MD61 Group2 - Chronic Venous Insufficiency (Presentation).pdf

1. Chronic Venous
Insufficiency

2. Chronic Venous Insufficiency
Keywords: Varicositas, Varicose vein, Venous Insufficiency, Venous Reflux
Disease, Chronic venous disease (CVD), Valvular Incompetence,
Subj: Hospital Surgery II
Prof. MOK THEAVY, DES
Group 2

3. Member
Hon Makara (1) Definition
(2) Epidemiology
(4) Physiology Anatomy
Hel Siyean (5) Pathophysiology
(6) Clinical Feature
(8) Diagnosis
Ro Sophara (9) Differential Diagnosis (10) Management
Measrithsomaly Sreypich (11) Complication (12) Prognosis
Map Ratanakvattey (3) Classification
Yi Bunyong (7) Etiology

4. Content
1). Definition
2). Epidemiology
3). Classification
4). Physiology Anatomy
5). Pathophysiology
6). Clinical Feature
7). Etiology
8). Diagnosis
9). Differential Diagnosis
10). Management
11). Complication
12). Prognosis

5. Overviews
 What is a Venous Disorder?
Acute venous diseases Chronic venous diseases
1) Leg vein thrombosis
2) Vein inflammation (phlebitis)
1) Spider veins
2) Varicose veins
3) Vein weakness: Venous insufficiency
4) Leg ulcer (ulcus cruris venosum)

6. I. Definition
• Chronic venous insufficiency (CVI) refers to functional changes that may occur in the
lower extremity due to persistent elevation of venous pressures.
• This most commonly results from venous reflux due to faulty valve function developing as
a long-term sequela of deep vein thrombosis (DVT) and recanalisation and may also
develop due to primary valvular incompetence without previous episode(s) of DVT.
• The term 'CVI' is usually reserved for more advanced disease involving oedema, skin
changes, or frank ulcers.
• Varicose Vein: Varicose veins are subcutaneous, Permanently dilated veins 3 mm or more
in diameter when measured in a standing position; however, they may not be visible.
• Varicosity (Plural varicosities): An enlarged vessel or nerve, particularly a blood vessel.

7. II. Epidemiology
Chronic venous insufficiency:
• CVI affects about 7% of the population.
• Prevalence of venous leg ulcers, the most extreme form of
• CVI, has been estimated to range from 1% to 2%.
• Following treatment, up to 7 in 10 wounds recur.
• The total cost of treating venous leg ulcers in the US alone was $3 billion in
2006.

8. Varicose veins:
• Generally, prevalence rates are higher in industrialised countries and in more developed
regions.
• Prevalence of visible varicose veins in the Western population aged over 15 years is 10%
to 15% in men and 20% to 25% in women.
• Prevalence rates in the US are 15% (range from 7% to 40%) in men and 27.7% (25% to
32%) in women.
• Visible varicose veins are more prevalent in Hispanic people (26.3%) and less prevalent in
Asian people (18.7%).
Mortality
Prevalence

9. III. Physiology Anatomy
• Capillaries and Venules, collect the used, oxygen-depleted blood from the muscles and
organs.
• Venous Return: Heart and Breathing, The venous valves, calf muscle pump, Vein tension
and vein dilation.
• Venous Flow: Saphenous veins (Greater, Smaller), Popliteal vein.
• Venous Type: Deep veins, Superficial veins, Perforating veins.
• Gravitational effects
• Blood flow travel against gravity: valves, muscle pumps.
• Venous valve function: Opening, Equilibrium, Closing, Closed.
• Contraction
• Relaxation (muscle pump) allows blood to refill to the deep venous system.

