Atherosclerosis

Definition and Core Concept

• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 465

Epidemiology

• Atherosclerosis-related ischemic heart disease is near-universal in high-resource nations, though risk reduction and improved therapies have reduced associated mortality over recent decades.
• Adoption of Western diet/lifestyle has increased prevalence in lower-resource nations - death rates from coronary artery disease in Africa, India, and Southeast Asia now exceed those in the United States.
• Eastern European countries have rates 3-5x higher than the US, and 7-12x higher than Japan.
• Myocardial infarction accounts for nearly a quarter of all deaths in the United States.
• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 465-466

Risk Factors

Non-modifiable (Constitutional)

Modifiable (Major)

Additional Factors

• Physical inactivity, obesity, hypertriglyceridemia, type A (hostile/competitive) personality, and diet all contribute.
• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 466-468

Pathogenesis - The "Response to Injury" Hypothesis

Step-by-Step Sequence

• Triggers include: hemodynamic stress (turbulent flow at arterial branch points), hypercholesterolemia, hypertension, cigarette smoke toxins, inflammatory cytokines, immune complexes.
• Injured endothelium shows: increased permeability, upregulation of adhesion molecules (VCAM-1, ICAM-1, E-selectin), impaired nitric oxide (NO) production, and a pro-thrombotic/pro-inflammatory state.

• LDL and oxidized LDL (oxLDL) accumulate in the subintimal space.
• OxLDL is particularly harmful: it stimulates further endothelial activation, is toxic to SMCs, and is phagocytosed by macrophages via scavenger receptors (bypassing normal LDL receptor feedback).

• Circulating monocytes adhere to activated endothelium, migrate into the intima, and differentiate into macrophages.
• Macrophages ingest oxLDL via scavenger receptors, becoming foam cells - the hallmark of early atherosclerosis.
• Foam cells aggregate to form fatty streaks (the earliest grossly visible lesion), visible as yellow intimal streaks.

• Growth factors (PDGF, FGF) and cytokines from platelets, macrophages, and ECs drive SMC migration from media to intima.
• Intimal SMCs proliferate and synthesize extracellular matrix (collagen, proteoglycans), forming the fibrous cap of the mature plaque.

• T cells are recruited and, upon recognizing antigens (e.g., oxLDL-protein complexes), secrete cytokines (IFN-γ) that further activate macrophages and inhibit SMC collagen synthesis - destabilizing the plaque.

• Foam cells die and release their lipid content, forming the soft, grumous lipid (necrotic) core.
• Extracellular cholesterol crystals accumulate; calcification may follow.
• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 468-470

Morphology of the Atherosclerotic Plaque

Gross Appearance

• Fatty streak: earliest lesion - flat yellow intimal streak composed of lipid-laden foam cells. Present even in aortas of children.
• Fibrolipid (atheromatous) plaque: raised, white-yellow firm lesion with:
  • A fibrous cap (SMCs + dense collagen + proteoglycans)
  • A lipid/necrotic core (cholesterol, cholesterol esters, foam cell debris, necrotic material)
  • Inflammatory infiltrate (macrophages, T cells, mast cells) at the shoulder regions
  • Variable calcification ("hardening of the arteries")

Microscopic Appearance

• Fibrous cap: SMCs and ECM
• Core: extracellular lipid, cholesterol clefts, necrotic debris, foam cells
• Base/shoulders: rich in macrophages, lymphocytes, and new blood vessels

Distribution

• Most severe in the abdominal aorta > coronary arteries > popliteal arteries > internal carotid > circle of Willis
• Predilection for branch points, bifurcations, and vessel curves - areas of disturbed (turbulent/oscillatory) flow and low shear stress

• Robbins Basic Pathology, p. 314-315; Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 470-472

Stable vs. Vulnerable (Unstable) Plaques

• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 472-473

Clinical Consequences

"Major consequences of atherosclerotic diseases include myocardial infarction, cerebral infarction, aortic aneurysms, and peripheral vascular diseases."

