Detailed presentation on Varicose veins, examination and management
Detailed presentation on Deep Vein Thrombosis, categories, staging and scoring systems and management.
Management also includes Endovascular and Surgical techniques.
Short notes made on IVC filters
3. Venous anatomy of lower limb
The venous system of the lower limb can be divided anatomically into
• the superficial venous system, which is located within the superficial tissues
• deep venous system, located deep to deep fascia and
• connected by fascial perforating veins.
5. Deep veins
• The deep veins of the lower limb
include three pairs of venae
commitantes, which accompany
the three crural arteries
• These six veins
intercommunicate and come
together in the popliteal fossa to
form the popliteal vein.
6. Fascial Perforators
Perforator Superficial vein Deep vein
Cockett’s Posterior arch
vein of
Leonardo
Posterior tibial
vein
Boyd’s Great
saphenous vein
Gastrocnemial
vein
Dodd Great
saphenous vein
Superficial
femoral vein
Hunterian Great
saphenous vein
Superficial
femoral vein
7. Pathophysiology of venous hypertension
• Venous return to heart is maintained by a pressure gradient between veins of leg and right
atrium.
• This is maintained by:
1. increase in thoracic volume during inspiration with a decrease in intrathoracic
pressure to -6 mm of Hg.
2. increase in the venous pressure by compression of the calf muscle pump
3. tone of the venous wall and
4. neuroendocrine factors.
8. Varicose Veins
• Varicose veins are dilated, tortuous elongated superficial veins ≥3 mm in diameter
measured in upright position with demonstrable reflux.
• There may be
• Primary varicose veins – idiopathic
• Secondary varicosities
9. Risk factors for primary varicose
veins
Risk factors for the development of varicose veins include
• Advancing age
• female gender
• Multiparity
• Obesity
• Heredity
• history of trauma to the extremity and
• prolonged standing.
10. Causes of secondary varicose veins
Pressure gradient dysfunction:
a. Increased abdominal or thoracic pressure:
1. COPD
2. Pregnancy
3. Obesity
4. Large tumour
5. Constipation
b. Decreased calf muscle pump function:
1. Immobility
2. Ankle joint fusion
3. Paralysis
Dysfunction of the venous system:
a. Venous structural deficit:
1. Valvular agenesis
2. Valvular incompetence
3. Venous dilatation
4. Loss of vein wall compliance and venous
tone
b. Venous occlusion by thrombosis
c. External venous compression:
1. May–Thurner syndrome
2. Pelvic/abdominal tumour
3. Pelvic/abdominal radiotherapy
11. Clinical features of venous hypertension
• Heaviness or aching in the leg present throughout day and increased by evening
• Discoloration
• Itching
• Cosmetic
12. Clinical features of venous hypertension
• Telangiectasia (spider veins): tiny intradermal venules less than 1 mm in diameter.
• Reticular vein: small dilated ‘bluish’ subdermal vein 1–2.9 mm in diameter.
• Varicose vein: subcutaneous dilated vein 3 mm in diameter or larger. They are elongated and
tortuous, with intermittent ‘blowouts’, and are defined by the presence of reflux.
• Saphena varix
• Corona phlebectatica (malleolar flare)
• Edema
• Eczema
13. Clinical features of
venous
hypertension
• Lipodermatosclerosis (LDS): chronic
inflammation and fibrosis of the skin and
subcutaneous tissues, resulting in a tight,
contracted, ‘woody’ leg on examination.
• Atrophie blanche: localized areas of
atrophic, white skin, often surrounded by
telangiectasia and pigmentation.
• Venous ulcer
14. Brodie - Trendelenburg’s test
• There are two components to this test. First, with the patient supine, the leg is elevated 45° to
empty the veins, and the GSV is occluded with the examiner’s hand or with a rubber
tourniquet. Then, with the GSV still occluded, the patient stands, the compression on the GSV
is released, and the superficial veins are observed for filling with blood.
• Sudden filling of veins on standing when GSV is released indicates incompetence of sapheno-
femoral junction .
• With the GSV still occluded, if there is filling of veins on standing for 1-minute, it indicates
incompetent perforators.
15. Tests for Varicose veins
Test Method and Interpretation
Morrissey’s test Cough impulse test
Modified Perthes test
Tourniquet is applied around the upper part of the thigh and patient is asked to walk
quickly with tourniquet in the place.
Severe crampy pain is suggestive of deep venous obstruction.
Schwartz test
In long standing varicose veins if the lower part of varicosity is tapped, an impulse is
felt at the saphenous opening.
Fegan's test
Palpation to find the fascial defects to locate incompetent perforators
16. Investigations
• Duplex ultrasonography (DUS) augmented by
color flow imaging is now the standard
diagnostic method in the evaluation of the
venous system.
