JC01 (Surgery) - Vein diseases Flashcards
Describe the course of the great saphenous vein
□ Arises from medial side of dorsal venous
arch of foot
□ Ascends immediately anterior to medial
malleolus together with saphenous n.
□ Runs up leg posteriorly to run posterior to
medial femoral condyle
□ Ascends obliquely up medial thigh
□ Empties at saphenofemoral junction (SFJ)
into femoral vein (deep venous system)
Define location of the saphenofemoral junction (SFJ)
→ 2.5cm below and lateral to pubic
tubercle
Describe the course of small saphenous vein
□ Arises from lateral side of dorsal venous arch of foot
□ Ascends posterior to lateral malleolus
□ Ascends along midline of posterior leg accompanied
by the sural nerve
□ Empties at saphenopopliteal junction (SPJ) into
popliteal vein (deep venous system)
Function and locations of perforating veins
Penetrate deep fascia to form communication between deep and superficial venous systems
→ SFJ and SPJ → Hunterian perforator at proximal thigh → Dodd’s perforator at distal thigh → Boyd’s perforator around knee level → Cockett’s perforators at 5, 10, 15cm from medial malleolus
Define chronic venous insufficiency
ambulatory venous hypertension
arises from congenital, primary or secondary causes (Etiology)
giving rise to reflux or obstruction or both (Pathophysiology)
in deep or superficial veins (Anatomy)
Risk factors of chronic venous insufficiency (7)
□ Gender: F>M
□ Age
□ Stature: ↑with BMI and height
□ Pregnancy: hormone-related weakness in venous wall
□ Occupation: long periods of standing
□ Family Hx: 50% if 1 parent, up to 80% risk if both parents
□ Causes of deep venous obstruction, eg. pelvic tumours
Symptoms of chronic venous insufficiency (5)
Symptoms:
□ Disfigurement
□ Pain: dull, in calf and lower leg (eg. nocturnal cramps)/ throughout day/ with prolonged standing
□ Pitting ankle oedema
□ Skin manifestations: hyperpigmentation, eczema, lipodermatosclerosis
□ Venous ulcer
Complications of varicose veins
→ Bleeding (due to thinning of skin)
→ Thrombosis (due to tortuosity of veins)
→ Superficial thrombophlebitis: red, painful tender lumps
→ Cellulitis
→ Other skin changes: eczema, lipodermatosclerosis, ulcerations
3 major etiologies of ambulatory venous hypertension
Primary (majority): inherent/ congenital weakness in venous walls
Secondary: Post-thrombotic
- Thrombosis obstruct deep veins
- WBC removal of thrombus cause valvular destruction and insufficiency
Postural/ Prolonged standing: increase venous pressure and dilatation
Explain regulation of venous pressure in lower limb
Normal venous pressure in foot ≈ 100mmHg
(column of blood from heart)
Muscle pump required to return venous
blood to heart → ambulatory venous BP ≈20-30mmHg
Flow of venous blood in lower limb during muscle contraction and relaxation?
1) Muscle contraction
→ deep veins compressed
→ blood ejected proximally
2) Muscle relaxation
→ ↓deep venous pressure
→ blood inflow from superficial veins via perforating veins
Explain pigmentation, edema and inflammatory changes in CVI
□ Pigmentation due to extravasation of RBC and hemoglobin
□ Pitting oedema due to extravasation of fluid and overloading of lymphatics
□ Inflammatory changes due to extravasation of WBC and plasma protein
→ Result: itchiness, skin thickening and ulcers
Varicose veins = chronic venous insufficiency. True or False? Why?
False
- VV is merely a reflection of the status of superficial veins
- Presence of VV often does NOT correlate with other
clinical manifestations of ambulatory venous HTN - VV should not be understood as the (sole) cause
or ‘precursor’ of more severe CVI manifestations
Causes of varicose veins
□ Primarily perforator incompetence → reflux of blood into superficial veins and dilatation
□ Primarily deep vein reflux/obstruction → perforators gradually become incompetent → reflux of blood into superficial veins → dilatation
□ Primarily superficial vein reflux/obstruction (uncommon)
Classification for clinical manifestations of CVI?
