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SRB’s Manual of Surgery
Fig. 1.393: Long saphenous vein with perforator
incompetence with venous ulcer.
Calf musculovenous pump: During contraction phase of
walking, pressure in the calf muscles increases to 200–300
mmHg. This pumps the blood towards the heart. During
relaxation phase of walking, pressure in the calf falls and so
it allows blood to flow from superficial to deep veins through
perforators. Normally while walking, pressure in the superficial system at the level of ankle is 20 mmHg.
During walking, foot pump mechanism propels blood from
plantar veins into the leg.
Gravity.
Note:
Pressure in arteriolar end of the capillary is 32 mmHg; venular end of
capillary is 12 mmHg.
FACTORS RESPONSIBLE FOR VENOUS RETURN
B
x Negative pressure in thorax
x Peripheral pump—calf muscles
x Vis-a-tergo of adjoining muscles
x Nonrefluxing valves in course of veins
DEEP VEIN THROMBOSIS
Deep vein thrombosis (DVT) is called as phlebothrombosis.
It is semisolid clot in the vein which has got high tendency to
develop pulmonary embolism and sudden death. Common site
of beginning of thrombus is soleal veins which later propagate
proximally, often getting detached to cause acute massive
pulmonary embolism or moderate sized emboli can cause
pyramidal/wedge shaped pulmonary infarcts.
Aetiology: Factors
VIRCHOW’S TRIAD
B
x Stasis; Hypercoagulability; Vein wall injury
Causes
Following childbirth.
Trauma—to leg, ankle, thigh, pelvis.
Muscular violence.
Immobility: Bedridden patients, individuals on long duration
air or bus travel (Traveller’s thrombosis).
Debilitating illness, obesity, immobility, bed rest, pregnancy,
puerperium, oral contraceptives (increases the risk by 5
times), estrogens.
Postoperative thrombosis (Most common cause): Common
after the age of 40 years. Incidence following surgeries
is 30%. In 30% of cases both legs are affected. Usually
seen after prostate surgery, hip surgery, major abdominal
surgeries, gynaecological surgeries, cancer surgeries.
Bedridden for more than 3 days in the postoperative period
increases the risk of DVT.
Spontaneous thrombosis is common in visceral neoplasm
like carcinoma pancreas or carcinoma stomach. It is often
migrating type.
Thrombus may start in a venous tributary which eventually
may extend into the main vein causing DVT.
Axillary vein thrombosis
¾
It can occur sponta neously, following compression by
cervical rib, by various causes of thoracic inlet syndrome,
or arm being in the hyperabduction state for prolonged
period (e.g. painting the ceiling), after axillary lymph node
block dissection, after radiotherapy to axilla, occasionally
as a compli cation of venous cannulation.
¾
Upper limb DVT is rare compared to lower limb DVT (5%
of all DVT). It may be axillary or subclavian vein or both.
¾
But 30% of upper limb DVT can cause pulmonary
embolism.
¾
Primary upper limb DVT is Paget-Schroetter syndrome,
is due to subclavian vein compression that occurs in
thoracic outlet syndrome. It may be precipitated by exertion of arms, swimming, exercise, etc.
¾
Idiopathic upper limb DVT is rare. Occult underlying
malignancy should be thought of.
¾
Secondary upper limb DVT is due to CVP line, pacemaker
thrombocytosis, malignancy, surgeries, radiotherapy, etc.
¾
Unilateral arm, forearm swelling with bluish discolouration, pain, pitting oedema, often with skin blebs are the
features.
¾
Investigations are—Duplex scan, MR venography (as
clavicle obscures proper duplex evaluation), BT, CT, PT,
APTT, platelet count estimation.
¾
Treatment is similar, with heparin/LMWH/warfarin,
thrombolysis using tissue plasminogen activator, elevation of the arm, using compression stockings.
Polycythaemia vera, thrombocytosis.
Deficiencies of antithrombin III, protein C, protein S, factor
V of Leiden, thrombophilia.
Recent myocardial infarction, heart failure, nephrotic
syndrome.
Thrombosis can occur in individuals who sit with computers
for long time—‘ethrombosis’.
Sites
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Pelvic veins—not uncommon; involves internal iliac veins. It is
a.
more common in PID (pelvic inflammatory disease) in females.
In males prostatic veins may be the site of origin. It is difficult to
identify clinically even though rectal or vaginal examination may
help.
Leg veins—very common in veins of soleus muscle in calf.
b.