• Robbins, Cotran & Kumar Pathologic Basis of Disease, p. 474

Calcification

• Guyton and Hall Textbook of Medical Physiology, p. 851

Key Molecular Players Summary

Sources

• Robbins, Cotran & Kumar Pathologic Basis of Disease (10e), Chapter 11, pp. 465-474
• Robbins & Kumar Basic Pathology (11e), Chapter 8, pp. 313-316
• Guyton and Hall Textbook of Medical Physiology (14e), Chapter 69, p. 851

• Bailey and Love's Short Practice of Surgery (28th Ed)
• Sabiston Textbook of Surgery
• Schwartz's Principles of Surgery (11th Ed)
• Fischer's Mastery of Surgery (8th Ed)
• Mulholland & Greenfield's Surgery (7th Ed)
• Current Surgical Therapy (14th Ed)
• S Das - A Manual on Clinical Surgery (13th Ed)

Atherosclerosis

Bailey and Love's Short Practice of Surgery (28th Edition)

Definition / Overview

• Plasma lipoproteins
• Leukocytes (monocytes/macrophages, T lymphocytes)
• Vascular endothelial cells
• Smooth muscle cells

Progressive Stages of Atherosclerosis

1. The Fatty Streak

• The first evidence of atherosclerosis can be found in children aged 10-14 years
• Appears as a yellow streak running along the major arteries
• Consists of:
  • Smooth muscle cells filled with cholesterol
  • Foam cells (lipid-laden macrophages)

2. Fibrous Plaque

• Consists of large numbers of smooth muscle cells, foam cells, and leukocytes
• As the fibrous plaque grows, it projects into the vessel lumen, causing narrowing
• This narrowing leads to ischaemia or infarction

3. Complicated Lesion

• Occurs when the fibrous plaque ruptures
• Provokes activation of the coagulation cascade and formation of thrombus
• End result: a calcified, ulcerated plaque with areas of haemorrhage and thrombus

Clinical Manifestations (IHD due to Atherosclerosis)

• Chest pain / angina (most characteristic)
• Breathlessness
• Fatigue
• Peripheral oedema
• Palpitations
• Syncope

Risk Factors for IHD (Summary Box 59.4)

Investigations

Non-Invasive

Invasive

Vascular Disorders

Bailey and Love's Short Practice of Surgery, 28th Edition - Chapter 61

Introduction

• Heart (coronary thrombosis and MI)
• Brain (stroke)
• Peripheral arterial system (limb ischaemia)

I. ARTERIAL STENOSIS AND OCCLUSION

Cause and Effect

• Predominantly caused by atherosclerosis and/or thromboembolic disease; also trauma
• Symptoms relate to the organ supplied:
  • Lower limb: claudication, rest pain, gangrene
  • Brain: TIAs and stroke
  • Myocardium: angina and MI
  • Intestine: abdominal pain and infarction
• Severity depends on:
  • Size of vessel occluded
  • Whether occlusion is acute (sudden, in a previously normal artery) or chronic (gradual, with collateral development)
• In chronic stenosis, a collateral circulation may develop as an alternative - albeit less effective - route for blood supply

II. CHRONIC LOWER LIMB ISCHAEMIA

Symptoms

• Cramping pain in the calf (most common), thigh or buttock on walking - relieved by rest
• Typical of femoral/popliteal disease (calf claudication) or aortoiliac disease (buttock/thigh)
• Fontaine classification describes severity of PAD

• Rest pain (worse at night, relieved by hanging leg down)
• Tissue loss: ulceration or gangrene

Clinical Examination

• Acute ischaemia: cold, white, paralysed, insensate
• Chronic ischaemia: equilibrates with surroundings; no paralysis; sensation usually intact
• Sunset foot sign (dependent rubor): on elevation - venous guttering + pallor; on dependency - red/purple discolouration; indicates severe ischaemia
• Capillary refill: normally 2-3 seconds; may be prolonged to 10 seconds in severe ischaemia

