34493078 Diseases of Veins
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Transcript of 34493078 Diseases of Veins
Diseases of the veins
Dr. Pisake Boontham M.D., Ph.D.
Department of surgeryPhramongkutklao hospital
Lecture Objectives
Anatomy of leg veinsVenous Insufficiency: varicose veinsDeep Vein Thrombosis
MAJOR VEINS
Anatomy principles
Superficial venous systemLong saphenous veinShort saphenous vein
Deep venous systemPerforating veins
Anatomy
Perforating Veins
Valves
More frequent distally Ensure one way flow
SUPERFICIAL TO DEEP DISTAL TO PROXIMAL
Essential to passive calf pump system of venous return
Varicose veins Varicose veins affect
20 - 25% of adult females 10 - 15% of adult males
75,000 operations are performed annually in United Kingdom
20% of operations are for recurrent disease
May develop anywhere in body, but most develop in lower extremities: Long Saphenous
Factors associated with varicose veins
InheritedFemale > Male: age > 35 yearsPregnancy – smooth muscle relaxationWestern lifestyle: Whites > BlacksProlonged standing
Varicose Veins
CausesSevere damage or trauma to saphenous
veinEffects of gravity produced by long periods
of standing
TypesPrimary: no deep veins involvedSecondary: caused by obstruction of deep
veins (Most Common)
The long saphenous vein (LSV) and its tributaries most often form varicose veins The short saphenous vein (SSV) and its tributaries can also become
varicose but less often
The veins in the leg are divided into two systems; the deep and the superficial veins The two systems are linked periodically by perforating veins. A superficial vein can
become varicose because a perforating vein is allowing blood to flow the wrong way (outwards)
Normal vs Abnormal
Varicose veins
Consequence of superficial vein valve failure (incompetent valves)
Pooling of blood distal to incompetent valve (blood flows backwards, from deep to superficial veins)
Vein wall distended
Pathophysiology
Thin-walled, unsupported veinsFew valvesAbnormalities in collagenPregnancyGravityUpright position
Pathophysiology Major cause: sustained stretching of
vascular wall die to long-standing increased intravenous pressure
Valves become incompetent because they cannot close properly due to stretching
Prolonged standing, the force of gravity, lack of lower limb exercise, & incompetent venous valves all weaken muscle-pumping mechanism, & return of venous blood to heart decreases
As client stands for long time, blood pools and vessel wall continues to stretch, and valves become increasingly incompetent
Varicose veins-pathophysiology
Congenital or acquired valvular incompetence of the deep and superficial veins along with weakness of the venous wall
Self-perpetuating cycle of venous reflux leading to further vein dilatation and valve failure.
Venous hypertension leads to fluid and protein extravasation into the subcutaneous tissue-edema
Edema & high venous pressure results in reduced local capillary flow and reactive hypoxia leading to further inflammation and tissue damage.
Clinical Manifestations No symptoms Leg fatigue &/or heaviness Itching over affected leg (stasis dermatitis) Feelings of heat in the leg Visibly dilated veins
Telangiectasia veins Reticular varices Varicose veins
Severe, aching pain in leg Thin, discolored skin above ankles Complications: insufficiency, stasis ulcers,
chronic stasis dermatitis, thrombophlebitis
Signs of venous hypertension
Perimalleolar oedema Pigmentation Lipodermatosclerosis Eczema Ulceration
Pathogenesis
Result of severe impairment of venous return causing venous hypertension; often with deep vein incompetence
Haemosiderin deposition – eczema – calf muscle hypertrophy – oedema – lipodermatosclerosis
+/- ulceration
Lipodermatosclerosis
Venous ulcer
Assessment of varicose veins
History
Examination; Identify distribution of
varicose veins - long saphenous (LSV) vs
short saphenous (SSV) No specific labsDiagnostic
Doppler ultrasound
Assessment: Labs & Diagnostics
No specific labsDiagnostics
Doppler ultrasound flow tests & angiographic studies or Duplex Doppler ultrasound
Trendelenburg tests assists w/diagnosis
Indications for duplex scanning
Suspected short saphenous incompetence
Recurrent varicose veins
Complicated varicose veins (e.g. ulceration, Lipodermatosclerosis)
History of deep venous thrombosis
Treatments
Treat varicose veinsSymptom control with compression
therapySclerosant injection for Telangiectasia &
Reticular veinsSurgery to strip veins/disconnect
perforator veinsSuperficial vein ablation – laser/foam