• The scan should commence in the groin, using
a transverse view to identify the GSV and CFV
lying medial to the common femoral artery (the
‘Micky Mouse’ sign)
18. Treatment of Varicose veins
Varicose veins
treatment
Compression
dressing
Endothermal
ablation
Non-endothermal
non-tumescent
ablation
Catheter guided
sclerotherapy with
mechanical ablation
Foam Sclerotherapy
Open surgery
Saphenofemoral ligation and
great saphenous stripping
Saphenopopliteal junction
ligation and small saphenous
stripping
19. Compression dressing
• Compression dressing creates a graduated
external pressure of 30-40 mm Hg to
improve deep venous return and reduce
venous pressures.
• They significantly improves varicose vein
symptoms but has poor compliance and
long-term tolerance.
• They further will not prevent the
occurrence or progression of varicose
veins.
• Incorrect application of compression
hosiery can cause pressure necrosis,
tourniquet effects.
20. Endothermal ablation
• Endothermal ablation technologies replaced surgical ligation and stripping as the gold standard
treatment.
• It is cost effective as it can be performed as an outpatient procedure under local anesthetic.
• The basic concept is that a treatment device is inserted into the incompetent axial vein percutaneously.
• The vein is surrounded by tumescent local anesthetic solution causing:
1. compression of vein onto the treatment device, emptying it of blood.
2. hydro-dissects tissues such as nerves away from the zone of injury
3. it acts as a heat sink
21. Endothermal ablation
• The treatment device then
produces thermal energy
that destroys the structure of
the vein, resulting in
permanent occlusion.
• Two broad technologies
exist: laser and
radiofrequency ablation
23. Non-endothermal non-tumescent ablation –
Tessari Foam sclerotherapy
• This technique does not require tumescent anaesthesia.
• It involves injection of sclerosing agent into the vein.
• Sclerosing agents used are - Sodium tetradecyl sulfate, polidochanol and
ethanolamine.
• Destroys lipid membranes of endothelial cells causing them to shed, leading to
thrombosis, fibrosis and sclerosis.
• Foam sclerotherapy was developed as foam used will displace the blood from the
vessel and drug dose can be minimized.
24. Tessari Foam
sclerotherapy
• Sclerosant : air ratio is 1:3
or 1:4.
• Complications:
• Anaphylaxis
• Thrombophlebitis
• Thrombosis
• Skin ulceration
• Skin discoloration
25.
26. Catheter guided sclerotherapy with
mechanical ablation
• This involves deployment of a catheter within the vein lumen and an angled wire
attached to a motorized handle is inserted from the end.
• The trigger on the handle is depressed, spinning the wire around and liquid
sclerosant is infiltrated via the catheter simultaneously during catheter withdrawal.
• The spinning wire causes physical damage to the endothelium and deeper
penetration of the sclerosant into the vein wall.
27. Open Surgery -
Saphenofemoral
ligation & vein
striping
Saphenofemoral ligation and great
saphenous stripping:
• An oblique groin incision made just lateral to pubic
tubercle
• Long saphenous vein identified and dissected till SFJ.
• 6 tributaries identified and ligated.
• Flush ligation of GSV done followed by striping of the
vein to the knee. .
Complications:
• Bleeding
• Postoperative pain
• Permanent skin discoloration
• Saphenous nerve injury
28. Minimally invasive surgery
Sole incompetent perforators or distal perforators following junctional ligation are
managed by:
1. Conventional phlebectomy (stab avulsion)
2. Powered phlebectomy
3. Subfascial endoscopic perforator vein surgery (SEPS)
29. Recurrence of Varicose veins
Recurrence is due to:
1. Neovascularization
2. Reflux in residual axial vein
3. Inadequate ligation
4. New junctional reflux
31. Deep Vein Thrombosis - epidemiology
• Deep vein thrombosis (DVT) and venous thromboembolism (VTE), remain an
important preventable cause of morbidity and mortality in a surgical patient.
• The incidence of VTE is approximately 100 per 100,000 people per year in
the general population, with 20% of the diagnoses made within 3 months
of a surgical procedure.
32. Deep Vein Thrombosis - epidemiology
• Of the symptomatic patients, one-third will present with PE and two-thirds
with DVT.
• Acute DVT poses several risks and has significant morbid consequences viz.,
edema, pain, immobility and the most dreaded sequel of pulmonary embolism.
33. Etiopathogenesis of DVT – Virchow’s Triad
Virchow’s
triad of
thrombosis
Circulatory
stasis
Hypercoag
ulability
Vascular
damage
34. Etiopathogenesis of DVT
• Of these risk factors, relative hypercoagulability appears most
important in cases of spontaneous VTE, or so-called idiopathic
VTE, whereas stasis and endothelial damage likely play a
greater role in secondary VTE.