• Examine: femoral, popliteal, posterior tibial, dorsalis pedis
• Always examine abdomen for aortic aneurysm (may coexist)
• Pulsation distal to occlusion is usually absent
• After exercise (walking to claudication), pulse at iliac stenosis may disappear as vasodilation reduces pulse pressure
• Arterial bruit = turbulent flow = suggests stenosis (but tight stenoses may have no bruit)

III. INVESTIGATIONS

Non-Invasive

• Ratio of systolic ankle pressure to ipsilateral brachial systolic pressure
• Highest pressure among dorsalis pedis, posterior tibial, or peroneal artery used as numerator

• Drop of >20% in ABI after exercise = flow-limiting arterial disease
• In diabetics: Toe-Brachial Index (TBI) preferred (toe arteries rarely calcify); TBI <0.6 = significant lesion
• Absolute toe pressure <50 mmHg = severe ischaemia likely to prevent ulcer healing

• B-mode ultrasound imaging combined with Doppler flow analysis
• Colour coding visualises flow direction, velocity, turbulence
• As accurate as angiography in experienced hands; non-invasive and cost-effective
• Limitation: aortoiliac segment can be difficult to image (bowel gas)

• CT Angiography (CTA): detailed anatomical imaging of entire arterial tree
• MR Angiography (MRA): no radiation; good for distal vessels
• Duplex surveillance for graft monitoring

Invasive

• Gold standard for anatomy; used when intervention planned
• Usually via common femoral artery (CFA) approach

IV. MANAGEMENT

Risk Factor Modification

• Modifiable risk factors for PAD mirror those for CAD: smoking, diabetes, hypertension, hyperlipidaemia
• 50% of claudicants die within 10 years from MI or stroke
• Decrease in ABI of 0.1 below 0.9 = 10% increase in relative risk of major cardiovascular event

Non-Surgical Management

• Structured exercise programme: minimum 2 hours/week for 3 months - improves claudication distance and reduces cardiovascular risk
• Smoking cessation: most important modifiable factor
• Diabetes control + weight loss in obese patients

Drug Treatment

• Statins (HMG-CoA reductase inhibitors): prescribed even with normal lipids - stabilise atherosclerotic plaques and protect against cardiac death independently of lipid levels
• Antiplatelet therapy: Clopidogrel 75 mg/day (first line) OR Aspirin 75 mg/day
• Antihypertensives: caution with β-blockers (may exacerbate claudication)
• Vasodilators: unlikely to provide significant or sustained benefit

Transluminal Angioplasty and Stenting

• Percutaneous transluminal angioplasty (PTA): balloon inflation to dilate stenosis
• Stenting to maintain lumen patency after vessel recoil
• Best results for: short segment iliac stenoses (>90% patency at 3 years), femoral/popliteal lesions (variable)

Bypass Surgery

• Aortobifemoral bypass: for aortoiliac occlusive disease; midline abdominal incision; Dacron or PTFE graft; tunnelled retroperitoneally to groins
• Femoropopliteal bypass: for SFA/popliteal disease; autologous long saphenous vein preferred conduit (minimum 3 mm diameter); PTFE used if no suitable vein
• Femorodistal bypass: for tibial/crural disease; high early failure rate (~30% at 30 days); only for limb salvage

V. GANGRENE

• Death of macroscopic tissue - turns black (haemoglobin breakdown → iron sulphide formation)
• Usually affects most distal part of limb due to arterial obstruction

Zone of Demarcation

• Granulation tissue forms between dead and living parts
• In dry gangrene: line forms in days if proximal supply adequate
• In wet gangrene: infection spreads proximally - demarcation more proximal

VI. ACUTE ARTERIAL OCCLUSION

• Usually caused by an embolus; also from thrombosis on atherosclerotic plaque (less dramatic - collaterals usually present)

Sources of Embolus

• Left atrium in atrial fibrillation (most common)
• Left ventricular mural thrombus after MI
• Vegetations on heart valves (infective endocarditis)
• Thrombi in aneurysms or on atherosclerotic plaques

