Literally means “hard arteries”, caused by thickening of the blood vessel wall.
There are three pathologic patterns:
Atherosclerosis
Arteriolosclerosis
Mönckeberg medial calcific sclerosis
B. Atherosclerosis
Definition and Morphology
Characterised by the formation of an intimal plaque that obstructs blood flow.
The plaque consists of a necrotic lipid core (mostly cholesterol) with a fibromuscular cap; the plaque often undergoes dystrophic calcification.
Distribution
Affects large- and medium-sized arteries such as the abdominal aorta, coronary arteries, popliteal arteries, and internal carotid arteries.
Risk Factors
Modifiable: Hypertension, hypercholesterolaemia (with LDL increasing risk and HDL being protective), smoking, and diabetes.
Non-modifiable: Age (number and severity of lesions increase with age), gender (increased risk in males and postmenopausal females; estrogen is protective), and genetics (family history is highly predictive).
Pathogenesis
Damage to the endothelium permits leakage of lipids into the intima.
Oxidised lipids are taken up by macrophages via scavenger receptors, forming foam cells.
Inflammatory processes and healing lead to deposition of extracellular matrix and proliferation of smooth muscle cells.
Morphologic Stages
Begins as fatty streaks (flat yellow lesions of the intima consisting of lipid-laden macrophages) that are present early in life (seen in most teenagers).
Progresses to atherosclerotic plaque.
Complications
Stenosis of medium-sized vessels results in impaired blood flow and ischaemia, leading to:
Peripheral vascular disease
Angina (coronary arteries)
Ischaemic bowel disease (mesenteric arteries)
Plaque rupture with thrombosis may result in myocardial infarction (coronary arteries) and stroke (e.g. middle cerebral artery).
Plaque rupture with embolisation causes atherosclerotic emboli (characterised by cholesterol crystals within the embolus).
Weakening of the vessel wall may result in aneurysm formation (e.g. abdominal aortic aneurysm).
C. Arteriolosclerosis
Definition
Refers to the narrowing of small arterioles.
Types
Hyaline Arteriolosclerosis:
Caused by the deposition of proteins in the vessel wall (seen as pink hyaline on microscopy).
Often a consequence of long-standing benign hypertension or diabetes.
Leads to reduced vessel calibre and end-organ ischaemia, classically producing glomerular scarring (arteriolonephrosclerosis) that progresses slowly to chronic renal failure.
Hyperplastic Arteriolosclerosis:
Involves thickening of the vessel wall due to hyperplasia of smooth muscle cells, producing an ‘onion-skin’ appearance.
Occurs in malignant hypertension.
Leads to reduced vessel calibre and end-organ ischaemia; may result in fibrinoid necrosis with haemorrhage, classically causing acute renal failure with a ‘flea-bitten’ appearance.
D. Mönckeberg Medial Calcific Sclerosis
Definition
Involves calcification of the media of muscular (medium-sized) arteries.
Clinical Significance
This calcification is non-obstructive.
Often an incidental finding on imaging studies (e.g. X-ray or mammography).
Asymptomatic: Until the aneurysm expands significantly (>5 cm) or ruptures.
Possible Presentations:
Back, Flank, Abdominal, or Groin Pain
Compression of Femoral Nerves: May cause paraesthesia of the anterior thigh and quadriceps weakness.
Embolic Phenomena: Leading to acute lower limb ischaemia.
Pulsatile Sensation or Mass in the abdomen.
1.5 Diagnosis
Abdominal Ultrasound: Quick, non-invasive, no radiation, used for screening and detection of AAA.
Computerised Tomography (CT): More detailed anatomical information, identifies involvement of other vessels (e.g., renal or iliac arteries) and detects thrombus.
Differential Diagnoses: Oesophageal varices, gastric ulcer, bowel obstruction, kidney stones, gallstones, etc. (each with different clinical clues).
1.6 Immediate Management
Risk Factor Management: Mainstay of conservative treatment (smoking cessation, controlling hypertension and hypercholesterolaemia).
Ruptured AAA:
Emergency Open Surgery is indicated if rupture occurs.
High mortality if not managed urgently.
1.7 Long-Term Management
Screening
Ultrasound in men over 65 (in some regions) to detect and monitor AAA before rupture.
Watchful Waiting
Employed for aneurysms <5.5 cm due to low rupture risk at this size.
Regular follow-up ultrasound once or twice a year to observe expansion rate.
Elective Endovascular Aneurysm Repair (EVAR)
Stent Placement (Teflon-covered) to seal the aneurysm from the native aorta.
