Varicose Veins are dilated, tortuous, elongated veins in the leg. There is reversal of blood flow through its faulty valves. It is permanently elongated, dilated vein/veins with tortuous path causing pathological circulation.

1. en love da Homoeopathy
VARICOSE
VEINS

2. VARICOSE
VEINS

3. VARICOSE VEINS
DEFINITION
• They are dilated, tortuous,
elongatedveins in theleg.
• There is reversal of blood
flow through its faulty
valves.
• It is permanently elongated,
dilatedvein/veins with
tortuous pathcausing
pathologicalcirculation.

4. RISKFACTORS
• Heredity
• female sex
• occupationthat demands
prolongedstanding
• Immobility
• raised intra-abdominal
pressure like in sports
• tight clothing
• Pregnancy
• raised progesterone level
and altered estrogen-
progesteroneratio
• chronic constipation
• highheels.
• Prevalence of varicoseveins
is 35%
• severe varicoseveins is
10%
• chronic venous
insufficiency (CVI) is 8%
• ulcer is 2%

5. CLASSIFICATION
ClassificationI
• Long/great saphenous vein
varicosity.
• Short/small saphenous vein
varicosity.
• Varicose veins due to
perforator incompetence
ClassificationII
• Thread veins (ordermal
flares/telangiectasis/spider
veins/Hypenveins are 0.5–1
mm in size):
• Are small varices in the
skinusuallyaround
ankle
• whichlook likedilated,
red or purple network
of veins (Venulectasia)
• Spider naevi/venous
flares are common in
females.

6. • Reticular varices (1–3 mm
in size)
• Are slightly larger
varices thanthread
veins locatedin
subcutaneous/subder
mal region.
• Varicose veins
• They are dilated,
tortuous, elongated
superficial veins located
in the subcutaneous
tissue(saphenous
compartment)
• equal or more than3
mm in diameter
measuredin standing
position.
• Combination of any
of theabove

7. ClassificationIII
• classificationof Lower Limb
Varicose Veins
(2004)CEAP classification
• C—clinical signs (grade
0–6);(A) for asymptomatic
or (S) for symptomatic
presentation
• E—Etiological
classification:
• Congenital (Ec)
• Primary (Ep)
• Secondary(Es)
• No venous etiology (En)
• A— anatomicdistribution:
• Superficial (As)
• Deep (Ad) or Perforator
(Ap)
• No venous location
identified(An)
• P— Pathophysiologic
dysfunction:
• Reflux (Pr)
• Obstructive (Po)
• Both or No
pathophysiology
identified(Pn)

8. GRADINGCLINICAL SIGN
• 0—No visible or palpable
signs of venous diseases
• 1—Telangiectases, reticular
veins or malleolar flare
• 2—Varicoseveins
• 3—Oedema without skin
changes
• 4—Skin changes due to
venous diseases like
pigmentation, eczema or
lipodermatosclerosis
• 4a—pigmentation
• 4b—lipodermatosis,
atrophia blanche
• 5—Skinchanges as above
with healed ulceration
• 6—Skin changes as above
with active ulceration
COMMONSITES
• Lower limb
• Pampiniformplexus of veins
• Vulva, perineum
• Sites of portosystemic
anastomosis.

9. PRE-DISPOSINGFACTORS
• Age
• Sex
• Race
• Obesity
• Height
• left > right
• Occupation
• familyhistory
• erect posture.
AETIOLOGY
• commonin lower limb
↓
becauseof erectposture& long
column of blood has to be
supported
↓
whichcan lead to weakness and
incompetencyof valves.
Primary varicosities due to:
• Congenital incompetence or
absence of valves.