The 6 Ps of Acute Limb Ischaemia (ALI)

Embolus vs. Thrombosis

Management of ALI

1. Immediate IV heparin (5000 U bolus)
2. Embolectomy: via Fogarty balloon catheter through arteriotomy in CFA - catheter passed proximal and distal, balloon inflated, withdrawn with clot; repeated until backbleeding
3. Thrombolysis: intra-arterial tissue plasminogen activator (tPA) if ischaemia not immediately limb-threatening; catheter embedded in clot via CFA approach; serial angiograms to monitor lysis
4. Post-procedure: heparin → warfarin (long-term anticoagulation) to prevent re-embolism

VII. AMPUTATION

Indications (The 3 Ds)

Levels of Amputation

• Distal/toe: small vessel disease with good proximal supply (diabetes)
• Transmetatarsal: several toes affected but proximal circulation adequate
• Below-knee (BKA): preserves knee joint; better rehabilitation
• Above-knee (AKA): poorer stump healing; worse rehabilitation

VIII. ANEURYSMAL DISEASE

Definition and Classification

• Aneurysm: abnormal localised dilatation >50% of normal vessel diameter (below 50% = ectatic)
• True aneurysm: all three layers of arterial wall (intima, media, adventitia) in sac
• False (pseudo)aneurysm: single layer of fibrous tissue (e.g. post-trauma, post-puncture)

Abdominal Aortic Aneurysm (AAA)

• Majority asymptomatic - found incidentally on USS or CT
• Symptomatic: pulsatile abdominal mass, back/loin pain (expansion), abdominal pain
• Thrombus within sac may give false impression of diameter on angiography

• USS: screening; monitors size; cannot diagnose rupture
• CT: definitive; measures size accurately; detects rupture; guides EVAR planning

• Diameter ≥5.5 cm
• Rapid expansion (>1 cm/year)
• Symptomatic aneurysm
• Ruptured aneurysm (emergency)

• Midline or transverse abdominal incision (avoid transverse - divides inferior epigastric collateral vessels)
• Small bowel retracted right; posterior peritoneum opened; aorta exposed below renal arteries
• Heparin 5000 U IV; clamps above and below lesion
• Dacron inlay graft anastomosed end-to-end proximally; distally to aortic bifurcation or iliac arteries

• Stent-graft deployed via femoral arteries under radiological guidance
• Less invasive; faster recovery; lower short-term mortality
• NICE 2020 (UK): recommends open repair unless contraindicated; EVAR for high-risk patients
• ESC 2019: EVAR as first-line; open for patients with long life expectancy
• EVAR first-line for anatomically suitable ruptured AAA

• Classic triad: severe abdominal/back pain + hypotension + pulsatile abdominal mass
• Rupture: 80% posterolateral (retroperitoneal) - may be temporarily tamponaded; 20% anterior (free peritoneal) - rapidly fatal
• Less than 50% survive to reach hospital; operative mortality ~50%; overall mortality 80-90%
• Management: IV access; permissive hypotension (systolic <100 mmHg - just enough to maintain consciousness); CT to confirm; immediate transfer to theatre; EVAR if anatomically suitable

Popliteal Aneurysm

• Most common peripheral aneurysm
• Over 50% bilateral; associated with AAA in 30-40%
• Complications: distal embolisation (causing foot ischaemia), thrombosis, rarely rupture
• Chronic embolisation occludes run-off vessels → eventual thrombosis → ischaemic foot
• Elective repair: bypass with vein graft via medial approach (preferred over posterior approach for better exposure)
• Acute thrombosis: poor prognosis; limb loss rate ~50%

Femoral Aneurysm

• True femoral aneurysm: uncommon; complications <3%; conservative unless large
• Always look for associated AAA or popliteal aneurysm (>50% association)
• False femoral aneurysm: 2% after arterial surgery; or post-puncture
  • ≤3 cm: thrombin injection under USS guidance

  • 3 cm: open surgical repair

Iliac Aneurysm

• Usually associated with AAA; rarely isolated
• ~50% present already ruptured when isolated
• Treatment: inlay graft or endovascular repair

