Varicose Veins - Definition

• Robbins, Cotran & Kumar: Pathologic Basis of Disease

• Schwartz's Principles of Surgery, 11th Edition

Key Pathophysiology

• Increased venous pressure leads to progressive dilation of the vein wall
• Valve cusps become separated and incompetent, allowing retrograde (reflux) blood flow
• This creates a self-perpetuating cycle of further pressure elevation and dilation
• The superficial veins of the lower leg are most commonly affected because venous pressure at these sites can be elevated up to 10 times normal with prolonged dependent posture

Classification

Epidemiology

• Present in at least 10% of the general population (Schwartz's)
• Up to 20% of males and one-third of females develop lower extremity varicosities (Robbins)
• Risk factors: obesity, female sex, prolonged standing, pregnancy (compression of IVC by gravid uterus), family history, and inactivity

Sites Commonly Affected

• Lower limb superficial veins (great saphenous vein and small saphenous vein tributaries) - most common
• Esophageal varices - due to portal hypertension from liver cirrhosis
• Hemorrhoids - varicose dilation of the anorectal venous plexus

Clinical Consequences

• Stasis dermatitis ("brawny induration")
• Skin hyperpigmentation and lipodermatosclerosis
• Venous ulceration
• (Note: embolism from superficial varicose veins is very rare, unlike DVT)

• Robbins, Cotran & Kumar: Pathologic Basis of Disease - Varicose Veins, Vascular Pathology chapter
• Bailey and Love's Short Practice of Surgery, 28th Ed. - Chapter 62
• Schwartz's Principles of Surgery, 11th Ed. - Vascular Surgery section

Thread Veins (Telangiectasias)

• Histologically, they are dilated blood channels in normal dermal stroma with a single endothelial cell lining, limited muscularis, and adventitial layers. Most measure 26 to 235 µm in diameter and lie 175 to 382 µm below the stratum granulosum.
• They are classified as CEAP class C1 disease (the lowest clinical class of visible venous abnormality).
• Most telangiectasias arise from - and are fed by - underlying reticular veins. Treating the feeding reticular vein first is the key principle of management.
• Bailey and Love's Short Practice of Surgery, 28th Ed.; Pfenninger and Fowler's Procedures for Primary Care, 3rd Ed.

Reticular Veins

• They can be difficult to distinguish from a normal subdermal vein in someone with thin, pale, transparent skin.
• They are best visualised with the patient lying prone or supine (unlike varicose veins, which are best seen standing). Transillumination helps detail their relationship to overlying telangiectasias.
• They often act as the feeding source for overlying thread veins/telangiectasias.
• Bailey and Love's Short Practice of Surgery, 28th Ed.; Fitzpatrick's Dermatology

Comparison Table

Clinical Significance

• Telangiectasias
• Reticular veins
• Corona phlebectatica (malleolar flare) - a fan-shaped telangiectatic pattern at the ankle, signalling advanced venous disease
• Current Surgical Therapy, 14th Ed.; Bailey and Love's, 28th Ed.

Clinical Photo

CEAP Classification of Chronic Venous Disorders

• Sabiston Textbook of Surgery; Fischer's Mastery of Surgery, 8th Ed.

C - Clinical Classification

• S = Symptomatic (aching, pain, tightness, skin irritation, heaviness, muscle cramps)
• A = Asymptomatic

e.g., a patient with an active venous ulcer with symptoms is classified as C6,S

E - Etiologic Classification

A - Anatomic Classification

P - Pathophysiologic Classification

How CEAP Is Written in Practice

C3,S, Ep, As, Pr = Symptomatic edema, primary etiology, superficial vein involvement, due to reflux

C6,S, Es, Ad, Po = Active venous ulcer with symptoms, secondary etiology (e.g. post-DVT), deep vein involvement, due to obstruction

Supplementary Scoring Tools

• Sabiston Textbook of Surgery, 21st Ed.; Fischer's Mastery of Surgery, 8th Ed.; Harrison's Principles of Internal Medicine, 22nd Ed.

Pathophysiology of Venous Ulceration - The Competing Theories

1. Stasis / Hypoxia Theory (Original - now disproved)

2. Arteriovenous Fistula Theory (Disproved)

3. Fibrin Cuff Theory (Browse & Burnand, 1982)

• Venous hypertension → increased capillary pressure → endothelial damage → fibrinogen extravasation
• Fibrinogen polymerises around capillaries forming thick fibrin cuffs
• These cuffs act as a barrier to diffusion of oxygen and nutrients into the surrounding tissue
• Result: local ischaemia, tissue necrosis, fibrosis, and ulceration
• Pfenninger and Fowler's Procedures for Primary Care, 3rd Ed.

4. White Cell Trapping Theory (the "Leukocyte Trapping" Theory)

1. Venous hypertension slows capillary blood flow in the lower limb
2. Sluggish flow causes leukocytes (white blood cells) to marginate and adhere to capillary endothelium - a process normally reserved for acute inflammation
3. The adherent leukocytes physically obstruct the local capillaries, further impairing microcirculation
4. Trapped leukocytes become activated and migrate into the surrounding subcutaneous tissue
5. Activated leukocytes release:
   • Proteolytic enzymes (matrix metalloproteinases) - causing direct tissue destruction
   • Toxic metabolites and reactive oxygen species (free radicals) - causing oxidative tissue damage
6. This increases capillary permeability, worsening oedema and further perpetuating the cycle
7. End result: local ischaemia, tissue necrosis, and ulceration

• Pfenninger and Fowler's Procedures for Primary Care, 3rd Ed.; Bailey and Love's Short Practice of Surgery, 28th Ed.