Used for higher-risk patients unsuitable for open repair.
Shorter hospital stay (~2 days) but requires further studies for long-term survival data.
Open Surgical Repair
Elective for most unruptured aneurysms exceeding 5.5 cm in suitable patients.
Absolute Indication for ruptured aneurysms.
Involves abdominal incision, vascular clamp above and below the aneurysm, resection of the aneurysmal segment, and placement of a conduit graft.
Mortality up to 10%; complications (30%) include acute kidney injury, myocardial infarction, and lower limb paralysis.
1.8 Complications
Infection and Thromboembolic Events: Can cause acute limb ischaemia.
Rupture: The most feared complication, often presenting with hypotension and severe back/abdominal pain, leading to sudden death if untreated.
1.9 Thoracic Aortic Anuerysm
Epidemiology
Thoracic aortic aneurysm is a balloon-like dilation of the thoracic aorta.
It is frequently linked to tertiary syphilis, though it can also develop from general weakness in the aortic wall.
Aetiology
Tertiary Syphilis: Endarteritis of the vasa vasorum leads to decreased blood flow and atrophy of the vessel wall, resulting in the characteristic ‘tree-bark’ appearance of the aorta.
Major Complications
Aortic Valve Root Dilation: Expanding aneurysm at the aortic root can cause aortic valve insufficiency (regurgitation).
Compression of Mediastinal Structures: The enlarged aorta may compress the airway or oesophagus, producing respiratory or swallowing difficulties.
Thrombosis and Embolism: Slow or turbulent flow within the dilated segment can lead to clot formation, which may dislodge and embolise.
Aortic Dissection
2. Aortic Dissection
2.1 Epidemiology
Incidence: Most common in individuals aged 50–65 years.
Demographics: More frequent in African–Caribbean people; has a 2:1 male-to-female ratio.
Mortality Rate: Approximately 30%.
2.2 Aetiology
Congenital Causes:
Marfan’s syndrome or other connective tissue disorders (e.g., bicuspid aortic valve, coarctation of the aorta).
Acquired Causes:
Hypertension (accounts for >70% of cases)
Pregnancy (due to increased stress and hormonal changes causing cystic medial necrosis)
Atherosclerosis
Aortic aneurysm
Iatrogenic Causes:
Occurring during or after cardiac surgeries (valve replacement, coronary artery bypass grafting)
Sudden, severe, tearing chest pain in >90% of cases.
Often retrosternal, radiating to the back if the dissection extends into the descending aorta.
Pain radiating to the neck may indicate involvement of the aortic arch.
Stroke, syncope, or heart failure symptoms if dissection compromises arterial branches or cardiac function.
Mesenteric ischaemia (abdominal pain) if involvement of mesenteric arteries.
Renal or liver injury signs if involvement of corresponding arteries.
2.5 Diagnosis
Clinical Clues:
Difference in blood pressure >20 mmHg between arms suggests aortic dissection.
A new diastolic murmur may indicate aortic regurgitation if the dissection involves the aortic root.
Imaging:
Computerised Tomography (CT): Gold standard for diagnosing and classifying aortic dissection.
Determines whether it is proximal (Stanford type A) or distal (Stanford type B).
Clarifies the DeBakey classification (types I–III).
Transthoracic Echocardiography (TTE): May detect intimal flap in proximal ascending aorta; also assesses for aortic regurgitation.
Chest X-Ray: Shows widened mediastinum in about two thirds of cases.
Laboratory Findings:
Cardiac enzymes may be raised if coronary arteries are involved, causing myocardial ischaemia.
Urea/Creatinine may be elevated if renal perfusion is compromised.
2.6 Immediate Management
Blood Pressure Control:
Aim for systolic BP <120 mmHg to reduce propagation of the dissection.
Use intravenous antihypertensives (e.g., beta-blockers) under close monitoring.
Stanford Classification:
Type A (involving ascending aorta): Managed surgically (resection of the affected aorta, replacement with a conduit graft, possible aortic valve replacement or coronary artery bypass if involved).
Type B (no ascending aorta involvement): Typically managed medically unless complications arise (e.g., compromised organ perfusion or rupture).
2.7 Long-Term Management
Blood Pressure Monitoring: Maintain tight control of hypertension to prevent recurrence or extension of dissection.
Medication: Ongoing antihypertensives (e.g., beta-blockers) to keep systolic BP low.
Imaging Follow-Up: Periodic CT or echocardiography to monitor for expansion or additional dissection.
Aortic Regurgitation: If dissection extends into the aortic sinus.
Myocardial Infarction: Involvement of coronary ostia.