IX. ARTERIOVENOUS FISTULA

• Communication between artery and vein
• Congenital malformation or acquired (trauma)
• Surgically created AV fistulae used for haemodialysis access

X. VASOSPASTIC DISORDERS

Raynaud's Disease (Primary)

• Episodic digital vasospasm triggered by cold or emotion
• Triphasic colour change: white (pallor) → blue (cyanosis) → red (reactive hyperaemia)
• No underlying cause identified
• Management: keep warm; calcium channel blockers (nifedipine); sympathectomy in severe cases

Raynaud's Syndrome (Secondary)

• Peripheral arterial manifestation of underlying collagen disease (SLE, rheumatoid arthritis)
• Also caused by vibrating tools ("vibration white finger" - recognised industrial disease)
• More aggressive; may lead to digital necrosis and multiple amputations
• Treatment: directed at underlying condition; nifedipine, steroids, vasospastic antagonists
• Sympathectomy: disappointing results; not recommended

Note: The sections on varicose veins, deep vein thrombosis, and lymphatic disorders are covered separately in Bailey and Love (Chapters 62-63). Reply with "continue" if you'd like those sections covered with a fresh budget.

Vascular Disorders (Continued)

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

XI. ARTERITIS AND VASOSPASTIC CONDITIONS

Buerger's Disease (Thromboangiitis Obliterans)

• Occlusive disease of small and medium-sized limb arteries
• Thrombophlebitis of superficial or deep veins
• Raynaud's syndrome (vasospastic component)
• Occurs almost exclusively in young male smokers
• Histology: inflammatory changes in the walls of both arteries and veins leading to thrombosis

• Affects upper and lower limbs (unlike atherosclerosis, which predominantly affects lower limbs)
• Common in Middle East, Asia, Eastern Europe - less common in Western Europe
• No other atherosclerotic risk factors needed - smoking is the dominant and essential factor
• Thrombophlebitis migrans: flitting thrombophlebitis affecting different veins at different times; seen in Buerger's disease and malignancy (especially pancreatic)

• Rest pain and digital ischaemia in young men (<45 years) who smoke
• Ulceration and gangrene of digits (fingers and toes)
• Superficial thrombophlebitis (nodular tender cord along a vein)
• Raynaud's phenomenon
• Absent distal pulses with relatively preserved proximal pulses

• Total abstinence from smoking - the only effective treatment; arrests but does NOT reverse the disease
• Established arterial occlusions managed as for atheromatous disease (angioplasty, bypass if possible)
• Amputation may eventually be required (digits or limbs if gangrene develops)
• Sympathectomy may provide temporary relief

"Treatment is total abstinence from smoking, which arrests, but does not reverse, the disease." - Bailey and Love, Ch. 61

Other Forms of Arteritis

• Localised infiltration with inflammatory and giant cells → arterial occlusion
• Features: ischaemic headache, tender + palpable + pulseless (thrombosed) temporal arteries
• Emergency: irreversible blindness if ophthalmic artery occluded
• Surgeon's role: temporal artery biopsy (confirms diagnosis) - but must NOT delay immediate steroid therapy
• Steroids arrest and reverse the process before ophthalmic artery involvement

• Arteritis obstructing major arteries, particularly large vessels off the aortic arch
• Usually pursues a relentless course
• Young women; also called "pulseless disease"

• Accumulation of clear jelly (like a synovial ganglion) in the outer layers of a main artery, especially the popliteal artery
• Narrows the vessel → claudication in young patients without risk factors
• Investigation: Duplex scan (choice)
• Treatment: decompression by removal of myxomatous material; sometimes requires excision of diseased artery

XII. CHAPTER 62 - VENOUS DISORDERS

Venous Anatomy of the Lower Limb

• Three pairs of venae comitantes alongside anterior tibial, posterior tibial and peroneal arteries
• Converge in popliteal fossa → popliteal vein (also receives soleal and gastrocnemius veins)
• Popliteal vein → through adductor hiatus → femoral vein (receives profunda femoris vein in femoral triangle) → external iliac vein → common iliac vein → inferior vena cava