Femoral vein/iliofemoral vein thrombosis can occur along with
calf veins or independently without calf vein thrombosis which
shows adductor canal tenderness. Iliofemoral vein thrombosis
is common on left side due to its lengthy course/compression
by right iliac artery/often due to presence of web at its entry
into IVC. Incidence of bilateral leg DVT is 30% which should be
differentiated from bilateral pedal oedema due to other causes
like hypoproteinaemia, renal failure and cardiac causes.
c. Upper limb veins—not uncommon (Axillary vein thrombosis).
Phlegmasia Alba Dolens
It is DVT of femoral vein (deep femoral vein commonly) causing
painful congestion and oedema of leg, with lymphangitis, which
further increases the oedema and worsens the situation (white
leg).
FEATURES OF DVT
B
x Commonly it is asymptomatic—60%
x Fever—most common
x Tense, tender, warm, pale/bluish, shiny swelling calf
x Positive Homan’s, Mose’s or Neuhof’s signs
x Inverted champagne bottle sign
x Features of pulmonary embolism
Features
Fever—earliest symptom.
Pain and swelling in the calf and thigh (often). Pain is often
so severe that the patient finds it difficult to flex (or move)
the leg.
Leg is tense, tender, warm, pale or bluish with stretched and
shiny skin.
Positive Homan’s sign: Passive forceful dorsiflexion of the
foot with extended knee will cause tender ness in the calf.
Mose’s sign: Gentle squeezing of lower part of the calf from
side-to-side is painful. Gentleness is very important otherwise
it may dislodge a thrombus to form an embolus.
Neuhof’s sign: Thickening and deep tenderness elicited while
palpating deep in calf muscles.
Most often, DVT is asymptomatic and presents suddenly with
features of pulmonary embolism like chest pain, breathless-
ness and haemoptysis.
After applying tourniquet at saphenofemoral junction, patient
is made to walk and without removing the tourniquet, limb
is elevated—persisting prominent superficial veins will be
observed in DVT—Linton’s test.
Differential diagnosis for DVT: Ruptured Baker’s cyst;
Ruptured plantaris tendon; Calf muscle haematoma; Cellulitis
leg; Superficial thrombophlebitis.
217
CHAPTER 1N General Surgery: Venous Diseases
Fig. 1.394: Deep vein thrombosis (DVT) in both legs. 30%
cases of DVT are bilateral.
Fig. 1.395: Right leg venous gangrene. Note the discolouration,
blebs and oedema.
Phlegmasia Caerulea Dolens
It is extensive DVT of iliac and pelvic veins causing blue leg with
either venous gangrene or areas of infarction.
Peace begins with a smile. Beauty is power; smile is its sword.
Investigations
Venous Doppler with Duplex scanning: It shows noncom-
pressible vein which is wider than normal. On compression
over calf muscles, it does not show any augmentation of
flow. Normal venous sound at the area of femoral vein which
disappears during inspiration is conspicuously absent in
DVT.
Fig. 1.396: US showing IVC thrombosis.
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Venogram
¾
Contrast material is injected into venous system to get
detailed idea of the veins after applying tourniquet into
superficial system. Occlusive and nonocclusive thrombus
can be differentiated by this. But as it is invasive one, it is
not commonly done at present. MR venogram is under
trial at present. Impedance plethysmography is used to
measure the rate of venous emptying. Vein occlusion is
time should be done. Warfarin is given for 3–6 months
with regular monitoring, depending on the cause, risk
group, and severity of DVT. INR should be maintained
between 2.0 to 3.0.
¾
Oral anticoagulants being teratogenic cannot be used
during pregnancy. LMWH is the drug of choice used
during pregnancy and postpartum period.
For free thrombus:
done using cuff around upper thigh which is confirmed
FREE THROMBUS
125
B
x Fibrinolysins
x Thrombectomy using Fogarty’s catheter
x IVC filter
¾
Fibrinolysins: Streptokinase, 6 lakhs to start with and
later one lakh hourly. It is commonly infused directly into
the affected vein through a venous catheter. Urokinase
or tissue plasminogen activator may also be used to
dissolve thrombus (it should not be given when patient
is on heparin).
by flat electrical wave pattern. When cuff is released rapid
flow of wave is observed in normal; sluggish flow of wave
is seen in DVT.
SRB’s Manual of Surgery
Radioactive I
¾
Sodium iodide 100 mg orally is given to the patient 24
125
fibrinogen study
hours before the test to block the thyroid activity. I
labelled fibrinogen 100 µ
Curies is injected intravenously.
First radioactivity of heart is measured by placing the
scintillation counter over precordium. Reading obtained
by this is adjusted as 100%. After that legs are elevated
using adjustable stands and to prevent venous pooling,
scintillation counter is placed over the calf. Counting in
the leg is done from below upwards at 5 cm intervals.
Procedure is done in preoperative period; on 1st, 3rd
and 6th postoperative days. A 20% or more raise in
percentage value suggests deep vein thrombosis in
leg. I
125
labelled fibrinogen is used (earlier I
131
labelled
fibrinogen was used) because it has got shorter radioaction; its detectability is done with much lighter and mobile
apparatus.
Haemogram with platelet count; D-dimer test/analysis of
fibrin degradation products (FDP) are relevant tests used.
D-dimer test is measurement of cross-linked degradation
products which interprets the plasmin activity on fibrin.
Negative D-dimer test is of more value.
Ventilation—perfusion scanning with mismatched defects;
pulmonary artery CT scan with filling defect; pulmonary
angiography are the investigations to confirm the pulmonary
embolism.
FIBRINOLYSINS
B
x Tissue plasminogen activator—directly into the thrombus through
popliteal/femoral vein
x Urokinase—1,20,000 to 2,50,000 units/hour; derived from
human urine
x Reptilase—0.5-1 unit/hour
x Streptokinase—2.5 to 6 lakh to start with later one lakh hourly;
derived from streptococci
¾
Venous thrombectomy is done using Fogarty venous
balloon catheter.
¾
Thrombotic emboli is prevented from reaching the heart
by filtering it at IVC level using intracaval filters—Kim ray
Greenfield filter, suture sieve plication, stapler plication,
vena caval ligation, Mobin Uddin umbrella filter.
¾
Special thrombectomy device of 7–9 French sheath is
passed through the thrombosed segment to have partial
mechanical thrombectomy and through that thrombolytics (tissue plasminogen activator) are infused.
Thrombus can be removed nowadays through balloon
Treatment
Rest, elevation of limb, bandaging the entire limb with crepe
bandage.
Anticoagulants: Heparin/low molecular weight heparin,
warfarin, phenindione.
For fixed thrombus:
¾
Initially high dose of heparin of 25,000 units/day for 7
days is given. Then later patient is advised to continue
warfarin for 3–6 months. Dose is controlled by assessing
Activated Partial Thromboplastin Time (APTT). Duration
of heparin treatment is usually for 7–10 days. Dose of
heparin is often calculated as— 80 units/kg bolus of
heparin followed by 15 units/kg of infusion.
¾
Low molecular weight heparin is preferred to heparin.
¾
Warfarin should be started as early as possible (same
day of heparin therapy). Day one and day two—10 mg
each day; day three—5 mg. On day three prothrombin
angioplasty tube. Open venotomy and thrombectomy
also can be done.
Modified Well's criteria for predicting pulmonary
T
embolism
Modified Well’s criteria for predicting
pulmonary embolism (PE)
Clinical symptoms and signs of DVT 3
Alternative diagnosis less likely PE 3
Heart rate >100 1.5
Immobilization more than 3 days or surgery
within last 4 weeks
Previous DVT or PE 1.5
Haemoptysis 1.0
Malignancy in last 6 months 1.0
Score <4 = PE unlikely; score >4 = suggestive of PE.
Points
1.5
Fig. 1.397: Palma operation for iliofemoral block. Using opposite
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saphenous vein femoral vein is connected to other femoral vein.
Low dose heparin is given in suspected cases, in major
surgeries and continued during postopera tive period till the
patient is ambulated. 5,000 units is given subcutaneously
2 hours before surgery. Low molecular weight heparin is
preferred drug than heparin as it can be used once a day;
it does not require monitoring; it does not cause thrombocytopenia (like heparin); and there is lesser risk of bleeding.
Various measures like graduated static compres sion, elastic
stockings, electrical stimulation of calf muscles, pneumatic
compression are used to prevent sluggish flow of blood.
Dextran 70, intravenously 500 mL during surgery and another
500 mL postoperatively in 24 hours can also be used to
prevent DVT.
Smoking increases the viscosity of blood and so should be
stopped.
Patients on oral contraceptives or oestrogens should stop
the drug 6-8 weeks prior to any elective surgery.
EFFECTS AND SEQUELAE OF DVT
B
x Pulmonary embolism—15%
x Infection; venous gangrene
x Partial recanalisation, chronic venous hypertension around the
ankle region causing venous ulcers—chronic venous insuf-
ficiency—CVI
x Recurrent DVT—30%
x Propagation of thrombus proximally—20–30%
219
CHAPTER 1N General Surgery: Venous Diseases
Fig. 1.398: Crepe bandages applied to both legs in bilateral
varicose veins and DVT.
Palma operation: In iliofemoral thrombosis, common femoral
vein below the block is commu
nicated to opposite femoral
vein through opposite long saphenous vein.
May-Husni operation: When blockage is in popliteal vein,
popliteal vein below the block is anastomo
sed to long saphenous vein (end-to-end) so as to bypass the blood across the
popliteal block.
Prevention of DVT
x Categorise the patient as low/moderate and high-risk. Low-risk—
young patients undergoing surgery for less than 30 minutes.
Moderate-risk—patients above 40 years of age undergoing major
surgery. High-risk—one who had existing cardiac diseases,
stroke, previous history of DVT, suffering from malignancy
x Mechanical methods—elastic compression bandage; elevation;
external pneumatic bandage
x Pharmacological—low molecular weight heparin—once a day
Care has to be taken to see for proper positioning of legs with
no pressure on the calf muscles.
Pressure bandage to the legs has to be applied during
major surgeries, laparoscopic surgeries. During postoperative period, elevation, massa ging, pressure bandage, early
ambulation, main taining hydration are essential measures.
VARICOSE VEINS
It is permanently elongated, dilated vein/veins with tortuous
path causing pathological circulation. There is reversal of
blood flow through its faulty valves.
Risk factors being heredity; female sex; occupation that
demands prolonged standing; immobility; raised intraabdominal pressure like in sports, tight clothing, pregnancy,
raised progesterone level and altered estrogen-progesterone
ratio, chronic constipation, high heels.
Prevalence of varicose veins is 35%; severe varicose veins
is 10%; chronic venous insufficiency (CVI) is 8%; ulcer
is 2%.
A B
Figs. 1.399A to C: Typical varicose vein with skin changes and
venous ulceration.
C
Every heart has pain; some hide it in eyes; some hide in their smile!
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Classication I
Long/great saphenous vein varicosity.
Short/small saphenous vein varicosity.
Varicose veins due to perforator incompetence.
Fig. 1.402: Atrophic blanche.
• Small varicose vein is <4 mm in diameter. Large varicose vein is >4
SRB’s Manual of Surgery
mm in diameter.
• Corona phlebectatica are blue telangiectasias on the medial aspect of the
foot below the malleolus around ankle level. More than 5 such lesions
are the best independent predictor of the skin changes.
• Pulsatile varicose veins in lower limb is seen in Klippel-Trenaunay
syndrome
Classication III
CEAP Classication of Lower Limb Varicose
Veins (2004)
A B C
Figs. 1.400A to C: (A) Great saphenous vein varicosity. (B) Small
saphenous vein varicosity. (C) Perforator incompetence (blow outs).
Classication II
Thread veins (or dermal flares/telangiectasis/spider veins/
Hypen veins are 0.5–1 mm in size): Are small varices in the
skin usually around ankle which look like dilated, red or purple
network of veins (Venulectasia). Spider naevi/venous flares
are common in females.
Reticular varices (1–3 mm in size): Are slightly larger varices
than thread veins located in subcutaneous/subdermal region.
Varicose veins: They are dilated, tortuous, elongated
superficial veins located in the subcutaneous tissue (saphenous compartment) equal or more than 3 mm in diameter
measured in standing position.
Combination of any of the above.
Fig. 1.401: Thread veins are up to 1 mm diameter;
reticular veins are 1–3 mm in diameter.
Note:
• Atrophic blanche is localized white atrophic skin surrounded by hyper
pigmentation and dilated capillaries.
• Saphena varix is a large groin varicosity at SFJ which disappears on
lying down and imparts an impulse and thrill on coughing.