Stroke: If dissection compromises carotid or other cerebral arteries.
Regional Ischaemia: Limb, renal, or mesenteric ischaemia if respective arteries are involved.
Pleural or Pericardial Effusion: If the dissection extends into these spaces.
Carotid Artery Disease
3. Carotid Artery Disease
3.1 Epidemiology
Prevalence: Affects approximately 5% of the population.
Gender Difference: Twice as common in men than in women.
Age Distribution: Three times more common in individuals over 70 years of age compared to younger cohorts.
3.2 Aetiology
Primary Cause: Narrowing of the carotid arteries due to atherosclerosis.
Pathophysiological Mechanism: Rupture of an atherosclerotic plaque leads to thrombosis or embolism, which can occlude the carotid artery or travel to cerebral arteries.
3.3 Risk Factors
Shared with Atherosclerosis:
Hypertension
Hypercholesterolaemia
Smoking
Advanced age
Male gender
3.4 Symptoms
Typical Presentation: Often detected after an acute complication, such as:
Stroke (Cerebrovascular Accident) when a large vessel is occluded
Transient Ischaemic Attack (TIA) due to temporary occlusion of a small cerebral artery
Incidental Detection: Occasionally discovered when a carotid bruit is noted on neck examination.
3.5 Diagnosis
Carotid Ultrasound:
Identifies significant stenosis if >75% of the lumen is narrowed.
Clinical Relevance: Significant because lesions <70% or fully occluded (100%) are usually not amenable to intervention due to risk–benefit considerations.
3.6 Immediate Management
Stabilise Atherosclerosis
Reduce Thrombosis Risk
Control Blood Pressure
3.7 Long-Term Management
Medication:
Aspirin indefinitely to lower thrombotic risk.
Statins to stabilise plaques and slow atheroma progression.
Surgical / Radiological Intervention:
Indications: Symptomatic patients (TIA or stroke) with 70–99% stenosis.
Carotid Endarterectomy: Plaque removal under proximal and distal arterial clamping. Complication rate includes a 5% risk of stroke or bleeding.
Stenting: An alternative in patients with significant comorbidities or high surgical risk.
Acute Limb Ischaemia
4. Acute Limb Ischaemia
4.1 Epidemiology
Incidence: Affects around 0.1% of people per year worldwide.
Age: More frequent in older individuals.
Gender and Ethnicity: Incidence is not significantly influenced by gender or ethnicity.
4.2 Aetiology
Atherosclerosis: Responsible for >80% of cases. A plaque rupture leads to thrombosis and arterial occlusion.
Thromboembolism: Accounts for ~15%; most emboli originate from the left atrial appendage (e.g., in atrial fibrillation).
Trauma: May cause vessel injury or thrombosis, leading to ischaemia.
Surgical Graft Thrombosis: Blockage can occur within a vascular graft.
Coldness: Comparatively lower temperature than the contralateral limb.
Paraesthesia: Numbness or tingling in severe cases.
Paralysis (or weakness): Late and ominous sign.
4.5 Diagnosis
Clinical Examination:
Peripheral Pulse Assessment: Identifies level of occlusion (e.g., femoral pulse present, popliteal absent → occlusion between them).
Capillary Refill: Delayed in significant ischaemia.
Imaging:
Ultrasound: Helps locate arterial narrowing or occlusion.
CT Scan: Provides detailed anatomy, confirms site of blockage.
Laboratory Tests:
Generally non-specific for diagnosis but serve as baselines (e.g., for coagulation profiles, renal function).
4.6 Immediate Management
Heparin (Intravenous): Prevents clot extension.
Thrombolysis (e.g., Streptokinase, tPA): Intra-arterial catheter-delivered to dissolve clot.
Surgical or Radiological Intervention:
Embolectomy: Percutaneous or open surgical removal of the clot.
Bypass Surgery: If simpler measures fail, a graft (vein or synthetic) bypasses the occlusion site.
4.7 Long-Term Management
Anticoagulation:
Long-term Oral Therapy (e.g., warfarin) for embolic causes—particularly in atrial fibrillation—to prevent recurrence.
Risk Factor Control:
Strict management of atherosclerosis (stop smoking, control hypertension, treat hyperlipidaemia).
Aggressive cardiac risk modification to reduce further arterial events.
4.8 Complications
Irreversible Tissue Ischaemia: May require debridement or lead to gangrene.
Amputation: If necrosis and gangrene are extensive.
Compartment Syndrome: Swelling within fascial compartments; may require fasciotomy.
Chronic Limb Ischaemia
5. Chronic Limb Ischaemia
5.1 Epidemiology
Prevalence: Chronic limb ischaemia affects approximately 1 in 10 people worldwide.
Age: The incidence increases with age.
Demographics: Affects both genders and all ethnicities equally.
Cardiovascular Risk: Patients with peripheral arterial disease (PAD) are at high risk of developing and dying from ischaemic heart disease or cerebrovascular disease.
5.2 Aetiology
Underlying Pathology: Primarily caused by atherosclerosis in the arteries supplying the lower limbs.
Atherosclerotic plaques progressively narrow or occlude the arterial lumen.
This results in a reduced blood flow, particularly during increased oxygen demand (e.g. exercise).
Pathogenesis:
Flow-limiting stenosis means that during exercise the arterial supply cannot meet the tissue oxygen demand, leading to ischaemia.
Over time, this chronic ischaemia may progress from intermittent claudication to pain at rest, arterial ulceration, and gangrene.
Comparison: The phenomenon is analogous to angina pectoris but affecting the lower limbs (“angina of the legs”).
5.3 Risk Factors
Shared with Atherosclerosis:
Smoking
Hypertension
Hypercholesterolaemia
Diabetes mellitus
Obesity
Sedentary lifestyle
Other Factors:
Advanced age increases the risk.
The presence of other cardiovascular risk factors further heightens the likelihood of developing chronic limb ischaemia.
5.4 Symptoms
Intermittent Claudication:
Calf, leg or buttock pain during walking that is relieved by rest.
Rest Pain:
As the disease progresses, patients may develop pain at rest due to critically reduced blood flow.
Advanced Disease:
Arterial ulcers: Typically located on the distal lower limb.
Gangrene: In severe cases, irreversible tissue loss may occur.
General Comparison: Claudication is often referred to as “angina of the legs”.
5.5 Diagnosis
Ankle–Brachial Pressure Index (ABPI):
Calculation: Ratio of ankle systolic blood pressure to brachial systolic blood pressure.
Normal ABPI: Approximately 1.
Diagnostic Threshold: An ABPI of <0.9 indicates peripheral arterial disease.
Correlation with Severity:
0.95–1.0: Symptom-free.
0.5–0.95: Intermittent claudication.
0.3–0.5: Resting pain.
<0.2: Ulceration and gangrene.
Ultrasound Scanning:
Serves as the investigation of choice to confirm occlusion.
Demonstrates blood flow, location, severity, and extent of atherosclerotic disease.
Fontaine Classification:
Stage I: Asymptomatic.
Stage IIa: Intermittent claudication at >200 m.
Stage IIb: Intermittent claudication at <200 m.
Stage III: Resting limb pain.
Stage IV: Limb necrosis or gangrene.
Additional Imaging: CT or MR angiography may be used for detailed anatomical assessment, particularly if surgical planning is required.
5.6 Immediate Management
Initial Stabilisation:
Rapid evaluation of limb viability and identification of the level of arterial occlusion.
Pharmacological Therapy:
Intravenous Anticoagulation: Often initiated if there is concern for acute thrombosis or embolisation.
Revascularisation:
Endovascular Techniques:
Angioplasty and Stenting: Used to reopen short segments of occlusion; typically, 90% remain patent at one year.
Note a small complication risk (approximately 2%) including acute thrombosis, arterial rupture, and distal embolisation.
Surgical Options:
Bypass Surgery: Performed when endovascular techniques are unsuitable or unsuccessful.
Involves resection of non-viable tissue and bypass grafting (using either a harvested vein or an artificial conduit, such as Teflon) to bridge the occlusion.
Emergency Intervention: In cases where limb viability is threatened, urgent revascularisation is required to prevent irreversible tissue damage.
5.7 Long-Term Management
Risk Factor Modification:
Smoking Cessation.
Optimised Management of hypertension, diabetes, and hypercholesterolaemia.
Diet and Exercise: Encouraging regular aerobic exercise to improve cardiorespiratory fitness and increase HDL cholesterol.
Medical Therapy:
Antiplatelet Therapy: Long-term aspirin to reduce thrombotic risk.
Statin Therapy: To stabilise atherosclerotic plaques and slow disease progression.
Surveillance:
Regular follow-up ultrasound scans to monitor aneurysm size and progression, particularly in those managed conservatively.
Foot Clinics/Chiropody: Especially for diabetic patients, to detect early signs of ischaemia and prevent ulceration.
Lifestyle Advice:
Education on recognising symptoms of worsening ischaemia.
Regular review of cardiovascular risk factors.