35. Etiopathogenesis of DVT – stasis and
vascular damage
• The stasis may contribute to the endothelial cellular layer contacting
activated platelets and procoagulant factors, thereby leading to DVT.
• Though overt loss of endothelium exposing subendothelial ECM, is
required for thrombus formation, endothelium need not be denuded or
physically disrupted to contribute to the development of thrombosis; any
perturbation in the dynamic balance of the prothrombotic and
antithrombotic effects of endothelium can influence clotting locally.
36. Etiopathogene
sis of DVT –
hypercoagula
bility
Primary (genetic) causes:
• Factor V Leiden
• Prothrombin
20210A
• Antithrombin
deficiency
• Protein C deficiency
• Protein S deficiency
• Factor XI elevation
• Dysfibrinogenemia
Mixed causes:
• Antiphospholipid
antibody
syndrome
• Homocysteinemi
a
• Factors VII, VIII,
IX, XI elevation
37. Secondary (acquired) causes of DVT
Advanced age
Hospitalization/immobilization
Hormone replacement therapy & OC pills usage
Pregnancy and puerperium
Prior venous thromboembolism
Malignancy
Major surgery
Obesity
Nephrotic syndrome
Trauma or spinal cord injury
Varicose veins
Polycythaemia
38. Diagnosis of DVT – clinical evaluation
• Diagnosis of DVT requires a high index of suspicion.
• Usually, there may be no or few clinical findings such as pain,
swelling or erythema.
• On examination there may be tenderness, erythema and dilated
superficial veins with Homan’s sign being positive occasionally.
• History and physical examination are often nonspecific and
unreliable.
41. Pre-test probability – modified WELL’S
scoring
Variable Score
Lower limb trauma or surgery or immobilization in a plaster cast 1
Bedridden for >3 days or surgery in last 4 weeks 1 1
Previous DVT 1
Malignancy (including treatment up to 6 months ago) 1
Pitting edema 1
Dilated collateral superficial veins (not varicose veins) 1
Entire limb swollen 1
Tenderness along the line of femoral or popliteal veins 1
Calf circumference >3 cm than the other side (10 cm below the tibial tuberosity) 1
Intravenous drug abuse 3
Alternative diagnosis more likely than DVT -2
42. Clinical suspicion of DVT – Modified wells scoring
Suspicion unlikely (score ≤2)
D-dimer
Normal
Diagnosis ruled out
Raised
Duplex ultrasound
Likely DVT (score >2)
Duplex ultrasound
43. Diagnosis of DVT –
Duplex ultrasound
• Most commonly performed test for
the detection of DVT.
• Uses real-time B-mode ultrasound
with compression and flow
augmentation amneuvres combined
with venous Doppler.
• It is a non-invasive method -
visualizing venous anatomy, detecting
completely and partially occluded
venous segments, and demonstrates
physiologic flow characteristics.
44. Diagnosis of DVT – Fibrinogen Uptake (FUT)
• Iodine-125 fibrinogen uptake (FUT) involves IV administration of
radioactive fibrinogen and monitoring for increased uptake in
fibrin clots.
• An increase of 20% or more in one area of a limb indicates an
area of thrombus.
• FUT can detect DVT in calf, but high background radiation from
pelvis and urinary tract limits its ability to detect proximal DVT.
• It also cannot be used in an extremity that has recently
undergone surgery or has active inflammation.
45. Diagnosis of DVT - Venography
• Venography is the gold standard method.
• Done by placing a small catheter in a dorsal
foot vein and a radiopaque contrast agent is
injected. Radiographs are obtained after
injection.
• A positive test result is failure to fill the deep
system with passage of the contrast medium
into the superficial system or demonstration of
filling defects.
• A normal study result virtually excludes the
presence of DVT.
46. Differential diagnosis of DVT
• Cellulitis
• Lymphoedema
• Chronic venous insufficiency
• Haematoma and
• Ruptured Baker cyst.
47. Treatment of DVT
• Anticoagulation is the mainstay of treatment for DVT and patient
with confirmed DVT on duplex imaging should be anticoagulated
rapidly.
• The aim of it is to reduce mortality, thrombus extension,
recurrence, and the risk of PTS (after DVT) and chronic
thromboembolic pulmonary hypertension (after pulmonary
embolism).