10. • Weaknessor wasting of
muscles—defective
connective tissue and
smoothmuscle in the
venous wall.
• Stretching of deepfascia.
• Inheritance (familyhistory)
with FOXC2 gene.
• Klippel-Trenaunay
syndrome
• Avalvulia
• Parkes-Weber syndrome.
• Here varices are of atypical
distribution.
Secondaryvaricosities:
• Recurrent thrombophlebitis
• Occupational—standing
for long hours (trafficpolice,
guards, sportsman)
• Obstructionto venous
return likeabdominal
tumour, retroperitoneal
fibrosis, lymphadenopathy,
ascites.
• Pregnancy(due to
progesterone hormone)

11. • Obesity
• chronic constipation
• AV malformations—
congenital or acquired.
• Iliacveinthrombosis.
• Tricuspidvalve
incompetence
PATHOGENESIS
• Fibrin cuff theory
• White cell trapping theory.
Incompetence leads to stasis
of blood
↓
Chronicamubulatoryvenous
Hypertension
↓
Defective micro circulations
↓
RBCdiffuses in to tissue
places- lysis of RBC
↓
Releaseof Haemosiderin

12. ↓
Pigmentation
↓
Dermatitis Capillary
endothelial changes
↓
Prevention of diffusion and
exchange of Nutrients
↓
Severe Anoxia
↓
chronic venous ulceration.
↓
Inappropriate activation of
trappedleucocytes
↓
release proteolytic enzymes
whichcausecell destruction and
ulceration
↓
White cell trapping theory.
↓
Fibrin deposition, tissue death,
scarring occurs together, called
as
↓
Lipodermatosclerosis
↓
Secondaryvalvular failure

13. ↓
venous reflux
↓
venous wall dilatation
↓
Effects
↓
Weakening of the venous
endothelial wall and valves occur
due to raised venous wall tension
Venous systemin the lower limb
is maintainedby—
• (1) Valvular competence
• (2) Venous patency
• (3) Calf muscle pump
whichis venous
channel/plexus withinthe
soleus muscle
• Chronicvenous
insufficiency (CVI) is a
syndrome resulting from
continuous chronic venous
hypertension/ambulatory
venous hypertension
• Varicose vein is a condition
of progressive deterioration
evenoftenwith
interventions

14. CLINICALFEATURES
• Dragging pain
• postural discomfort
• Heaviness in the legs
• Night time cramps—usually
late night
• Oedema feet, itching (feature
of CVI)
• Discolouration/ulceration in
thefeet/painful walk
• It is more common in females
(10 : 1)
• Oftenit is familial.
• Familial varicoseveins
beginin younger age group,
seen bilaterally, involves all
veins including deep veins.
SIGNS
• Visible dilatedveins in the
leg withpain
• Distress
• nocturnal cramps
• feeling of heaviness
• pruritus.
• Pedal oedema
• Pigmentation

15. • Dermatitis
• Ulceration
• Tenderness
• restrictedanklejoint
movement.
• Bleeding, thickening of tibia
occurs due to periostitis.
• Positive coughimpulse at
the saphenofemoral
junction.
• Saphena varix—a large
varicosity in the groin, which
becomes visible and
prominent on coughing.
SIGNS-TEST
Brodie-Trendelenburg test:
• Veinis emptied by elevating
thelimb
↓
and a tourniquet is tied
↓
just belowthe saphenofemoral
junction (or using thumb,
saphenofemoral junction is
occluded).
↓
Patient is askedto stand
quickly.

16. ↓
When tourniquet or thumb is
released
↓
rapidfilling fromabovesignifies
saphenoemoral incompetence.
This is Trendelenburg test I.
↓
In Trendelenburg test II, after
standing tourniquetis not
released
↓
Filling of blood from
below upwards rapidly
can be observedwithin 30–60
seconds
↓
It signifies perforator
incompetence

17. Perthe’s test
• The affected lower limb is
wrappedwithelastic
bandage
↓
and the patient is askedto walk
aroundand exercise
↓
Development of severe cramp
likepain in the calf
↓
signifies DVT.
Modified Perthe’s test:
• Tourniquet is tiedjust below
the saphenofemoral junction
↓
without emptying the vein.
↓
Is allowedto have a briskwalk
↓
whichprecipitates bursting pain
in the calf and
↓
also makes superficial veins
more prominent.
↓
It signifies DVT