5.8 Complications
Arterial Ulcers: Due to chronic ischaemia.
Gangrene: May develop if ischaemia becomes irreversible, potentially necessitating limb amputation.
Disabling Symptoms: Persistent claudication can significantly impair mobility and quality of life.
Thrombosis/Embolism: Continued risk of clot formation or embolisation leading to further ischaemic events.
Deep Vein Thrombosis
6. Deep Vein Thrombosis (DVT)
6.1 Epidemiology
Prevalence: Approximately 1 in 20 individuals will develop DVT during their lifetime.
Risk Demographics:
Increased risk in males.
Higher prevalence in those of white ethnicity.
Risk rises with increasing age.
6.2 Aetiology
Definition: Deep vein thrombosis is the formation of a blood clot in a deep vein of the lower limb.
Pathogenesis:
Often results from Virchow’s triad, which includes:
Disruption in normal blood flow: Stasis and turbulence promote clot formation (e.g. prolonged immobility, immobilisation due to casts or bed rest).
Endothelial cell damage: Injury to the vessel wall from trauma or inflammatory processes exposes subendothelial tissue, triggering thrombosis.
Hypercoagulable state: Inherited or acquired conditions increase the tendency of blood to clot.
Prevention Focus: Avoidance of prolonged stasis, especially during situations like long-haul flights, is key.
Asymptomatic Cases: Approximately 50% of DVT cases may be asymptomatic.
Symptomatic Presentation:
Pain in the affected limb.
Swelling and warmth over the area.
Erythema (redness) of the skin.
Differential Diagnoses: Ruptured Baker’s cyst, trauma, or cellulitis should be considered.
6.5 Diagnosis
6.5.1 Clinical Assessment
History and Physical Examination:
Assess for symptoms of leg pain, swelling, and tenderness.
Palpation of Peripheral Pulses: An occlusion is suggested when pulses are diminished distal to the clot.
Wells Score for DVT:
The Wells score aids in estimating the probability of DVT, thereby guiding further investigation.
A simplified version is shown in the table below:
Criterion
Score
Active cancer
+1
Unilateral calf swelling ≥3 cm
+1
Unilateral swollen veins
+1
Unilateral pitting oedema
+1
Previous DVT
+1
Swelling of the entire leg
+1
Deep venous localised tenderness
+1
Paralysis, paresis or recent cast
+1
Recently bedridden or major surgery
+1
Alternative diagnosis as likely as DVT
−2
Well’s Score for DVT
Interpreting the Wells Score:
High risk: Score ≥2 (approximately 50% likelihood of DVT) → Proceed directly to imaging (venous ultrasound).
Moderate risk: Score 1–2 (approximately 20% likelihood) → Consider D-dimer test; if positive, then imaging is indicated.
Low risk: Score <1 (approximately 5% likelihood) → A negative D-dimer may exclude DVT; if positive, further imaging is warranted.
6.5.2 Laboratory Investigations
D-dimer Test:
Purpose: A by-product of fibrinolysis; a raised level suggests activation of the coagulation system.
Interpretation:
High sensitivity: A normal D-dimer makes DVT unlikely.
Poor specificity: Elevated levels can occur in many other conditions (e.g. trauma, recent surgery, infection, malignancy, pregnancy).
6.5.3 Imaging Studies
Venous Ultrasound:
Primary Diagnostic Tool: Visualises the venous lumen and detects the presence, location, and extent of a thrombus.
Context: Particularly indicated if clinical suspicion is moderate to high or if D-dimer is elevated in a patient with low-to-moderate Wells score.
6.6 Immediate Management
Anticoagulation:
Initiate Intravenous LMWH immediately to prevent further clot propagation.
Concurrent Warfarin Loading: Begin warfarin while administering LMWH. Continue LMWH until the International Normalised Ratio (INR) stabilises between 2 and 3.
Monitoring:
The INR is calculated by dividing the patient’s prothrombin time by the normal prothrombin time, raised to the power of the international sensitivity index, standardising results across different laboratories.
Alternative Anticoagulants:
If patients have poor venous access, unstable INR, bleeding, or poor concordance with warfarin, a novel oral anticoagulant (NOAC) may be prescribed, or the patient may remain on LMWH.
Inferior Vena Cava (IVC) Filter:
Consider in patients with recurrent DVT or contraindications to warfarin/LMWH, to prevent embolisation to the lungs.
6.7 Long-Term Management
Continuation of Anticoagulation:
Maintain warfarin therapy for 3–6 months once the INR is stabilised.
