MBBS IV WCS 001 – Varicose Veins

Varicose veins
 Anatomy
o Superficial venous system
o Deep venous system
o Separated by deep fascia, perforating venous system (communicating vein)
o Blood flows from 1. superficial to deep veins; and 2. bottom to the top
o Veins have thin walls – not supposed to stand high pressure

 Long saphenous system

o Medial side  empties into deep veins (femoral vein) in saphenous opening
(2cm lateral below pubic tubercle)
o Superficial veins: often examine long saphenous system
o Anterior to medial malleolus (if need emergency access)
 Short saphenous system
o Lateral side  behind calve  popliteal vein in knee joint area (less constant
junction; rarely examined on pathology in short saphenous vein)
 Sapheno-femoral junction
o Many branches of superficial vein (from near sapheno-femoral junction) 
need to ablade deep vein as close as possible  cannot regurgitate as easy
 Perforating and communicating veins
o Traverse the deep fascia
o Converge at locations in the lower limb
 Lower, middle, upper calf, knee, mid thigh perforators
o Connected to a branch axial vein (instead of axial vein itself)  should ablade
the axial vein when surgery
MBBS IV WCS 001 – Varicose Veins

2 main pathologies
 1. Incompetence: valves not functioning well (chronic venous insufficiency)
 2. Obstruction: clots  inflammation  blockage of flow (thrombosis)

1. Chronic venous insufficiency (valvular malfunction – incompetence)

 Mildest: varicose veins  severe: reflux, ulceration
 2 common presentations of chronic venous insufficiency (in wards, exams)
o 1. Varicose veins (clinical description of chronic venous insufficiency)
 Dilated veins
 Reflux
 Thin walls  cannot withstand pressure  dilated, expanded veins
o 2. Leg swelling, chronic non-healing leg ulcers

 Pathophysiology – subjected to higher venous pressure

o Competent valves
 Stand erect, free the upper limbs
 Venous blood under low pressure – column of blood (weight of blood)
 exerted to the lowest part of the leg
 Return to the heart  rely on muscles in the lower limb  using the
calf muscles to pump the blood back to the heart
 Relax muscle  blood drawn from superficial to knee veins
 Valves in all 3 systems
o Incompetent valves
 Causes: damaged, relaxed (pregnancy: hormones), congenital
 Leaky valves
 When muscles contract  blood pumped upwards and downwards
(valves cannot prevent backward flow of blood)
 Pumped back into superficial system as well (higher pressure)
MBBS IV WCS 001 – Varicose Veins

o Pressure chart: normal

 Blood pull to catheter  stop at level to the heart (weight of the blood)
compared to weight of manometer
 Venous pressure in lowest part of leg (when static)
 When walking  blood is pumped back towards the heart  venous
pressure at the lowest part will be reduced  thus, have a lower
pressure during exercise  rest (blood pressure come back)
o Pressure chart: superficial reflux - valve incompetence
 Pressure will drop, but some blood reflux back into the distal limbs 
not drop as low  ambulatory venous hypertension (in the “varicose
veins” line) (elevated venous pressure when walking)
 Elevation of pressure  symptoms (aching, pain)
 High venous reflux  overloads lymphatic system (cannot absorb the
insterstitial fluid)

 Results in a spectrum of clinical disease

 1. Swelling
 2. RBC come out  stay in tissue  die (hemoglobin stays in
tissues) = hemosiderin  brownish pigmentation in lowest
part of the leg
 3. Proteins in blood diffuse out (do not return)  white cells
activated  chronic inflammation  thickened skin (itchy)
 protein form a layer of cuff around the capillaries
 4. Ulcers (due to protein layer covering the capillaries)
 Clinical symptoms
o 1. Disfigurement
o 2. Swelling and ache (venous pressure)
o 3. Complications: bleeding, thrombosis (if close to the surface)
 Etiology (insufficiency/incompetence of valves)
o Primary (unknown cause)
 Congenital
 Posture (e.g. surgeons, teachers)
o Secondary (previous episode of DVT  valves damaged  removal of clots 
attacking the clot AND valves)
 Post-thrombotic (after recanalization  no longer valves  pressure
transmitted to superficial veins)
MBBS IV WCS 001 – Varicose Veins

