After completing this section, you will be able to approach a patient with suspected peripheral vascular disease in the Kenyan context, understanding its causes, presentation, examination, and initial investigations. Always consult the Kenya MoH guideline and hospital formulary for specific drug doses and local protocols.

Peripheral vascular disease

Definition

Peripheral vascular disease (PVD) refers to conditions affecting blood circulation outside of the heart and brain, primarily involving the arteries and veins of the limbs. This note focuses on arterial PVD, often termed peripheral arterial disease (PAD).

Anatomy and physiology you need

The peripheral arteries are a network of vessels branching from the aorta, supplying oxygenated blood to the extremities. Key vessels include the iliac arteries, femoral arteries, popliteal arteries, and tibial arteries. Arterial walls are composed of three layers: intima, media, and adventitia. Smooth muscle in the media allows for vasodilation and vasoconstriction to regulate blood flow. Veins return deoxygenated blood to the heart, aided by valves to prevent backflow. Adequate blood flow is essential for tissue oxygenation and metabolic waste removal.

Causes and risk factors

In Kenya, PVD is influenced by a combination of global and local factors:

• Atherosclerosis: The most common cause, characterized by plaque buildup within arteries.
  • Modifiable Risk Factors:
    • Hypertension: High blood pressure damages arterial walls.
    • Diabetes Mellitus: High blood sugar leads to endothelial dysfunction and accelerates atherosclerosis.
    • Dyslipidaemia: Abnormal cholesterol levels contribute to plaque formation.
    • Smoking: Nicotine causes vasoconstriction and damages the arterial lining.
    • Obesity: Associated with other risk factors like hypertension and diabetes.
    • Sedentary Lifestyle: Contributes to obesity and poor cardiovascular health.
  • Non-Modifiable Risk Factors:
    • Age: Risk increases with age.
    • Family History: Genetic predisposition.
• Inflammatory Conditions:
  • Rheumatic Diseases: Conditions like rheumatoid arthritis can cause vasculitis.
  • Systemic Lupus Erythematosus (SLE): Can lead to inflammation of blood vessels.
• Infectious Causes:
  • HIV/AIDS: Increased risk of accelerated atherosclerosis and opportunistic infections affecting blood vessels.
  • Tuberculosis (TB): Can cause arteritis, particularly in endemic areas.
  • Malaria: Chronic or severe malaria can lead to vascular complications.
• Haematological Disorders:
  • Sickle Cell Disease: Vaso-occlusive crises can lead to arterial occlusion and tissue damage.
• Trauma: Direct injury to arteries.
• Vasculitis: Inflammation of blood vessel walls from various causes.
• Thromboembolic Disease: Blood clots forming in situ or travelling from elsewhere.

Pathophysiology

Atherosclerosis:

Endothelial Injury/Dysfunction ↓ Lipid Infiltration (LDL) ↓ Macrophage Activation & Foam Cell Formation ↓ Fatty Streak Formation ↓ Fibrous Plaque Development ↓ Plaque Progression & Calcification ↓ Arterial Stenosis (Narrowing) or Occlusion (Blockage) ↓ Reduced Blood Flow to Tissues

Sickle Cell Disease (Vaso-occlusion):

Sickling of Red Blood Cells ↓ RBCs block small blood vessels ↓ Ischemia and Infarction of Tissues ↓ Pain and Organ Damage

Inflammatory Vasculitis:

Inflammation of Arterial Wall ