Varicose Veins

Definition

Pathophysiology

• Inflammatory cell infiltration and activation
• Dysfunctional smooth muscle cell proliferation
• Collagen deposition and decreased elastin content
• Increased matrix metalloproteinases
• Loss of compliance, dilatation, and elongation (causing tortuosity)
• Secondary valvular dysfunction

Aetiology

• Valve incompetence - the most important factor; may be a sequel of venous thrombosis
• Erect posture - not seen in other animals; occurs in those who stand for prolonged periods (policemen, tram drivers, conductors)
• Pregnancy - progesterone-related smooth muscle relaxation plus uterine compression of pelvic veins
• Obstruction to venous return: abdominal tumours, fibroids, ovarian cysts, abdominal lymphadenopathy, retroperitoneal fibrosis, ascites
• Congenital arteriovenous fistulae - particularly in younger patients
• Hereditary - runs strongly in families

Clinical Features

Epidemiology

• Middle-aged individuals most commonly affected
• Women > men (ratio approximately 10:1)
• Less common in primitive civilisations (Africa, Far East)

Symptoms

• Aching pain in the leg, worst toward the end of the day, relieved by elevation
• Ankle swelling by end of day
• Itching of the skin over the leg
• Night cramps
• Bursting pain on walking (suggests coexisting deep vein thrombosis)
• Varicose ulcer on medial malleolus

Note: Symptoms do not necessarily correlate with the degree of visible varicosity. Asymptomatic varicose veins on one side and severe symptoms with minimal visible veins on the other side are both possible.

Clinical Classification (CEAP)

Examination

Inspection

• Note which system is involved - long (great) saphenous or short (small) saphenous, or both
• Great saphenous: trunk on medial side of leg from in front of medial malleolus to saphenous opening in groin
• Small saphenous: trunk from behind lateral malleolus up the posterior calf to popliteal fossa
• Look for skin changes: eczema, pigmentation (haemosiderosis), lipodermatosclerosis, ulceration, scarring

Clinical Tests (Palpation)

Complications

1. Haemorrhage - may be profuse due to high venous pressure; elevation of the limb is first aid
2. Superficial thrombophlebitis (phlebitis) - spontaneous or post-trauma; vein becomes tender and firm, overlying skin red and oedematous, may have pyrexia
3. Venous ulceration - typically on the medial malleolus, often associated with underlying deep vein thrombosis; follows lipodermatosclerosis
4. Eczema / dermatitis - erythematous, itchy, may progress to blistering
5. Lipodermatosclerosis - chronic inflammation and fibrosis resulting in "woody," contracted leg
6. Haemosiderosis - brownish skin discoloration around ankle from haemoglobin breakdown

Investigations

• Reflux defined as retrograde flow lasting ≥ 0.5 seconds in superficial/crural veins
• Reflux in proximal deep veins requires ≥ 1 second
• The SFJ is identified in the groin using transverse view - the "Mickey Mouse sign" (CFV + CFA + GSV)
• Elicited by calf/foot squeeze release, Valsalva, or pneumatic cuff deflation

Treatment

1. Conservative

• Compression hosiery (not a curative treatment but reduces symptoms)
• Elevation, weight loss, mobility

2. Endothermal Ablation (First-line for truncal incompetence)

• Catheter placed under ultrasound guidance to the lowest point of reflux
• Perivenous tumescent anaesthesia administered
• Energy delivery ~60-80 J/cm used; catheter withdrawn during energy delivery
• Post-procedural compression applied

• Similar principle using radiofrequency energy instead of laser
• Slightly less painful than EVLA; similar efficacy

3. Non-Thermal, Non-Tumescent Techniques

• Sclerosing agent (sodium tetradecyl sulphate most common) made into foam via Tessari method (1:3 or 1:4 sclerosant:air ratio, oscillated ~20 times)
• Foam stable for ~2 minutes; injected with leg elevated
• Effective for trunk and tributaries; higher recanalisation rates than thermal ablation

• Spinning wire physically damages endothelium while sclerosant is simultaneously injected
• No tumescent anaesthesia usually required
• Good option for needle-phobic patients; higher long-term recanalisation than endothermal

• Adhesive applied in 0.1 mL increments via catheter; vein compressed to seal lumen
• Minimal procedural pain; no tumescent anaesthesia
• Higher consumable cost; long-term data still emerging

4. Open Surgery (Traditional)

• Complete dissection of SFJ with flush ligation + stripping of GSV
• Usually under general anaesthesia
• Now superseded by endothermal techniques in most centres; reserved for complex or recurrent cases

• Preoperative duplex marking of SPJ highly recommended
• Prone position; risk of sural nerve and popliteal vein injury

• Small stab incisions using mosquito forceps or phlebectomy hooks
• Used as adjunct to truncal ablation or as sole treatment for isolated tributary incompetence

Summary of Key Points

Types of Ischemic Heart Disease (IHD)