• Great Saphenous Vein (GSV): longest vein in the body; ascends medially; joins femoral vein at saphenofemoral junction (SFJ) in the groin
• Small Saphenous Vein (SSV): runs posterolaterally; joins popliteal vein at saphenopopliteal junction (SPJ) in popliteal fossa

Calf Muscle Pump Physiology

• Venous pressure in foot on standing ≈ 100 mmHg (hydrostatic column to heart)
• Blood returns against gravity via:
  1. Inspiration → decreased intrathoracic pressure creates suction
  2. Calf muscle pump: compression of deep veins raises pressure to 200-300 mmHg during contraction; one-way valves direct flow toward heart
• Calf pump reduces superficial venous pressure to ≈30 mmHg (two-thirds reduction)
• Venous hypertension occurs when: valves incompetent, deep veins obstructed, or pump failure

XIII. VARICOSE VEINS

Definition

Prevalence

• 30-50% of the adult population
• More common in women; increases with age; Edinburgh Vein Study prevalence rose from 11.5% (age 18-24) to 55.7% (age 55-64)
• Risk factors: female sex, increasing age, pregnancy, family history, obesity, tall stature

Pathophysiology

• Primary failure of venous valves → retrograde blood flow (reflux) → venous hypertension
• Raised pressure → vein wall weakening via matrix metalloproteinases → loss of compliance, dilatation, elongation, further valvular dysfunction
• Secondary varicose veins: arise post-DVT (post-thrombotic limb) or in congenital abnormalities (e.g. Klippel-Trénaunay syndrome)

CEAP Classification (Clinical features)

Symptoms

• Aching, heaviness, throbbing, burning, bursting sensation
• Worse throughout the day and with prolonged standing
• Relieved by elevation or compression hosiery
• Itching, ankle swelling
• Symptoms independent of degree of incompetence

Investigation

• Duplex ultrasound: mandatory for ALL patients; assesses:
  • Site and source of reflux
  • Deep vein patency (obstruction)
  • Suitability of veins for treatment (diameter, tortuosity, thrombus)
  • Pelvic source of reflux
• Reflux defined: retrograde flow ≥0.5 seconds in superficial veins (≥1 second in proximal deep veins)
• Hand-held Doppler and tourniquet tests have been abandoned

Treatment

• Compression hosiery (graduated elastic stockings)
• Suitable for patients unfit for intervention or who decline treatment

• Endovenous Laser Ablation (EVLA): laser fibre inserted percutaneously; tumescent local anaesthetic surrounds vein; thermal energy destroys vein permanently; wavelength typically 1470 nm
• Radiofrequency Ablation (RFA): similar principle using radiofrequency energy; may have marginally less post-procedure pain
• Both preceded by tumescent anaesthesia injection around vein (compresses vein, dissects nerve, acts as heat sink)
• RFA preferred for veins <15 mm; EVLA better for very large veins (>15 mm) and cheaper consumables

• Ultrasound-guided foam sclerotherapy (UGFS): sclerosing agent (sodium tetradecyl sulphate) foamed and injected into vein; causes endothelial destruction, thrombosis, fibrosis, obliteration; blood deactivates agent so foam used to maximise contact
• Mechanochemical ablation (MOCA): combined mechanical disruption + sclerosant
• Cyanoacrylate (glue) ablation: no tumescent anaesthetic needed

• Saphenofemoral junction (SFJ) ligation + GSV stripping (Trendelenburg operation)
• Saphenopopliteal junction (SPJ) ligation + SSV stripping (prone position; preoperative duplex mapping mandatory)
• Phlebectomy: stab avulsion of varicosities through small incisions using mosquito forceps/phlebectomy hooks; performed concomitant or sequentially; can be done under local anaesthetic
• Perforator ligation: subfascial endoscopic perforator surgery (SEPS) if indicated