Ongoing Risk Factor Modification:
Encourage mobilisation and leg exercises to prevent stasis.
Review and manage modifiable risk factors, such as obesity and smoking.
Monitoring:
Regular follow-up appointments to check INR (if on warfarin) or assess for any complications if on NOACs/LMWH.
Reassessment of DVT risk, particularly in patients with recurrent events.
6.8 Complications
Pulmonary Embolism (PE):
A thrombus may dislodge and travel through the pulmonary circulation, potentially causing a life-threatening PE.
Post-Thrombotic Syndrome (PTS):
Chronic pain, swelling, and a feeling of heaviness in the affected limb due to persistent venous insufficiency after DVT.
Venous Ulcers:
Result from long-standing venous hypertension and stasis, often in the lower leg.
Bleeding:
A potential complication of anticoagulant therapy if not appropriately managed.
Varicose Veins
7. Varicose Veins
7.1 Epidemiology
Prevalence:
Affects approximately 40% of women and 20% of men worldwide.
Demographic Trends:
More common in western populations.
Incidence increases with age.
Higher prevalence in individuals who are obese and inactive.
7.2 Aetiology
Pathophysiology:
Result from chronic incompetence of the one-way venous valves, leading to retrograde blood flow.
The resulting venous insufficiency causes pooling and engorgement of the veins.
Underlying Mechanism:
Venous dilatation and reduced venous return from the lower limbs.
7.3 Risk Factors
7.3.1 Non-Modifiable Risk Factors
Genetic Factors: Although the specific genes are as yet unknown.
Ageing: Natural wear on the venous system with time.
7.3.2 Modifiable Risk Factors
Prolonged Standing: Leads to increased venous pressure.
Obesity: Increases pressure on the venous system.
Chronic Abdominal Straining: Often due to constipation.
Pregnancy: Increases venous pressure and can compromise valve function.
7.4 Symptoms
Leg Discomfort:
Aches and a sensation of heavy legs.
Swelling:
Noted during the day, particularly after prolonged standing.
Visual Changes:
Appearance of telangiectasia (small, red, spidery veins).
Additional Features:
Varicose eczema: Dry, pruritic (itchy) skin overlying the affected veins.
Leg cramps.
Delayed healing of minor injuries.
7.5 Diagnosis
7.5.1 Clinical Evaluation
History and Examination:
Identification of symptomatic varicose veins.
Presence of skin changes such as pigmentation and varicose eczema.
Detection of a palpable, often tortuous, venous network.
Doppler Ultrasound:
Gold Standard for diagnosing varicose veins.
Assesses venous anatomy and evaluates for truncal reflux (backflow through a main superficial vein).
7.6 Immediate Management
Asymptomatic Patients:
Reassurance and conservative management; drug therapy is not required.
Symptomatic Patients or Those with Complications:
Referral to a vascular service if there are symptoms or skin changes (e.g. varicose eczema), superficial vein thrombosis, or venous ulceration.
Investigation with Doppler ultrasound to guide treatment decisions.
7.7 Long-Term Management
Conservative Management:
Lifestyle Modifications:
Weight loss.
Regular exercise.
Avoidance of prolonged standing.
Compression Stockings:
Used to reduce venous stasis and relieve symptoms.
Interventional Options (for patients with disabling symptoms or complications):
Endothermal Ablation.
Endovenous Laser Treatment.
Ultrasound-Guided Sclerotherapy.
Surgical Stripping: Considered if interventional procedures are unsuitable.
7.8 Complications
Venous Ulcers:
May develop due to chronic venous insufficiency.
Deep Vein Thrombosis (DVT):
Occurs as a result of prolonged venous stasis.
Pain and Tenderness:
Persistent symptoms that affect quality of life.
Superficial Thrombophlebitis:
Inflammation and clot formation in superficial veins.
Superficial Thrombophlebitis
8. Superficial Thrombophlebitis
8.1 Epidemiology
Prevalence: Affects approximately 5% of the population worldwide.
Demographics:
More common in women.
Increased incidence in the elderly.
Frequently observed in patients with varicose veins.
8.2 Aetiology
Definition: Superficial thrombophlebitis is the presence of both a thrombus (clot) and venous inflammation(phlebitis) within the superficial veins of the lower limb.
Pathological Process:
The thrombus forms within a superficial vein, and the inflammatory process affects the vein wall.
8.3 Risk Factors
Gender: Higher prevalence in women.
Age: More common in the elderly.
Venous Insufficiency:
Associated with varicose veins, which predispose to valve incompetence and venous stasis.
8.4 Symptoms
Localised Pain: Affected area is painful.
Erythema and Swelling: The involved limb shows redness and swelling.
Palpable Cord: A cord-like, tender vein can be felt on examination.
8.5 Diagnosis
Clinical Diagnosis:
Typically based on patient history and physical examination findings.
Diagnosis is straightforward when confined to the lower limb.
Use of Ultrasound:
If symptoms or signs extend above the knee, an ultrasound is required to exclude deep vein thrombosis (DVT).
8.6 Immediate Management
Conservative Measures:
Elevation of the affected limb to promote venous return.
Use of compression stockings to reduce venous stasis.
Application of warmth to alleviate discomfort.
Administration of non-steroidal anti-inflammatory drugs (NSAIDs) to reduce pain and inflammation.
These measures help to reduce symptoms and prevent propagation of the clot.
8.7 Long-Term Management
In many cases, conservative management is sufficient since the venous lumen can become recanalised over time.
Ongoing Risk Factor Modification:
Address underlying venous insufficiency (e.g. managing varicose veins) and encouraging regular leg movement.
8.8 Complications
Extension into Deep Veins:
The clot may extend, resulting in deep vein thrombosis.
Venous Ulcers:
Chronic venous insufficiency may lead to ulceration.
Persistent Thrombosed Vein:
The thrombosed vein may remain as a palpable nodule.
Raynaud’s Phenomenon
9. Raynaud’s Phenomenon
9.1 Epidemiology
Prevalence:
Primary Raynaud’s disease affects approximately 10% of the population worldwide.
Age of Onset:
Typically presents in the second or third decade of life.
Affected Areas:
Most commonly affects the peripheries (fingers, toes, and other appendages), though other areas may be involved.
9.2 Aetiology
Underlying Mechanism:
Raynaud’s phenomenon occurs due to excessive transient vasoconstriction (vasospasm) that compromises blood flow.
Triggers:
Exposure to cold and emotional stress are recognised triggers.
Subtypes:
Primary Raynaud’s Disease: Occurs in the absence of an underlying condition and is considered a benign vasospastic disorder.
Secondary Raynaud’s Syndrome: Occurs in the context of another disease
9.3 Risk Factors
Primary Raynaud’s:
More common in younger individuals (typically second or third decade).
Secondary Raynaud’s:
Associated with various underlying conditions (see section 9.6 for mimic conditions).
Common Triggers:
Cold exposure, smoking and caffeine are well recognised to provoke an attack.
9.4 Symptoms
Colour Changes in Affected Digits:
White/Pale: Occurs due to vasospasm causing a reduction in blood flow.
Blue: Resulting from cyanosis as blood oxygen saturation drops.
Red: Occurs during reactive hyperaemia as blood flow is restored.
Associated Symptoms:
Pain in the affected digits.
Sensations of coldness and numbness during an attack.
Pattern of Attacks:
Typically bilateral and triggered by exposure to cold or emotional stress.
9.5 Diagnosis
Clinical Diagnosis:
Based primarily on the patient’s history and physical examination during an attack.
Attacks characteristically produce a sequential colour change (white → blue → red).
Distinguishing Primary from Secondary:
In primary Raynaud’s, attacks occur in the absence of an identifiable underlying cause.
If a secondary cause is suspected (e.g. features suggestive of connective tissue disease), further investigations such as antinuclear antibody titres and referral to rheumatology are warranted.
Conditions That Mimic Raynaud’s Phenomenon:
A variety of disorders may present with similar symptoms; see the table below.
Avoidance of triggers: Keep peripheries warm, use protective clothing in cold weather.
Pharmacological Therapy:
Calcium Channel Blockers: First-line agents to induce vasodilatation.
In Severe Cases:
Additional treatments may include:
Alpha-adrenergic Blockers (e.g. prazosin).
ACE Inhibitors or Angiotensin Receptor Blockers (ARBs).
Topical Nitrates.
Phosphodiesterase Inhibitors (e.g. sildenafil).
Prostaglandins (e.g. iloprost).
9.7 Long-Term Management
For Primary Raynaud’s:
Continued emphasis on lifestyle modifications and avoidance of triggers.
Regular follow-up to assess symptom frequency and severity.
For Secondary Raynaud’s:
Management of the underlying disease is paramount.
Symptomatic treatment with calcium channel blockers is typically continued.
Patient Education:
Instruct patients on recognising early signs of an attack and measures to reduce exposure to triggers.
9.8 Complications
Arterial Ulcers:
In extreme cases, persistent ischaemia can lead to the formation of ulcers.