CEAP CLASSIFICATION
B
C— Clinical signs (grade 0–6); (A) for asymptomatic or (S) for
symptomatic presentation
E— Etiological classification: Congenital (Ec), Primary (Ep),
Secondary (Es),
Anatomic distribution: Superficial (As), Deep (Ad) or Perforator
A—
(Ap), No venous location identified (An)
P— Pathophysiologic dysfunction: Reflux (Pr), Obstructive (Po),
Both, or
GRADING OF CLINICAL SIGNS (C)
B
0—No visible or palpable signs of venous diseases
1—Telangiectases, reticular veins or malleolar flare
2—Varicose veins
3—Oedema without skin changes
4—Skin changes due to venous diseases like pigmentation, eczema
or lipodermatosclerosis 4a—pigmentation; 4b—lipodermatosis,
atrophia blanche
5—Skin changes as above with healed ulceration
6—Skin changes as above with active ulceration
ANATOMICAL DISTRIBUTION (A)
B
As—superficial system:
1–Telangiectases, reticular veins
2–Great saphenous vein above the knee—ostial and preterminal
3–Great saphenous vein below the knee
4–Small saphenous vein
5–Nonsaphenous—43%
Ad—deep system:
From 6 to 15
Ap—perforator system:
17–Perforator vein (PV) of the thigh
18–Perforator (PV) of the calf and leg
An—no anatomical lesion identified
No venous etiology (En)
No pathophysiology identified (Pn)
Pathogenesis
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TWO THEORIES
B
x Fibrin cuff theory
x White cell trapping theory
Incompetence of venous valves
↓
Stasis of blood
↓
Chronic ambulatory venous hypertension
↓
Defective microcirculation
↓
RBC diffuses into tissue planes
↓
Lysis of RBC’s
↓
Release of haemosiderin
↓
Pigmentation
↓
Dermatitis
↓
Capillary endothelial damage
↓
Prevention of diffusion and exchange of nutrients
↓
Severe anoxia
↓
Chronic venous ulceration (Fibrin cuff theory).
Inappropriate activation of trapped leucocytes release proteo-
lytic enzymes which cause cell destruction and ulceration—
White cell trapping theory. Fibrin deposition, tissue death,
scarring occurs together, called as lipodermatosclerosis.
Secondary valvular failure → venous reflux → venous wall
dilatation → effects. Weakening of the venous endothelial wall
and valves occur due to raised venous wall tension by—(1)
Shearing stress pressures of blood flow, (2) Increased matrix
metalloproteinases (MMPs) activity on endothelium and
smooth muscle cells reducing structural integrity of venous
wall with decreased elastin content in the media of the vein,
(3) Changes in normal venous constriction and relaxation
properties, (4) Recurrent inflammation.
Venous system in the lower limb is maintained by—(1)
Valvular competence, (2) Venous patency, (3) Calf muscle
pump which is venous channel/plexus within the soleus
muscle. Any change in any of these systems can cause
venous insufficiency.
Chronic venous insufficiency (CVI) is a syndrome resulting
from continuous chronic venous hypertension/ambulatory
venous hypertension [AVP] (>80 mmHg venous pressure at
ankle) in the erect posture either on standing or exercise (in
normal people venous pressure in superficial system falls
during calf contraction). CVI consists of postural discomfort,
varicose veins, oedema, pigmentation, induration, dermatitis,
lipodermatosclerosis and ulceration. CVI patients may be
having superficial vein incompetence (30%) with or without
perforator incompetence or deep vein incompetence (30%)
or having previous DVT with complete obliteration or partial
recanalisation with incompetence called as post-thrombotic
syndrome (30%).
Varicose vein is a condition of progressive deterioration even
often with interventions.
A
Figs. 1.403A and B: Lipodermatosclerosis is pigmentation,
thickening, and induration of the skin due to venous diseases.
B
Predisposing factors for varicose veins are—age, sex, race,
obesity, height, left > right, occupation, family history, erect
posture.
Fig. 1.404: Typical site of venous ulcer. Note the
pigmentation and chronicity.
SITES WHERE VARICOSITIES CAN OCCUR
B
x Lower limb, Sites of portosystemic anastomosis
x Vulva, perineum, Pampiniform plexus of veins
REMEMBER
B
20% of population suffers from varicose veins. Prevalence of varicose veins increases with age (from 11% at 18 years of age to 55%
at 55 years). Veins are three times of arteries. 70% of blood in the
circulation is in veins at a given point of time.
Contd...
221
CHAPTER 1N General Surgery: Venous Diseases
One negative thought can burn all positive thoughts.
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Contd...
Superficial veins carry 10% of venous system. Superficial veins of
the lower limb have thick muscular wall and are located in condensed
superficial fascia (between skin and deep fascia called as saphenous
fascia), have low pressure; have plenty of valves to propagate blood.
Blood from these veins enter into the femoral vein through SFJ and
through SPJ and through perforators into the deep veins. Long saphenous vein (LSV) is the longest vein in the body has 10–20 valves.
Posterior arch vein of Leonard starts behind the medial malleolus
ascending upwards to join the LSV at knee level; anterior superficial
vein (along the shin joining the LSV at knee level); posteromedial
SRB’s Manual of Surgery
and anterolateral accessory veins in the thigh join LSV near SFJ.
Superficial epigastric, superficial circumflex iliac and superficial
external pudendal veins are tributaries at SFJ.
Deep venous system in the leg comprises femoral and popliteal veins;
pairs of venae commitantes of the tibial, posterior tibial and peroneal
arteries (total 6 venae comitantes, soleal and gastrocnemius veins
join to form popliteal vein); being valveless blood takes within the calf
muscles communicates with superficial system via saphenofemoral
junction, mid-thigh perforators, short saphenopopliteal junction and
calf perforators.
Primary varicose veins are often familial; with unknown cause
could be due to weak valve or wall. It is seen in younger age, main
saphenous veins are usually affected; deep veins are usually patent;
only Trendelenburg test-I is positive; complications are less and late
to occur. Occupation prolonged standing and muscular weakness
are contributory factors. Congenital is; due to absence valve; it is
uncommon.
Secondary type is acquired one; it occurs in adult and old; saphenous,
perforators and often deep veins are affected; both Trendelenburg
tests I and II are often positive; complications are common and
quick to develop.
Perforators normally drain only from superficial to deep veins across
a valve (through deep fascia); in perforator incompetence flow
reverses from deep veins towards superficial veins as ‘blow outs’
which are more prominent during calf contraction. Communicating
veins are one which communicates between one or more superficial
venous system; example is communicating vein between long and
short saphenous veins.
Symptom classification: Asymptomatic is group I with venous
telangiectasia, thread/reticular/varicose veins; symptomatic group II
with cramps, heaviness, tenderness, itching, swelling; complicated
group III is with haemorrhage, superficial thrombophlebitis, eczema,
lipodermatosclerosis and venous ulcers. CEAP classification is also
important. Symptoms are less severe in morning than at evening.
In atrophie blanche white patches develop in skin due to severe varicose veins. Dermal flares are thread veins seen in the skin with <1
mm diameter; they are seen in 30% of superficial vein incompetence.
Reticular veins are 1–3 mm in diameter; lie just deep to the skin as
small varices in 30% of superficial vein incompetence. Varicose veins
are usually >3 mm in diameter.
INR (International Normalised Ratio): Ratio of measured PT to a
mean lab control PT corrected for the sensitivity of thromboplastin
Aetiology of Varicose Veins
Varicosities are more common in lower limb because of erect
posture and long column of blood has to be supported which
can lead to weakness and incompe tency of valves. Incidence is
5% of adult population.
Primary varicosities due to:
¾
Congenital incompetence or absence of valves.
¾
Weakness or wasting of muscles—defective connective
tissue and smooth muscle in the venous wall.
¾
Stretching of deep fascia.
¾
Inheritance (family history) with FOXC2 gene.
¾
Klippel-Trenaunay syndrome, avalvulia, Parkes-Weber
syndrome. Here varices are of atypical distribution.
Secondary varicosities:
¾
Recurrent thrombophlebitis.
¾
Occupational—standing for long hours (traffic police,
guards, sportsman).
¾
Obstruction to venous return like abdominal tumour,
retroperitoneal fibrosis, lymphadeno pathy, ascites.
¾
Pregnancy (due to progesterone hormone), obesity,
chronic constipation.
¾
AV malformations—congenital or acquired.
¾
Iliac vein thrombosis.
¾
Tricuspid valve incompetence.
Features
SYMPTOMS IN VARICOSE VEINS
B
x Dragging pain, postural discomfort
x Heaviness in the legs
x Night-time cramps—usually late night
x Oedema feet, itching (feature of CVI)
x Discolouration/ulceration in the feet/painful walk
CAUSES OF PAIN/CRAMPS IN VARICOSE VEINS/VENOUS
B
DISEASES
x Increased venous wall tension—chronic venous hypertension
x Hypoxia of tunica media of the venous wall due to altered function
of vasa vasorum
x Increased capillary pressure
x Hyperviscosity of red cells—haemorrheological disorders
x Platelet hyperaggregation
x Reduction in capillary permeability causing capillary functional
disorder
x Altered cutaneous microcirculation due to leucocyte adhesion and
accumulation into the venous wall; release of free radicals cause
microvascular lesional disease
OEDEMA IN VENOUS DISEASES
B
x Can be localised or generalised
x Localised oedema is due to ankle flare or dilatation of medial
marginal vein
x Cellulitis and lymphangitis association causes oedema
x Scarring and thickening of dermal and subdermal tissues—lipo-
dermatosclerosis (brawny induration)
x Ankle becomes narrower due to contraction of skin and subcu-
taneous tissues but calf remains prominent—champagne bottle
appearance
x Pale atrophic skin with white patches surrounded by dilated capil-
laries and pigmentation—atrophic blanche
It is more common in females (10:1). Often it is familial.