CAEP Classification: Clinical
C1 = Telangiectasia/ reticular veins C2 = Varicose veins C3 = Unilateral pitting Edema C4 = Pigmentation, eczema, dermatosclerosis C5 = Healed ulcer C6 = active ulcer
Investigations for chronic venous insufficiency
Venous duplex ultrasound**: for incompetent perforators and venous reflux
Handheld continuous wave Doppler: at SFJ and SPJ
Options for conservative treatment of CVI
1) Foot care
- Encourage: walking, running on the spot, tiptoe exercise
- Avoid: standing still, tight clothing constricting pelvis/hip, heavy lifting
2) Graduated compression stocking: prefer class 2 elastic stockings
3) Venoactive drugs, eg. Daflon, Paroven, Escin
Increase venous tone
Surgical options for local varicosities?
Treatment of local varicosities (cosmesis only)
→ Stab avulsion for branch varicosities
→ Injection sclerotherapy for reticular veins
→ Surface laser therapy for telangiectasiae
Open and Minimally invasive surgical options for severe CVI?
1) Ligation/ Stripping/ Stab avulsion of incompetent perforators: at SFJ, SPJ or other perforators
2) Ablation of diseased veins: MMI
- Thermal: endovenous laser therapy (EVLT), radiofrequency ablation (RFA)
- Non-thermal: microfoam sclerotherapy, mechanical-chemical ablation (eg. ClariVein)
Describe venous ulcer:
- site
- shape
- edge
- base
- depth
- discharge
- surrounding skin
→ Site: gaiter area of lower leg (medial distal 1/3 of leg)
→ Shape/size: irregular
→ Edge: gently sloping, pale pink (when healing)
→ Base: usually fixed to deep tissues
- Yellow slough
- Pink granulation tissue (when healing)
- Whitish fibrous tissue (if chronic and indolent)
→ Depth: shallow
→ Discharge: seropurulent or blood-stained
→ Surrounding skin: signs of CVI
Differential diagnosis of leg ulcers
□ Arterial: signs of PAD (gangrene, trophic changes), very painful, at pressure areas
□ Venous: signs of CVI, good pulse, less painful, at gaiter area
□ Neurogenic: painless, signs of neuropathy
□ Malignant: irregular, everted edges, lymphadenopathy
□ Infectious (rare): chronic osteomyelitis, syphilis
□ Traumatic
Describe malignant changes for chronic venous ulcers
Marjolin’s ulcer:
→ Aggressive SCC arising from long-standing
venous ulcer
→ Suggestive features
- Enlarged
- Became painful and malodorous
- Raised or everted edge
- Lymphadenopathy
Management of venous ulcers
□ Posture: Elevation leg to lower venous pressure
□ Ulcer: analgesics, antibiotics, compression bandage
□ Skin graft over ulcer
□ Surgical Tx:
- Venous surgery for superficial venous reflux
- Venous reconstruction for deep venous reflux (rarely done)
Pathophysiology of CVI (2 mechanisms)
- Venous reflux
Defined as >0.5s of reverse flow detected by duplex scans due to valvular insufficiency - Venous obstruction
May occur in deep veins (DVT, pelvic tumours) or
superficial veins
When resolved, may result in damage of valves leading to secondary reflux
Clinical features of DVT? (3)
Phlebothrombosis (blood clot in a vein that is not inflamed)
Thromboplebitis (clot in vein with inflammation)
Venous gangrene
Specific sign used for clinical diagnosis of DVT
Homan’s sign
positive Homans’s sign: calf pain at dorsiflexion of the foot
Investigation of DVT
Venous duplex ultrasound: constant flow not augmentable by compression
Venogram
Complications of DVT
- Pulmonary embolism (commonly from ilio-femoral or proximal vein DVT)
- Venous hypertension causing chronic venous insufficiency/ obstruction
Which leg more susceptible to DVT and why?
Left leg
Due to anatomical compression of left iliac vein by right common iliac artery
4 goals of DVT treatment
Prevent pulmonary embolism
Relieve acute symptoms
Prevent recurrent DVT
Prevent post-thrombotic sequelae
Treatment modalities for DVT
- Bed rest
- Leg elevation to reduce venous pressure
- Anticoagulant therapy
- Catheter-directed thrombolysis
- Venous thrombectomy + stenting
Outline anticoagulant therapy for DVT
Heparin 5 days
Low-molecular-weight heparin or NOAC for 3-6 months
Post-operative management of DVT
Avoid stasis: physical exercise, pneumatic or stocking compression, posture
Avoid trauma
Avoid coagulability by heparin/ anti-coagulants
Treatment of recurrent pulmonary embolism despite anticoagulation therapy?
IVC filter insertion