Overview

Pathophysiology - The Two Core Mechanisms

1. Fixed ("Chronic") Atherosclerotic Occlusion

2. Acute Plaque Change with Thrombosis / Vasospasm

• Sudden rupture, fissuring, ulceration, or erosion of a partially occlusive plaque exposes thrombogenic material
• Rapid thrombosis follows, causing abrupt complete or near-complete occlusion
• This underlies the three catastrophic ACS presentations: unstable angina, MI, and sudden cardiac death

The Four Clinical Syndromes of IHD

1. Angina Pectoris

A. Stable Angina (Exertional Angina)

• Caused by fixed high-grade atherosclerotic stenosis (> 70%)
• Pain occurs predictably at certain levels of exertion and is relieved by rest or nitrates
• Imbalance between a fixed maximum coronary supply and increased demand (exercise, emotion)
• ST depression on ECG during episodes
• No myocardial necrosis

B. Vasospastic Angina (Prinzmetal Angina)

• Caused by coronary artery spasm - transient intense vasoconstriction of a coronary vessel
• Often occurs at rest, without obvious precipitant, and can occur even without significant fixed stenosis
• May be due to hyperreactivity of vascular smooth muscle or endothelial dysfunction
• ST elevation (not depression) during episodes - unlike stable angina
• Can be a precursor to MI if spasm is sustained

C. Unstable Angina

• Part of the Acute Coronary Syndrome (ACS) spectrum
• Caused by acute plaque disruption with non-occlusive or transiently occlusive thrombus
• Pain occurs with progressively less exertion, at rest, is more prolonged, or crescendo in pattern
• No troponin elevation (distinguishes it from NSTEMI)
• High short-term risk of progressing to MI

"Unstable angina is the most common initial presentation of ischemic heart disease." (Robbins, p. 352)

2. Myocardial Infarction (MI)

A. STEMI (ST-Elevation MI)

• Results from complete, abrupt occlusion of an epicardial coronary artery
• Causes transmural infarction - full-thickness necrosis of the ventricular wall
• ST elevation on ECG; Q waves develop later
• Treated with emergency reperfusion (primary PCI or thrombolysis)
• Higher in-hospital mortality (~10%)

B. NSTEMI (Non-ST-Elevation MI)

• Coronary thrombus is non-occlusive or transiently occlusive (or spontaneously lysed)
• Causes subendocardial infarction - limited to the inner third of myocardium
• No ST elevation; troponin IS elevated (distinguishes from unstable angina)
• In-hospital mortality ~6%

Coronary artery territory and infarct location:

Patterns of infarction:

• Transmural: Full thickness; due to complete epicardial occlusion + atherosclerosis → STEMI
• Subendocardial: Inner 1/3 of myocardium; due to transient or partial occlusion → NSTEMI; subendocardium is most vulnerable (last to receive blood, highest intramural pressures)

Cardiac Biomarkers after MI:

Complications of MI (nearly 3/4 of patients experience at least one):

1. Myocardial rupture (1-5% of MIs; peaks 3-7 days post-MI when granulation tissue is maximal):
   • Ventricular free wall rupture → fatal hemopericardium/tamponade
   • Interventricular septum rupture → VSD (most common type of rupture)
   • Papillary muscle rupture → acute severe mitral regurgitation
2. Arrhythmias - cause 80-90% of cardiac deaths in IHD setting (ventricular fibrillation)
3. Left ventricular failure / cardiogenic shock
4. Pericarditis (Dressler syndrome - autoimmune, weeks later)
5. LV thrombus → systemic embolism
6. Ventricular aneurysm - late complication of scar formation

3. Chronic IHD with Congestive Heart Failure

• Also called ischemic cardiomyopathy
• Results from progressive cardiac decompensation after acute MI or accumulated effect of multiple ischemic insults
• Viable but non-functional myocardium ("hibernating myocardium") contributes to pump failure
• "Stunned myocardium" - reversible non-contractile state after ischemia, before tissue death
• Eventually leads to mechanical pump failure (CHF)
• Prognosis is poor; treated with standard HF therapy + revascularization if viable myocardium present

4. Sudden Cardiac Death (SCD)

• Death within 1 hour of symptom onset, typically due to a lethal arrhythmia (ventricular fibrillation)
• In 80-90% of cases, underlying coronary artery disease is present
• Myocardial ischemia creates electrical instability of ischemic regions → VF
• May be the first manifestation of IHD in up to 20% of patients
• One-third of individuals with STEMIs die out-of-hospital before receiving care
• Survivors require ICD implantation and aggressive risk factor modification

Acute Coronary Syndrome (ACS) - Umbrella Term

ACS
├── Unstable Angina      (no biomarker rise, no ECG ST elevation)
├── NSTEMI               (biomarker rise, no ST elevation → subendocardial)
└── STEMI                (biomarker rise + ST elevation → transmural)

Summary Table