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Familial varicose veins begin in younger age group, seen bilaterally, involves all veins including deep veins.
Signs
A
Brodie-Trendelenburg test: Vein is emptied by elevating
the limb and a tourniquet is tied just below the sapheno-
femoral junction (or using thumb, saphenofemoral junction
is occluded). Patient is asked to stand quickly. When tourni-
quet or thumb is released, rapid filling from above signifies
saphenoemoral incompetence. This is Trendelenburg test I.
In Trendelenburg test II, after standing tourniquet is not
released. Filling of blood from below upwards rapidly can
be observed within 30–60 seconds. It signifies perforator
incompetence.
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CHAPTER 1N General Surgery: Venous Diseases
B
Figs. 1.405A and B: Thread (<1 mm) and reticular veins (1–3 mm).
Visible dilated veins in the leg with pain, distress, nocturnal
cramps, feeling of heaviness, pruritus.
Pedal oedema, pigmentation, dermatitis, ulceration, tender-
ness, restricted ankle joint movement.
Bleeding, thickening of tibia occurs due to perio stitis.
Positive cough impulse at the saphenofemoral junction.
Saphena varix—a large varicosity in the groin which
becomes visible and prominent on coughing.
Fig. 1.406: Site of saphena varix—in the lower part of groin just
below the inguinal ligament.
Fig. 1.407: Brodie-Trendelenburg test. Note the reversal of blood
flow while releasing the tourniquet.
A
Figs. 1.408A and B: Tourniquet tests for long saphenous vein and
short saphenous vein.
Perthe’s test: The affected lower limb is wrapped with
B
elastic bandage and the patient is asked to walk around and
exercise. Development of severe cramp like pain in the calf
signifies DVT.
Modified Perthe’s test: Tourniquet is tied just below the
saphenofemoral junction without emptying the vein. Patient is
Be tough but look soft; be a winner but look like a beginner; be simple but look stylish; be tensed but look cool.
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allowed to have a brisk walk which precipitates bursting pain
in the calf and also makes superficial veins more prominent.
It signifies DVT.
DVT is contraindicated for any surgical intervention of super-
ficial varicose veins. It is also contraindicated for sclerosant
therapy.
Three tourniquet test: To find out the site of incompetent
perforator, three tourniquets are tied after emptying the vein.
1. At saphenofemoral junction.
2. Above knee level.
3. Another below knee level.
Patient is asked to stand and looked for filling of veins and site
SRB’s Manual of Surgery
of filling. Then tourniquets are released from below upwards,
again to see for incompetent perforators.
Schwartz test: In standing position, when lower part of the
long saphenous vein in leg is tapped, impulse is felt at the
saphenous junction or at the upper end of the visible part
of the vein. It signifies continuous column of blood due to
valvular incompetence.
Fegan’s test: On standing, the site where the perforators enter
the deep fascia bulges and this is marked. Then on lying down,
button like depression (crescent like) in the deep fascia is felt
at the marked out points which confirms the perforator site.
Pratt’s test: Esmarch bandage is applied to the leg from below
upwards followed by a tourniquet at saphenofemoral junction.
After that the bandage is released keeping the tourniquet in
the same position to see the “blow outs” as perforators.
Morrissey’s cough impulse test: The varicose veins are
emptied. The leg is elevated and then the patient is asked to
cough. If there is saphenofemoral incompe tence, expansile
impulse is felt at saphenous opening. It is a venous thrill due
to vibration caused by turbulent backflow.
Ian-Aird test: On standing, proximal segment of long saphe-
nous vein is emptied with two fingers. Pressure from proximal
finger is released to see the rapid filling from above which
confirms saphenofemoral incompetence.
Examination of the abdomen has to be done to look for pelvic
tumours, lymph nodes, which may compress over the veins
to cause varicosity.
COMPLICATIONS OF VARICOSE VEINS
B
x Haemorrhage: Venous haemorrhage can occur from the ruptured
varicose veins or sloughed varicose veins, often torrential, but
can be controlled very well by elevation and pressure bandage.
x Pigmentation (hemosiderosis), eczema and dermatitis.
x Periostitis causing thickening of periosteum. It delays healing of
ulcer due to poor perfusion of ulcer bed.
x Venous ulcer.
x Marjolin`s ulcer—due to unstable scar of long duration—very
well-differentiated squamous cell carcinoma.
x Lipodermatosclerosis.
x Ankylosis of the ankle joint is due to fibrosis of soft tissues around
ankle joint—fibrous ankylosis.
x Talipes equinovarus—wherein patient walks on the tip of toes
like horse.
x Calcification of the wall of varicose veins or of sclerosed soft
tissue.
x Recurrent thrombophlebitis, clot formation on the superficial
system often at perforator level which often get infected causing
fever and tenderness over the spot.
x Deep venous thrombosis per se due to varicose vein is rare but
can occur if there is associated deep vein disease or recurrent
thrombophlebitis.