Current Status of the Theory

• Polymorphonuclear leukocytes (neutrophils) were NOT consistently found within the peri-ulcer tissues
• Instead, increased numbers of mast cells, monocytes, and lymphocytes were found in periulcer tissues
• The concept remains relevant but has been modified rather than accepted wholesale
• Bailey and Love's Short Practice of Surgery, 28th Ed.

5. Trap Hypothesis (Unifying Theory)

• Venous hypertension causes extravasation of red blood cells from the capillary bed in addition to fibrin and leukocytes
• These "trapped" red blood cells break down in the tissues and release haemoglobin, which is metabolised to haemosiderin
• Haemosiderin is responsible for the characteristic brown hyperpigmentation ("brawny oedema") of advanced CVI
• The fibrin cuffs and resultant fibrosis produce the thin, glistening, indurated skin of lipodermatosclerosis
• These ischaemic, fibrotic areas develop stasis dermatitis with intense pruritus → scratching → skin breakdown → ulceration
• Pfenninger and Fowler's Procedures for Primary Care, 3rd Ed.

Additional Factors Now Recognised

The Accepted Bottom Line

Ambulatory venous hypertension is the only universally accepted underlying cause of venous ulceration. This also explains why venous ulcers are never seen in the upper limb (where venous pressures are not comparably elevated by gravity and standing).

• Bailey and Love's Short Practice of Surgery, 28th Ed.

Anatomy of the Superficial Venous System

Great Saphenous Vein (GSV) - Long Saphenous Vein

Origin

• Arises from the medial end of the dorsal venous arch of the foot
• The dorsal arch runs in the subcutaneous tissues over the metatarsal heads (the plantar surface drains preferentially dorsally to avoid pressure damage)

Course

1. Passes anterior to the medial malleolus at the ankle
2. Ascends the medial aspect of the leg, lying in the superficial tissues medial to the tibia, accompanied by the saphenous nerve
3. Loops posteriorly at the level of the medial condyle of the femur
4. Continues up the medial thigh
5. In the groin, unites with several tributaries corresponding to branches of the common femoral artery
6. Pierces the cribriform fascia covering the saphenous opening (fossa ovalis), located approximately 2.5 cm below and lateral to the pubic tubercle
7. Terminates by draining into the common femoral vein (CFV) at the saphenofemoral junction (SFJ)

Key Facts

• The longest vein in the body
• Most frequently affected superficial vein in varicose disease (involved in ~60% of cases)
• Throughout its course it receives variable superficial tributaries

Important Tributary - Anterior Accessory GSV (AAGSV)

• One of the most common tributaries
• Commonly originates around the lateral border of the knee (sometimes as low as the lateral end of the dorsal arch)
• May course up the medial thigh anterolateral to the GSV, and drain into the GSV at or near the SFJ
• Frequently mistaken for the GSV itself (called a "duplex GSV" by some surgeons; a true duplex GSV is rare)

Small Saphenous Vein (SSV) - Short Saphenous Vein

Origin

• Arises from the lateral end of the dorsal venous arch of the foot

Course

1. Passes posterior to the lateral malleolus
2. Ascends the posterior midline of the leg, accompanied by the sural nerve
3. In the proximal calf sits in the groove between the two heads of gastrocnemius
4. Pierces the fascia of the popliteal fossa and typically terminates by draining into the popliteal vein at the saphenopopliteal junction (SPJ)

Termination - Highly Variable

Comparison Summary

Anatomy Diagram

• Bailey and Love's Short Practice of Surgery, 28th Edition, Chapter 62

Named Tributaries

Tributaries at the Saphenofemoral Junction (SFJ)

Clinical note: Dilated superficial epigastric veins ("caput medusae" pattern on the abdominal wall) indicate incompetence of the SEV and should alert the clinician to underlying deep venous obstruction, usually at the iliofemoral segment.

• Dermatology 2-Volume Set 5e; Imaging Anatomy - Bones, Joints, Vessels and Nerves

Named Tributaries of the GSV in the Leg

Visual: SFJ and Tributaries

Named Perforating Veins

Thigh Perforators

Knee Perforators

Upper Medial Leg Perforators (Paratibial)

Lower Medial Leg Perforators

Cockett's perforators are the most clinically significant - their incompetence directly causes the high venous pressures responsible for skin changes and ulceration in the "gaiter area" (medial ankle/lower calf). Note that they connect to the posterior accessory GSV (Leonardo's arch), NOT the main GSV trunk directly.

Summary Table of Named Perforators

Clinical Significance of Incompetent Perforators

• Incompetent perforators transmit the high pressure of the deep venous system directly into the superficial system during calf muscle contraction
• Number and size of incompetent perforators correlate directly with severity of chronic venous disease
• Cockett's perforators are the key drivers of ankle/gaiter area skin changes and venous ulceration
• Subfascial Endoscopic Perforator Surgery (SEPS) was developed specifically to interrupt incompetent Cockett perforators
• Fitzpatrick's Dermatology; Bailey and Love's Short Practice of Surgery, 28th Ed.; Imaging Anatomy Vol. 3