18. Three tourniquet test
• To find out the site of
incompetent perforator
↓
three tourniquets are tied after
emptying the vein.
↓
At saphenofemoral junction.
Above knee level. Another
below knee level.
↓
Patient is askedto stand and
lookedfor filling of veins and
site of filling
↓
Then tourniquets are released
frombelow upwards
↓
againto see for incompetent
perforators
Schwartz test
• In standing position
↓
whenlower part of the long
saphenous vein in leg is
tapped
↓
impulse is felt at the
saphenous junction

19. ↓
or at the upper end of the
visible partof the vein.
↓
It signifies continuous column
of blood due to valvular
incompetence
Pratt’s test
• Esmarchbandageis
applied to the leg
↓
frombelowupwards followed
by a tourniquet at
saphenofemoral junction
↓
After that the bandage is
released
↓
keeping the tourniquet in the
same positionto see the “blow
outs” as perforators.
Fegan’s test
• On standing
↓
the site where the perforators
enter the deepfascia bulges
and this is marked

20. ↓
Thenon lying down, buttonlike
depression (crescentlike)
↓
in the deep fascia is felt at the
markedout points
↓
whichconfirms the perforator
site.
Morrissey’s cough impulse test:
• The varicose veins are
emptied.
↓
The leg is elevated and then the
patient is askedto cough.
↓
If there is saphenofemoral
incompetence, expansile impulse
is felt at saphenous opening
↓
It is a venous thrill due to
vibration caused by turbulent
backflow. .

21. INVESTIGATION
• Venous Doppler
• Duplex scan
• Ultrasoundabdomen
• peripheral smear
• plateletcount
• other relevant
investigations are done
depending on the cause
of the varicosevein
• PlainX-rayof the part is
takento look for
periostitis
TREATMENT
Conservative treatment:
• Elasticcrepe bandage
applicationfrombelow
upwards or use of
pressure stockings to the
limb—pressure gradiant
of 30–40 mmHg is
provided.
Elevationof the limb
• relieves oedema.
• Two short times, during
day and full night

22. • elevationof foot with feet
above the level of heart and
toes
• above the level of nose is the
method
Unna boots
• provide nonelastic
compression therapy.
• It comprises a gauze
compressiondressingsthat
contain zinc oxide,
calamine, and glycerine
that helps to prevent
further skinbreak down.
• It is changedonce a week.
Pneumatic compression
method.
• Drugs used for varicose
veins: Calcium
dobesilate—500 mg BD.
Injection—sclerotherapy:
Fegan’s technique:
• By injecting sclerosants
into the vein, complete
sclerosis of the venous
walls canbe achieved.

23. Indications –
• Uncomplicated perforator
incompetence.
• In the management of
smaller varices—reticular
veins, threadveins
(telangiectasis).
• Recurrent varices.
• Isolatedvaricosities.
• Aged/unfit patients
• Sclerosantsused are:
• Sodiumtetradecyl
sulphate 3% (STDS)—
commonly used
• Sodiummorrhuate
• Ethanolamine oleate
• Polidocanol—3%or
1%

24. Mechanisms of action
• Causes asepticinflammation
• Causes perivenousfibrosis
leading to block
• Causes approximationof
intima leading to obliteration
by endothelial damage
• Alters intravascular
pH/osmolality
• Changes surface tension of
plasma membrane
Contraindications for
sclerotherapy
• Saphenofemoral
incompetence
• Deep venous thrombosis
• Huge varicosities—may
precipitate DVT
• Peripheral arterial
diseases
• Hypersensitivity/immobili
ty
• Venous ulcer—relative
contraindication

25. Advantages of sclerotherapy
• It can be done as an
outpatient procedure.
• It does not require
anaesthesia.
Disadvantages of
sclerotherapy
• Inadvertentsubcutaneous
injection can causeskin
necrosis or abscess
formation.
• Anaphylaxis
• vasovagal shock
• Allergy
• Hyperpigmentation.
Surgery
• Trendelenburg operation
• Stripping of vein
REFERENCE
1. SRB's Manual of Surgery
by SriramBhatM
2. A Manual on Clinical
Surgeryby Das
3. A Concise textbookof
Surgeryby Das

26. A
Special Thanks
To A Very
Special Doctor