Investigations
Venous Doppler:
¾
With the patient stand ing, the Doppler probe is placed
at saphenofemoral junction and later wherever required.
Basically by hearing the changes in sound, venous flow,
venous patency, venous reflux can be very well-identified.
¾
Doppler test: When a hand held Doppler (continuous
wave 8 MHz flow detector) is kept at SFJ, typical audible,
‘whoosh signal’ >0.5 sec while performing Valsalva
manoeuvre is the sign of reflux at SFJ. It is also used at
SPJ and at perforators.
VENOUS DISABILITY SCORING SYSTEM
B
Score 0 Asymptomatic
Score 1 Symptomatic but able to carry out activities without any
therapy
Score 2 Symptomatic—can do activities only with compression/
limb elevation
Score 3 Symptomatic—unable to do daily activities even with
compression or limb elevation
Venous segmental disease score (venous clinical scoring
system/VCSS) is done based on different symptoms/signs/
ulcer activity/compression therapy with 10 parameters with
each having 3 scores as mild/moderate/severe.
Fig. 1.409: Doppler machine to assess venous
system and its problems.
Note:
All clinical/phlebological tests mentioned above have been superseded by
Doppler test. Doppler test is considered to be a clinical method.
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CHAPTER 1N General Surgery: Venous Diseases
A
Fig. 1.411: Venous haemodynamic mapping (VHM)
of the lower limb.
VENOUS DOPPLER IN VARICOSE VEINS
B
x To find out DVT—very important
x To find out saphenofemoral, saphenopopliteal incompetence
x To find out perforator incompetence
x Uniphasic signals signify flow in one direction—normal
x Biphasic flow signifies reversal flow with incompetence
x To find out thrombus/thrombophlebitis in superficial veins
B
Figs. 1.410A and B: Duplex scan for venous diseases of lower limb
should also be done in standing position.
Duplex scan:
¾
It is a highly reliable U/S Doppler imaging technique (here
high resolution B mode ultrasound imaging and Doppler
ultrasound is used) which along with direct visualisation
of veins, gives the functional and anatomical informa tion,
and also colour map. Examination is done in standing,
lying down position and also with Valsalva manoeuvre.
Hand-held Doppler probe is placed over the site and
visualised for any block and reversal of flow. DVT is very
well-identified by this method.
¾
Venous haemodynamic mapping/VHM/Cartography is
essential prior to surgery.
Note:
• Proper venous haemodynamic mapping (VHM) is essential.
• Saphenous eye (Egyptian eye) at SFJ should be identified in duplex US.
• Reflux is defined as retrograde blood flow in reverse direction lasting
for more than 0.5 seconds.
• ‘Mickey mouse sign’ is the duplex scan transverse B mode image
showing great saphenous vein (GSV) and femoral vein medially and
femoral artery laterally.
¾
Digitally coded free flow (B flow) USG (Professor Feder
Lurie of Hawaii) allows simultaneous visualisation of
flowing blood/blood cells and surrounding stationary
structures to give proper haemodynamic imaging with
functioning mechanism of venous valves, valve leaflets
and flow across leaflets. This may be the ideal tool of
investigation in future.
x Ultrasound abdomen, peripheral smear, platelet count, other
relevant investigations are done depending on the cause of the
varicose veins.
x If venous ulcer is present, then the discharge is collected for
culture and sensitivity, biopsy from ulcer edge is taken to rule
out Marjolin’s ulcer.
x Plain X-ray of the part is taken to look for periostitis.
x IVUS (Intravenous ultrasound) is often used.
Plethysmography:
¾
It is a noninvasive method which measures volume changes
in the leg. It gives functional information on venous volume
changes and calf muscle pump insufficiency.
¾
Photoplethysmography: Using probe transmission
of light through the skin, venous filling of the surface
venules which reflects the superficial venous pressure
is measured. Initially patient performs dorsiflexion at
ankle for 10 times to empty the venules and pressure
tracing falls in photoplethysmography. Patient takes rest
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