10. Venous Pressure
• Normal Venous Pressure (Refill Time > 20 seconds)
(1) Resting Standing Pressure: 80 – 90 mmHg
(2) Drop in Exercise: 20 – 30 mmHg
• Abnormal Venous Pressure (Refill Time < 20 seconds)
(1) Resting Standing Pressure: Higher than normal
(2) Drop in Exercise: Blunt (decrease 50%)
• Abnormal Venous Pressure , Venous Obstruction
(1) Resting Standing Pressure: Higher than normal
(2) Not-Drop in Exercise

11. IV. Clinical Feature
Common:
1) Corona phlebectatica (malleolar flare or
ankle flare)
2) Ankle swelling
3) Hyperpigmentation
4) Lipodermatosclerosis
5) Atrophie blanche
6) Leg ulcers
Uncommon:
1) Leg fatigue, aching, and/or discomfort
2) Heavy legs
3) Leg cramps
4) Telangiectasias
5) Reticular veins
6) Dilated tortuous veins
7) Dry and scaly skin
Atrophie blanche:
• L'atrophie blanche est la traduction clinique d'une ischémie cutanée par occlusion localisée
des petits vaisseaux du derme superficiel.

12. Telangiectasias
• Telangiectasias are small, widened blood
vessels on the skin.
• They are usually harmless, but may be
associated with several diseases.
Reticular veins
• Reticular veins are the visible veins below
your skin that appear blue-purple in colour,
• They don't bulge out as varicose veins do.
Telangiectasias

13. Corona phlebectatica:
• Corona phlebectatica is a cutaneous sign of chronic venous insufficiency, characterized
by abnormally dilated veins around the ankle.
• It is characterised by the presence of abnormally visible cutaneous blood vessels at the
ankle with:
1) Venous cups
2) Blue and red telangiectasis
3) Capillary stasis spots

14. V. Etiology
• Primary varicose veins are thought to be due to genetic or developmental defects in the
vein wall that cause
1) Diminished Elasticity
2) Valvular Incompetence.
• Secondary varicose veins arise from destruction or dysfunction of valves caused by:
1) Trauma
2) Deep Venous Thrombosis
3) Arteriovenous Fistula
4) Nontraumatic Proximal Venous Obstruction (Pregnancy, Pelvic Tumor)

15. • Severe CVI usually results from:
1) Chronic Valvular Reflux
2) Venous Obstruction
3) Frequently from a combination of both.

16. Diminished Elasticity

17. Arteriovenous Fistula
(1) Arteriovenous (AV) fistula is an irregular
connection between an artery and a vein.
(2) Blood flow avoids tiny blood vessels
(capillaries) and moves directly from an artery into
a vein.
(3) Arteriovenous (AV) fistula is an irregular
connection between an artery and a vein.
(4) Due to: Injuries that pierce the skin, Congenital
arteriovenous fistulas, Genetic conditions,
Dialysis-related surgery.

18. Trauma

19. Pregnancy

20. Pelvic Tumor

21. VI. Physiopathology
• Chronic Venous Insufficiency, Retrograde blood flow.
• Venous Return ( calf and foot muscle pumps, patent veins, and
competent valves).
• Venous insufficiency or Chronic Venous Insufficiency (CVI).
• Venous Reflux

22. Venous Reflux (1)
• Venous Reflux or Retrograde flow of blood serves to increase hydrostatic
pressures.
• Valve Incompetence lead to rapid refill and accumulation of fluid.
• This excessive local pressure can produce dilatation of the superficial
veins.
• Hydrostatic pressures: Vessel wall is thin, direct injury or Superficial
phlebitis.

23. Venous Reflux (2)
• Abnormal capillaries: accumulation of fluid, macromolecules, and
extravasated red blood cells into the interstitial space (oedema).
• The typical constellation of findings that ensue include:
1) Oedema
2) Lipodermatosclerosis
3) Ulceration
4) Hyperpigmentation
• Microangiopathy: Macrocirculation > Venous microangiopathy.