48. Various anticoagulants
Anticoagulant Indications Dose Route Adverse effects Monitoring
Contraindica
tions
Reversal agent
Unfractionated
heparin
• DVT
• PE
• Cancer-
associated
VTE
80 IU/
kg
intravenous
bolus, then
18 IU/
kg per hour
IV
infusion
PTT
at 60 to 80
seconds
Heparin-
induced
thrombocytop
enia
Protamine
Warfarin
• DVT
• PE
Typically
start with
5mg
Oral
Bleeding,
intracranial
haemorrhage,
not
safe in
Pregnancy
target INR
2.0–3.0
Intracranial
haemorrhage,
skin
necrosis,
pregnancy,
breastfeeding
Vitamin K,
prothrombin
complex
concentrate
49. Various anticoagulants
Anticoagulan
t
Indications Dose Route
Adverse
effects
Monitorin
g
Contraindications
Reversal
agent
Rivaroxaban
1. DVT
2. PE
15 mg oral
twice daily
for 21 days,
then 20 mg
daily
Oral Bleeding No
Severe renal and hepatic
impairment, pregnancy,
breastfeeding
Enoxaparin
1. DVT
2. PE
3. Cancer-
associated
VTE
Typically
start with
5mg
Oral Bleeding No
Heparin-induced
thrombocytopenia
within previous 100 days
Dabigatran
1. DVT
2. PE
150 mg oral
twice
daily
Oral
Bleeding,
dyspepsia No
Severe renal and hepatic
impairment, pregnancy,
breastfeeding
Idarucizu
mab
50. Duration of anticoagulation
Subgroup Duration of anticoagulation
proximal DVT provoked
1. by surgery or trauma
2. by a non-surgical transient risk factor
3. unprovoked isolated distal DVT and
4. for unprovoked DVT when the bleeding risk is high
3 months
DVT provoked by active cancer 6 months
1. recurrent DVT
2. for unprovoked proximal DVT when the bleeding risk is low
Extended anticoagulation
51. Treatment of DVT - Thrombolysis
• Catheter-directed thrombolysis (CDT) involves the percutaneous
insertion of a catheter and infusion of a thrombolytic typically
recombinant tissue plasminogen activator (tPA) directly into the
thrombus.
• There is no reduction in the risk of post-thrombotic syndrome (PTS)
but has increased bleeding risk.
• Indications – extensive iliofemoral DVT and phlegmasia cerulea
dolens.
52. IVC filters
• Indications of IVC filters include:
• manifestations of lower extremity VTE and
absolute contraindications to anticoagulation,
• patients having bleeding complication from
anticoagulation therapy of acute VTE
• who develop recurrent DVT or PE despite
adequate anticoagulation therapy and
• for patients with severe pulmonary
hypertension
53. IVC filters
Remove IVC
filterswithin 29 and 54
days after
implantation.
Complications include
thrombosis or bleeding
at the insertion site
misplacement of the
filter
thrombosis of the IVC,
DVT,
breaking, migration
Erosion of the filter
through the IVC.
54. Treatment of DVT – Surgical thrombectomy
• Surgical therapy is generally reserved for patients
1. worsening with anticoagulation therapy
2. phlegmasia cerulea dolens and
3. impending venous gangrene
• Patient with phlegmasia cerulea dolens - a fasciotomy.
• In iliofemoral DVT - a longitudinal venotomy in the common femoral vein with
venous balloon embolectomy of proximal thrombus and manual pressure removal
of distal thrombus with application of a tight rubber elastic wrap.
55. Treatment of
DVT –
Surgical
thrombectomy
For a thrombus extending into
IVC - IVC exposure
transperitoneally and thrombus
removal by gentle massage.
Every operated patient should
be anticoagulated with heparin
for several days.
58. Thromboembolism risk and recommended
thromboprophylaxis in surgical patients
LEVEL OF RISK
APPROXIMATE DVT RISK
WITHOUT
THROMBOPROPHYLAXIS
SUGGESTED
THROMBOPROPHYLAXIS
OPTIONS
Very low risk general or
abdominopelvic surgery
<0.5% (Rogers score <7;
Caprini score 0)
No specific thromboprophylaxis
Early ambulation
Low-risk general or
abdominopelvic surgery
∼1.5% (Rogers score 7–10;
Caprini score 1–2)
Mechanical prophylaxis
Moderate-risk general or
abdominopelvic surgery
∼3.0% (Rogers score >10;
Caprini score 3–4)
LMWH (at recommended doses),
LDUH, or mechanical prophylaxis
High-risk general or
abdominopelvic surgery
∼6% (Caprini score ≥5)
LMWH (at recommended doses),
fondaparinux and mechanical
prophylaxis
60. Duration of prophylaxis
• Thromboprophylax
is should be
continued until
discharge
Drug Dose and route Comment
Low dose
unfractionated
heparin
5000 IU 8-12hly;
subcutaneously
Maybe started 12
hours before
surgery
Enoxaparin 40mg once a day;
subcutaneously
Maybe started 12
hours before
surgery
