open repair for overall survival but has higher rate of secondary interventions. Good for high operative risk patients as less invasive
Screening for AAA
One-time USS for men >65
Re-screen
3.0-4.4cm yearly
4.5-5.4cm 3monthly
Investigations for carotid bruit
- Urinalysis: protein
- ECG: AF, ischaemia, LVH
- Bloods: FBC, U+Es, glucose, lipids
- Carotid duplex scan
- Carotid angiography (2% stroke risk)
- MRA
- Echo
- CT/MRI brain: looking for old infarcts
Consequence of carotid stenosis?
85% stokes thromboembolic caused by artherosclerosis at carotid bifurcation