24. Microangiopathy
• There have been several postulated mechanisms for the development of
Venous Microangiopathy, including:
1) Fibrin Cuff Hypothesis
2) White Blood Cell Trapping

25. • Fibrin Cuff Hypothesis , venous hypertension with resultant extravasation
of plasma proteins and fibrinogen into the soft tissue, resulting in a fibrin
cuff around the capillaries and Tissue Hypoxia.
(1) Venous hypertension
(2) Fibrinogen leaks from the capillaries
(3) Fibrinogen coagulates and hardens to form a fibrin cuff
(4) Cuff surrounds the capillaries
(5) Cuff establishes a barrier that prevents oxygen and nutrients
(6) Skin cannot reach of oxygen and nutritional
(7) Tissue hypoxia

26. • White cell trapping that white cells are trapped in capillaries due to
venous hypertension, with secondary escape of proteins into the interstitial
space and resultant Diminished Tissue Oxygenation.
(1) Increase Venous Blood Pressure
(2) Leukocyte surrounding tissue and attack to vessel wall.
(4) When, leukocytes are activated and releasing of pro-inflammatory and
cytokine.
(5) Then, present as ulceration.
(6) Chronic Inflammatory State / Chronic Venous Insufficiency

27. • After Ulceration / Cell Injury / Subcutaneous
• Lipodermatosclerosis characteristically results from capillary
proliferation, fat necrosis, and fibrosis of the skin and subcutaneous
tissues.
(1) Hypertension leads to an increase of leukocytes in the veins, which migrate
to surrounding tissue.
(2) Leukocytes are activated, releasing proinflammatory cells and cytokines,
inducing a chronic inflammatory state.
(3) Increased collagen production leads to the fibrosis of subcutaneous fat.
Lipodermatosclerosis

28. Hyperpigmentation
• Hyperpigmentation (usually a reddish-brown discoloration) of the ankle
and lower leg is also known as brawny oedema.
• It results from extravasation of blood and deposition of haemosiderin in
the tissues due to long-standing ambulatory venous hypertension.
(1) Hemosiderin (Protein Compound)
(2) Red Blood Cell contain Hemoglobin
(3) Hemoglobin carry Oxygen & Iron
(4) RBC breakdown, releasing of Iron from hemoglobin.
(5) Accumulated fluid lead to Iron Trap upper skin tissue.

29. Physiopathology (2): Varicose Veins
• The venous system acts as both a reservoir and a conduit in the return of blood to the heart
and lungs for oxygenation and re-circulation.
• End capillary venous pressure is low (20 mmHg). Veins are thin-walled and lack the
muscular walls of arteries.
• Therefore, veins require assistance in blood return. This is provided by valves and muscle
pumps - as one walks, the muscle pumps contract and push blood against gravity, and as
the muscle pump relaxes, the fall of the blood is stopped by the valve system.
• When one of these factors is not functioning properly, venous hypertension and
insufficiency can ensue, possibly leading to varicose veins.
• A normal vein wall has three smooth muscle layers that all help to maintain its tone.
• Varicose veins demonstrate marked proliferation of collagen matrix as well as decreased
elastin, leading to distortion and disruption of muscle fibre layers.

30. IV. Classification
Revised CEAP criteria:
• C = Clinical class
• E = Etiology
• A = Anatomy
• P = Pathophysiology

31. Clinical (C)
• C0: No visible sign of venous disease
• C1: Telangiectases or reticular veins
• C2: Varicose veins
• C3: Edema
• C4: Changes in skin and subcutaneous tissue
C4a: Pigmentation or eczema
C4b: Lipodermatosclerosis or atrophie blanche
• C5: Healed ulcer
• C6: Active ulcer

32. Etiologic (E)
• Ec: Congenital (eg, Klippel-Trenaunay syndrome)
• Ep: Primary
• Es: Secondary (eg, postthrombotic syndrome, trauma)
• En: No venous cause identified

33. Anatomic (A)
• As: Superficial
• Ad: Deep
• Ap: Perforator
• An: No venous location identified

34. Pathophysiologic (P)
• Pr Reflux
• Po Obstruction, thrombosis
• Pr,o Reflux and obstruction
• Pn No venous pathophysiology identified

35. Venous Disorder Stages
• Stage 0: No signs that can be seen or felt (like achy or tired)
• Stage 1: Visible blood vessels, including spider veins.
• Stage 2: Varicose veins at least 3 millimeters wide.
• Stage 3: Edema (swelling) but no skin changes.
• Stage 4: Changes to your skin’s color and/or texture.
• Stage 5: Healed ulcer.
• Stage 6: Acute (active) ulcer.