• Thrombophlebitis (superficial vein thrombosis)
• Bleeding (from varicosity - usually minor but alarming; elevate limb and apply pressure)
• Venous eczema
• Lipodermatosclerosis
• Venous ulceration

XIV. DEEP VEIN THROMBOSIS (DVT) AND VENOUS THROMBOEMBOLISM (VTE)

Pathophysiology (Virchow's Triad)

1. Venous stasis (immobility, surgery, long travel)
2. Endothelial damage (trauma, surgery, inflammation)
3. Hypercoagulability (thrombophilia, malignancy, OCP)

Risk Factors (Table 62.2)

Thrombophilia (Table 62.3)

• Antithrombin deficiency
• Protein C or protein S deficiency
• Factor V Leiden (activated protein C deficiency) - most common; present in 6-7% of white populations
• Prothrombin gene mutation
• Antiphospholipid syndrome
• Screen when: VTE with family history, no provoking factor, recurrent VTE, or young age

Clinical Features of DVT

• Calf pain, swelling, tenderness, erythema, warmth
• Homan's sign (calf pain on dorsiflexion of foot) - non-specific; should NOT be routinely elicited
• Tenderness in 75% - but also in 50% without DVT
• Clinical signs of PE in ~10% of confirmed DVT: cyanosis, dyspnoea, raised JVP, fixed split S2, pleural rub

Investigation - Modified Wells Score (Table 62.4)

• Score -2 to 0: Low probability (5%)
• Score 1-2: Moderate probability (17%)
• Score >2: High probability (17-53%)

• Venous Duplex Ultrasound: first-line; compression ultrasound - veins normally compress completely; in DVT, they do not
• CT Pulmonary Angiogram (CTPA): definitive for pulmonary embolism - shows filling defects in pulmonary arteries
• Pulmonary angiography: rarely required unless thrombolysis being considered

Prophylaxis

• Graduated elastic compression stockings
• External pneumatic compression (intermittent pneumatic compression - IPC)
• Avoid in peripheral vascular disease (can worsen ischaemia)
• Electronic nerve stimulators - insufficient evidence

• LMWH (low-molecular-weight heparin): once daily subcutaneous; no monitoring; lower bleeding risk; preferred in most patients
• Unfractionated heparin (UFH): IV or subcutaneous; used in renal impairment
• Risk stratification: low/medium/high risk for PE - medium and high risk groups should receive pharmacological prophylaxis

Treatment

1. Rapid anticoagulation: treatment-dose LMWH subcutaneously
   • Renal impairment: IV unfractionated heparin
   • Heparin-induced thrombocytopenia (HIT): fondaparinux (factor Xa inhibitor) or bivalirudin (direct thrombin inhibitor)
2. Oral anticoagulation for minimum 3 months (longer if persistent risk factors or recurrent DVT):
   • NOACs (preferred): rivaroxaban or apixaban (direct factor Xa inhibitors) or dabigatran (direct thrombin inhibitor)
   • Equally effective as warfarin; fewer major bleeding complications
   • Warfarin (VKA) if NOACs contraindicated
3. IVC filter: if anticoagulation contraindicated (bleeding risk); temporary/retrievable preferred
4. Endovascular surgery (selected patients, e.g. iliofemoral DVT): thrombus removal, thrombolysis, stenting - reduces risk of post-thrombotic syndrome

• Most: anticoagulation + observation
• Severe (right heart strain, haemodynamic compromise): systemic thrombolysis or catheter-directed embolectomy

Superficial Vein Thrombosis (Thrombophlebitis)

• Previously called thrombophlebitis
• Abnormal endothelium is more common precipitant than in DVT
• Causes: trauma to varicose veins, IV cannula (>24-48 hours), infusions of hyperosmolar solutions, Buerger's disease, malignancy (pancreatic cancer → thrombophlebitis migrans)
• Surface vein: solid, tender, overlying skin erythematous early → turns brown
• Management: anti-inflammatory drugs, compression, consider anticoagulation if near SFJ (risk of propagation to deep system)