Conservative Interventions
Conservative measures include antiembolism stockings and regular walking & leg elevation
Mild analgesics may relieve pain
Sclerotherapy
Only suitable for below knee varicose veins Need to exclude SFJ or SPJ incompetence Main use is for persistent or recurrent
varicose veins after adequate saphenous surgery
Complications of sclerotherapyExtravasation causing pigmentation or
ulcerationDVT
Indications for varicose vein surgery
Most surgery is cosmetic or for minor symptoms
Absolute indications for surgery :
Lipodermatosclerosis leading to venous ulceration
Recurrent superficial thrombophlebitis Bleeding from ruptured varix
Treatment of venous ulcer
AFTER EXCLUDING ARTERIAL DISEASE:4 layer compression bandagingTreat varicose veinsLong term compression
Venous Stripping
ENDOVENOUS LAZER:an alternative choice for surgery of varicose veins
Indication
Varicose veins with:Saphenofemoral junction refluxPrimary insufficiency of GSVLasser saphenous vein reflux
Contraindication
Technical unable to accessRisk for DVT: hypercoagulationPostphebitic limbInfected venous ulcerMedically high-risk patient
Advantages
Minimally invasive procedureAmbulatory procedureQuick methodNo scaring
Outcome
Follow up (yr) Treated/ occluded
Continued occlusion (%)
<1 231/218 94
1-2 247/245 99
2-3 151/151 100
>3 72/72 100
Procedure
Recurrent varicose veins
15 - 25 % of varicose vein surgery is for recurrence
Outcome of recurrent varicose veins surgery is less successful
Can be avoided with adequate primary surgery
Reasons for recurrence Inaccurate clinical assessment Confusion as to whether varicosities are in
LSV or SSV distribution Can be avoided with use of hand held
Doppler Inadequate primary surgery 10% cases SFJ not correctly identified 20% cases tributaries mistaken for LSV Failure to strip LSV 70% of those with SF incompetence treated
with sclerotherapy alone will develop recurrence
Neovascularisation
Deep vein thrombosis
Very common especially in hospital patients
Incidence of about 50-150 DVTs per 100,000
population per year
Asymptomatic in 30% (calf veins only)
10% pulmonary embolism when popliteal
vein and above involved
Deep Vein Thrombosis (DVT)
Most likely to occur in deep veins of the calf (80%)
25% of thrombi that occur in calf will extend to the popliteal & femoral veins
PE may be the first sign of DVT
Risk Factors
Hypercoagulable state
Age Obesity Immobility Surgery Pregnancy
OCP Malignancy Heart Failure Infection Inflammatory bowel Nephrotic syndrome
Hypercoagulable state
Factor V Leiden mutationProthrombin gene mutationProtein C or S deficiencyAntithrombin III deficiencyHomocysteineAntiphospholipid syndrome
Pathophysiology: Virchow’s Triad
Stasis of blood Increased blood coagulability Injury to vessel wall
2 of 3 factors must be present for thrombi to form
DVT Manifestations
When clot is in formative stage, may notice no
symptoms
Usually profound tenderness; affected extremity
may be larger (unilateral edema)
Dull aching esp when walking: Most common
Severe pain, esp when walking
Cyanosis of extremity
Slightly elevated temp
General malaise
Diagnosis of DVT
HistoryExamination – swelling, tender,
redness, dilated superficial veins, low grade pyrexia
Duplex US + d-dimer. If still uncertain, (MRI) venography
Homan’s Sign
Was long considered classic manifestation—this is no longer true
Sign is not specific to DVT & can be elicited by any condition of the calf
As calf muscles contract, there is risk of detaching thrombus from the wall
DVT
Prevention of DVT
Mobilise ASAPLow compression stocking for
inpatientsProphylactic LMW Heparin
Treatment of DVT
Medical therapyHeparinise immediatelyWarfarinise over next 3 daysLong term warfarin
Conservative therapyExclude risk factors IVC filter! For PE preventionSurgery
Conservative Therapy: DVT
Anticoagulants may be prescribed for severe
cases
Strict bed rest until symptoms of tenderness
& edema resolve
Legs elevated, knees slightly flexed, above
heart level to promote venous return &
discourage venous pooling
TED’s or pneumatic compression devices
IVC filter Re-embolism despite
anticoagulation Anticoagulation contraindicated Extensive thrombus persists
SurgeryVenous thrombectomy; done when
thrombi are lodged in femoral vein & excision of clots is required to prevent PE or to prevent gangrene
Venous surgery is rarely indicated.Venous stenting combined with catheter-
directed thrombolytic therapy is being used in some centers to treat patients with iliofemoral venous thrombosis and severe obstruction.