36. Varicose veins Edema

37. Link: https://www.elenaconde.com/en/chronic-venous-insufficiency-
from-a-dermatological-perspective/
Dermatological

38. VII. Diagnosis
1). Clinical Feature
2). Physical Examination
3). Noninvasive Testing
a) Venous Duplex Imaging
b) Air Plethysmography
c) Computed Tomographic or Magnetic Resonance Venography
d) Other Techniques
4). Invasive Testing
a) Contrast Venography
b) Intravascular Ultrasound
c) Ambulatory Venous Pressure

39. Clinical Feature
(1) Symptomatic
(2) Major
(3) Congenital

40. Symptomatic
1) Heavy legs, leg fatigue, aching, and/or discomfort.
2) Burning and itching of the skin and leg cramps.

41. Major
• CVI present with:
1) Dilated veins, varicose vein, tenderness
2) Edema
3) Leg pain
4) Cutaneous changes in the leg.

42. Congenital
• Congenital disorders are those that are present at birth but may be
recognized later in life.
• These include the well-recognized syndromes of:
(1) Klippel-Trénaunay Syndrome (varicosities and venous
malformations, capillary malformation, and limb hypertrophy) and
(2) Parkes-Weber (venous and lymphatic malformations, capillary
malformations, and arteriovenous fistulas).

43. Klippel-Trénaunay Syndrome
• A newborn boy was noted to have a diffuse
erythematous rash at birth.
• He had been born at 40 weeks of gestation to a 19-year-
old gravida 2, para 2 mother who had had adequate
prenatal care.
• The pregnancy had been complicated by chlamydia
infection with documented cure after treatment,
anemia, and an episode of self-limited hives.
• He had been born by spontaneous vaginal delivery and
had Apgar scores of 8 at 1 minute and 9 at 5 minutes.
• Physical examination findings were remarkable for a
diffuse erythematous macular rash with blanching on
his trunk and extremities.
https://www.consultant360.com/article/consultant360/kl
ippel-trenaunay-syndrome
Diffuse Erythematous Macular Rash

44. Klippel-Trénaunay syndrome
Lymphorrhea
Capillary-venolymphatic Malformation (CVLM)
Link: https://www.compva.com/patientexamples/klippel-trenaunay-syndrome-lymphorrhea

45. Link: https://www.nejm.org/doi/full/10.1056/NEJMicm1312948
Parkes-Weber Syndrome
• Fingertip ulcers
• Arteriovenous malformation of the left arm
• Hypertrophy, with a giant arteriovenous
malformation (Fingers, forearm, elbow, and
upper arm)
• Enlarged and tortuous arteries and veins
Parkes Weber syndrome consists of:
venous and capillary malformations

46. Physical examination
• Sign
• Tourniquet Test
(1) Brodie-Trendelenburg Test
(2) Perthes Test
(3) Delbet-Mocquot test
(4)

47. Sign
1) Early signs of CVI: Telangiectasias, Reticular Veins, Corona Phlebectatica
2) Palpation for bulges consistent with varicose veins.
3) Ankle swelling (usually unilateral but may be bilateral) due to oedema is
also common.
4) Severe CVI: Atrophie blanche, Lipodermatosclerosis, and
Hyperpigmentation.
5) Venous ulcers are located in the gaiter area.

48. • CVD represents a spectrum of conditions ranging from simple
telangiectases or reticular veins to more advanced stages, such as
skin fibrosis and venous ulceration.
Leg venous ulceration

49. Brodie-Trendelenburg Test
• Patient's leg is elevated to drain venous blood.
• Elastic Tourniquet (saphenofemoral junction mid thigh and the patient then
stands)
• Rapid filling (<30 seconds) of the saphenous system from the deep system
indicates perforator valve incompetence.
• When tourniquet is released, additional filling of the saphenous system
occurs if the saphenofemoral valve is also incompetent.