 Anatomical locations
o Sapheno-femoral incompetence (2cm lateral, below pubic tubercle)
 Commonly for primary etiologies
 First valve that goes
o System (can be a combination of all three)
 Superficial system
 Deep system
 Perforators
 Classification (CEAP):
o Clinical: 1-6 (C1: best prognosis; C6: worst prognosis)

o Etiology: congenital, primary, secondary

o Anatomy: superficial, perforator, deep
o Pathophysiology: due to reflux, obstruction (chronic venous obstruction can
produce exactly the same symptoms), both
 Physical examination: Tourniquet examination
o Varicose veins  greater saphenous veins reflux
o Lie patient down  tie below sapheno-junction
o Stand up  check if reflux is present (reflux +ve  if can be controlled by
tourniquet  can pinpoint the level of reflux)
 Investigations
o Ultrasound
 Reflux in axial system (greater saphenous vein)  large incompetent
communication (causing reflux from deep to superficial)
 Check the sapheno-femoral junction
 Use of Duplex scan (to see the flow)
 Incompetence: upward and downward flow (both directions of flow)
 done any segment = directional reflux in system (axial vein) and
perforating vein
MBBS IV WCS 001 – Varicose Veins

 Treatment
o Conservative treatment of varicose veins
*Principle: reduce venous pressure (if do not get up, do not get varicose viens)
 1. Elevation (above heart level)
 2. Postural adjustments
 3. Graduated compression stockings (woven tighter; lower = tighter
at ankle; lesser and lesser  creates a pressure gradient)
o Surgery: varicose treatment
*Ligate incompetent perforators (for cosmetics, symptoms, complications)
*Not absolutely indicated since not life threatening until complications
 i. Interrupt the perforators (source of reflux) – main source is at the
sapheno-femoral junction  ligate the incompetent junction (destroy)
 Sapheno-femoral flush/high ligation (2cm incision in
saphenous opening; at 2cm below, lateral pubic tubercle: find
common femoral vein and saphenous vein  find the junction
 put arteries into it – flow  cut saphenous vein NOT the
deep vein (as close to junction  to destroy all the tributaries)
 ii. Remove diseased veins (avoid blood getting in)  recurrent
symptoms
 Stripping of veins of incompetent LSV
o Removal of vein
o Smaller cuts below  tie  pull the vein up from under
the skin at the top (connect the two ends via stripper)
 Stab avulsion of branches (remove tributaries that cannot be
stripped)
 Interruption of perforating veins (identify via ultrasound)
o Minimally invasive surgery
 i. Thermal: laser (EVLT endovenous laser treatment EVLT, cheaper)
or radiofrequency (Venefit)
 More painful (need to reduce pain)
 Put catheter in the great saphenous vein (2cm behind sapheno-
venous junction)  inject saline to elevate the skin
 Connect catheter to machine  energy transmitted  closure
 ii. Non-thermal: mechanical  chemical ablation or glue (inject
into veins  glue the veins short)
 Not painful (but there is higher risk of recurrence)
o Sclerotherapy agents (an adjunct) (for cosmetic treatment, primary – destroy
junction and remove axial vein)
MBBS IV WCS 001 – Varicose Veins

 Indication: Reticular varicosis (network of veins in subcutaneous layer)

 Detergent (for esophageal varices as well)  destroy protein structure
using small needle  fill vein using sclerotherapy (protein in
endothelium will denature)
o External laser (cosmetic purposes)
 Telangiectasa (intra-dermal): capillaries  difficult to inject
  Severe chronic venous insufficiency (class 5 and 6)
o Other names
 Post-thrombotic/post phlebitis syndrome (thought it is a result of DVT)
 Chronic venous stasis
 Chronic venous hypertension

o Clinical features of severe chronic venous insufficiency

 1. Pigmentation
 2. Edema
 3. Eczema
 4. Ulcers (usually inside of the leg; medial side of the foot; where the
perforators are  skin are subjected to the highest level of pressure)
 Not extremely painful (arterial ischemia to nerve = painful)
 But ulcer is not painful, blood supply is good (unless infected)
 But very chronic ulcers  pigmentation and skin changes
o Pressure chart: post-phlebitic (whether walk or stand  venous pressure is still
high)  consistently high venous pressure (top line)

o Differential diagnosis of leg ulcers

 Arterial
 Signs (loss of pulse, skin changes, gangrene)
 Painful (affecting the nerves)
 Pressure areas
 Venous
 Signs of CVI (varicose veins), pigmentation, skin changes,
healing evidence (if remove pressure)
 Good pulse
 Less painful
 Site (medial side of leg)
 Neurogenic (leprosy, diabetes)
 Painless
 Neuropathy
MBBS IV WCS 001 – Varicose Veins