Gangrene:
Prolonged or severe episodes may result in tissue necrosis and gangrene, necessitating surgical intervention.
Functional Impairment:
Recurrent episodes can lead to chronic pain and disability.
Subclavian and Axillary Vein Thrombosis
10. Subclavian or Axillary Vein Thrombosis
10.1 Epidemiology
Prevalence:
A rare condition, accounting for approximately 1% of all venous thrombosis cases.
Demographics:
More commonly affects the dominant upper limb.
10.2 Aetiology
Definition:
Thrombosis in the subclavian or axillary veins involves the formation of a clot within the proximal veins of the upper limb.
Alternate Names:
Also known as effort thrombosis or Paget–von Schrötter disease.
Pathogenesis:
Typically occurs due to repeated and sustained overhead activity (e.g. painting) causing mechanical compression of the veins.
May also occur in association with malignancy, following radiotherapy, in the presence of an underlying thrombophilic state (e.g. protein C or S deficiency), or with long-term indwelling central venous catheters.
Mechanism of Venous Compression:
Venous return from the upper limb becomes restricted when the arms are positioned overhead due to:
Compression by soft tissue (e.g. anterior scalene muscle).
Compression by bony structures (e.g. first rib).
Endothelial damage from repetitive motion or cannulation.
Hypercoagulable states, which may be exacerbated by dehydration.
10.3 Risk Factors
Effort-Related:
Repeated overhead activity (occupational or recreational).
Thrombophilia:
Inherited conditions such as protein C or S deficiency.
Iatrogenic Causes:
Long-term indwelling central venous catheters.
Malignancy and Radiotherapy:
Presence of cancer or prior radiotherapy increases risk.
Anatomical Factors:
Venous compression due to structural factors in the thoracic outlet.
10.4 Symptoms
Local Signs:
Affected arm exhibits a feeling of heaviness, swelling, and weakness.
The limb may appear cyanotic.
Presence of distended superficial veins.
General Discomfort:
Pain in the upper limb, which may be exacerbated by movement or prolonged activity.
10.5 Diagnosis
10.5.1 Clinical Assessment
History:
Inquiry about repetitive overhead activities.
Assessment of any previous indwelling catheter use or recent malignancy treatments.
Physical Examination:
Inspection and palpation of the upper limb for swelling, tenderness, and the presence of a cord-like structure along the vein.
10.5.2 Imaging Studies
Ultrasound:
The first-line investigation to visualise the thrombus, assess venous patency, and evaluate blood flow.
May be limited by overlying bony structures (clavicle or sternum); if suspicion remains high, alternative imaging is warranted.
Alternative Imaging:
Computed Tomography (CT) may be used if ultrasound is inconclusive due to anatomical limitations.
10.6 Immediate Management
Anticoagulation Protocol:
Begin subcutaneous low-molecular-weight heparin (LMWH) immediately to prevent clot propagation.
Concurrently, initiate loading doses of warfarin.
Continue LMWH until the International Normalised Ratio (INR) is stable within the therapeutic range (typically 2–3), after which LMWH is discontinued.
Management of Anticoagulation:
The INR is calculated as the patient’s prothrombin time divided by the normal prothrombin time, raised to the power of the international sensitivity index. This standardises the result across different laboratories.
Alternative Options:
In patients with poor venous access, unstable INR, bleeding, or poor compliance with warfarin, consider the use of a novel oral anticoagulant (NOAC) or continuation on LMWH.
Inferior Vena Cava (IVC) Filter:
For patients with recurrent DVT or those who cannot tolerate warfarin/LMWH due to bleeding risk, an IVC filter may be inserted to prevent pulmonary embolisation.
10.7 Long-Term Management
Continuation of Anticoagulant Therapy:
Once the INR is stabilised, maintain warfarin for 3–6 months.
Monitoring:
Regular monitoring of INR (if on warfarin) to ensure continued therapeutic anticoagulation.
Periodic reassessment for any signs of recurrent thrombosis.
Risk Factor Modification:
Address and modify underlying risk factors such as immobility and dehydration.
Evaluate for and manage any underlying thrombophilic conditions appropriately.
10.8 Complications
Pulmonary Embolism:
Thrombus embolisation to the lungs, causing potentially life-threatening pulmonary embolism.
Post-Thrombotic Syndrome (PTS):
Chronic pain, swelling, and a sensation of heaviness in the affected limb due to persistent venous insufficiency.
Recurrent Thrombosis:
Increased risk of repeat clot formation if anticoagulation is inadequate.
Bleeding:
A potential complication of anticoagulant therapy if not carefully monitored.