50. (1) Negative Varicose Vein
• Patient standing with tourniquet, Varicose is not appearing
• If elastic tourniquet is release and varicose vein is not appearing
• Called: Negative Varicose Vein
(2) Positive Varicose Vein
• Patient standing with tourniquet, Varicose is not appearing
• If elastic tourniquet is release and varicose vein is appearing
• Due to Perforating Vein Incompetence
• Called: Positive Superficial Varicose Vein
(3) Double Positive Varicose Vein
• Patient standing with tourniquet
• Elastic tourniquet is not release but varicose vein is appearing
• Called: Positive Deep Varicose Vein

51. Brodie-Trendelenburg Test
Watch1: https://www.youtube.com/watch?v=b5l3PcoZ65A
Watch2: https://www.youtube.com/watch?v=UAtO1Zt-ydg

52. Perthes Test
• Purpose assess patency of the deep femoral vein.
• German surgeon Georg Perthes.
(1) The limb is elevated and an elastic bandage is applied firmly from the toes to the
upper 1/3 of the thigh to obliterate the superficial veins only.
(2) With the bandage applied the patient is asked to walk for 5 minutes.
(3) If deep system is competent, the blood will go through and back to the heart.
(4) If the deep system is incompetent, the patient will feel pain in the leg.

53. Delbet-Mocquot test
• French physicians Pierre Delbet and Pierre Mocquot.

54. Noninvasive Testing
 A variety of techniques may be employed to investigate patients with CVI:
1) Duplex Ultrasound
2) Ascending phlebography
3) Computed tomography (CT) and Magnetic Resonance Venography
4) Intravascular ultrasound (IVUS)
5) Air plethysmography

55. Duplex Ultrasound
• Speed of blood flow, and structure of the leg veins.
• Localize sites of obstruction and valvular reflux (deep and superficial
venous systems).
• Goal: Venous Reflux, Retrograde or reversed flow, valve closure time >0.5
seconds.

56. Ascending phlebography

57. Magnetic Resonance Venography

58. Intravascular ultrasound (IVUS)

59. Air Plethysmography

60. Invasive Testing
 Ambulatory Venous Pressure
• Gold standard assessment.
• Insert needle to dorsal foot vein with transducer.
• Detect: Refill time and Leg Pressure

61. Contrast Venography

62. Intravascular Ultrasound

63. Ambulatory Venous Pressure

64. VIII. Differential Diagnosis
1) Diabetic foot ulcer
2) Arterial ulcer
3) Squamous cell carcinoma (Marjolin)
4) Pyoderma gangrenosum
5) Kaposi's sarcoma
6) Lymphoedema
7) Congestive heart failure
8) Renal disease
9) Hepatic disease
• Excluded:
1) Acute Venous Problem
2) Deep Vein Thrombosis
• Included:
1) Heart failure
2) Nephrosis,
3) Liver
4) Endocrine disorders
Oedema

65. IX. Management
(*) Early Management:
1) Wound and Skin Care
2) Pharmacologic Therapy
3) Compressive Leg Garments
(*) Prevention:
• Exercise Therapy
• Conservative Management
(*) Interventional Management:
a) Superficial venous reflux (Saphenectomy,
Endovenous laser therapy, Foam
sclerotherapy)
b) Endovenous Ablative Therapy
c) Endovenous Deep System Therapy
d) Surgical Management
e) Surgery for Truncal Vein
f) Perforator Vein Surgery
g) Valve Reconstruction

66. Wound and Skin Care
• Moisturiser: moisturising cream to combat skin dryness and flaking in
eczematous skin changes and mild stasis dermatitis is generally thought to be
beneficial.

67. Compressive Leg Garments
• Graded Compression Stockings: CVI-related oedema, stasis
dermatitis, and small venous leg ulcers is use of graded compression
knee-high stockings.

68. Pharmacologic Therapy
1) Eczematous skin changes and mild stasis dermatitis
2) Venous leg ulcers
3) Leg pain
• Pentoxifylline or Diosmin: Pentoxifylline is used to
treat claudication, 400 mg orally three times daily.

69. Pentoxifylline
• Classes: Hemorheologic Agents
• Dosage Forms: 400mg
• Intermittent Claudication: Effects may be seen
within 2-4 weeks; recommended to continue
treatment for at least 8 weeks.
• Contraindications: Recent retinal or cerebral
hemorrhage.
Diosmin is most often used for hemorrhoids and leg
sores caused by poor blood flow.
• Side effects: stomach pain, diarrhea, dizziness,
headache, skin redness and hives, muscle pain, blood
problems, and altered heart rate.