 Malignant
 Squamous cancer (malignancy in skin)
o Irregular
o Raised edges
o Biopsy at the edge of the ulcer (not in the centre – dead tissue)
o Groin LNs (enlarged)
o Evidence of spread from the lymphatics
 Marjoin’s ulcer (chronic irritation  grow into malignant ulcer)
o Due to previous chronic venous ulcer
 Infection
 Chronic osteomyelitis (tuberculosis)
 Syphilis
 Trauma
o Treatment of severe venous ulcers
 1. Reduce venous pressure
 Bed rest: elevation of the leg
 2. Treat ulcer
 Compression therapy (wound nurse)
 Reduce infection
 3. Topical ulcer treatment
 Skin graft (for healing)
 4. Venous surgery
 Adjunct: identify superficial vein (can treat superficial vein)
 Superficial reflux can overload the deep veins  dilated deep
veins  secondary reflux of the deep veins (to help with the
deep vein reflux)
 5. Venous reconstruction
 Treat deep reflux (rarely done)

2. Deep vein thrombosis (obstruction)

 Virchow’s triad (remember)
o 1. Stasis (blood is not moving)
o 2. Trauma (injury to vein)
o 3. Coagulability (clotting causes)
o  Inflammation  pain, swelling, signs of inflammation (redness, warmth)
 Clinical features (suspect when having leg swelling, acute, pain, warmth)
o Silent (phlebothrombosis)
o Thrombophlebitis
 1. Swelling
 2. Tender
 3. Warmth
 4. Redness
 Homan’s sign (dorsiflex ankle joint, pain in the calf  stretch vein)
o Venous gangrene (poor blockage)
 Venous congestion, pressure cut off the capillary supply
o Note: Left common iliac vein crossed over by common iliac artery  thus left
side is more common
 Investigations
o Ultrasound (venous Duplex) (gold standard)
MBBS IV WCS 001 – Varicose Veins

 Filling defect without blood flow (no phasic flow after taking deep
breathe  since flow is sluggish)
 Squeeze the leg (press down with ultrasound probe, can compress the
vein and not the artery) = artery is on the medial side
 Deep vein with clots  filling defect in deep veins
o Venogram (not done commonly – injection in the vein, cutoff in the vein)
 Complications
o 1. Pulmonary embolism
 Occurs when there is major deep vein thrombosis (ileo-femoral DVT)
 Not everyone with DVT has PE, and not always die from PE either
o 2. Chronic venous insufficiency
 Varicose veins, ulcers
o 3. Chronic venous obstruction
 Veins are not re-canalized (not resolved)  block flow)
o 4. Venous hypertension (due to chronic venous insufficiency and obstruction)
 Treatment of DVT
o 1. Prevent pulmonary embolism (propagation of clot)
o 2. Relieve acute symptoms
  Conservative
 i. Bed rest
 ii. Elevation
 iii. Anti-coagulation (blood does not clot)
o Heparin 5 days followed by oral anticoagulants, or
o SC heparin/LMWH x 3 months
o  reduce risk of fatal PE to 0.3-0.4%
  Aggressive therapy
 Catheter directed thrombolysis (early): protect valve 
reduce the chance of chronic venous sequelae/venous gangrene
 Venous thrombectomy (using stent): squeeze out clot
o 3. Prevent recurrent DVT (prophylaxis)
 Indications: can be high risk
 Stasis: physical means/physical movement
 Posture
 Stocking
 Intermittent compression (keep pressure going)
 Trauma:
 Avoid (and better surgery)
 Coagulability: chemical agents
 Low dose heparin BEFORE operation (subcutaneous)
o 4. Prevent post-thrombotic sequelae
 IVC Filter
 Indications
o Recurrent pulmonary embolism despite adequate
anticoagulation
o Cannot give anticoagulation
 Trap the clots  prevent going to the heart