70. Interventional
1. Superficial venous reflux
 Saphenectomy,
 Endovenous laser therapy
 Foam sclerotherapy
2. Angiomata and varicosities
3. Perforating vein incompetence
4. Iliac vein obstruction
5. Deep venous reflux
a) Endovenous Ablative Therapy
b) Endovenous Deep System Therapy
c) Surgical Management
d) Surgery for Truncal Vein
e) Perforator Vein Surgery
f) Valve Reconstruction

71. (1) Saphenectomy (vein ligation and stripping)
• Painless technique is the sapheon closure device which uses glue to seal the vein.
• It is used to remove a damaged vein and prevent complications of vein damage.
• If several valves in a vein and the vein itself are heavily damaged, the vein (or the
diseased part of the vein) is removed (stripped).

72. (2) Radiofrequency Ablation Generator & Catheter
• The heating element burns the vein from the inside and the vein shuts down.

73. (3) Foam Sclerotherapy
• This is a relatively Painless
out patient procedure.
• This causes the walls of the
vein to stick together.
• Over time the collapsed vein
turns into scar tissue.
• Sclerotherapy is a non-
invasive procedure taking
only about 30 minutes to
perform.
• Affected: Bruising, Raised
red areas, Small skin sores.

74. (4) Endovenous Deep System Therapy

75. (5) Surgery for Truncal Vein

76. (6) Perforator Vein Surgery

77. (7) Valve Reconstruction

78. Prevention
 Primary prevention:
• No specific measures have been shown to prevent CVI.
• Activity
• Long-term treatment with low molecular weight heparin, rather than oral
anticoagulation after DVT, may reduce or prevent development of post-thrombotic CVI.
 Secondary prevention:
• Avoided: Prolonged standing, especially in one place.
• Advised to lose weight if obesity.

79.  Emerging treatments:
• Balneotherapy
• Spray-applied cell therapy
• Other pharmacological therapies
• Exercise
Balneotherapy is the set of methods and practices
which, based on scientific evidence, use medically and
legally recognized mineral-medicinal waters, muds,
and natural gases from natural springs for therapeutic
purposes inside the facilities of thermal spa centres.

80. X. Complication
1) Haemosiderin
2) Venous ulceration
3) Haemorrhage
4) Infection
5) Severe CVI:
• Atrophie blanche, Lipodermatosclerosis,
• and Hyperpigmentation.
Complication Related:
1) Spermatic cord (varicocele), Esophageal varices
2) Anorectum (hemorrhoids),
3) Varicosities of the legs, Trunk varices

81. Trunk varices
Anorectum (hemorrhoids

82. XI. Prognosis
(1) If CVI is left untreated it is usually progressive and leads to the post-phlebitic syndrome
and venous ulcers.
(2) Poor Prognosis: CVI + Diabetes and peripheral arterial occlusive disease.
(3) Lifelong graded compression: Patients with severe CVI (CEAP C4-6) or previous ulcers
generally require lifelong graded compression stockings of at least 30 to 40 mmHg.
(4) Recurrence of venous leg ulcers: Failure with stocking.
(5) Mortality rate was very low, 0.0056%.

83. XII. Reference
1) Robert T. Eberhardt, MD; Joseph D. Raffetto, MD
2) https://bestpractice.bmj.com/topics/en-gb/507/prognosis
3) https://www.medi.de/en/diagnosis-treatment/venous-disorders/anatomy-veins/
4) https://lajollaveincare.com/vein-conditions/venous-reflux-is-a-progressive-condition-worsens-
over-time/
5) https://my.clevelandclinic.org/health/diseases/16872-chronic-venous-insufficiency-cvi
6) http://www.sophierenton.co.uk/treatments-for-varicose-veins/
7) https://www.ahajournals.org/doi/10.1161/CIRCULATIONAHA.113.006898

85. THANKS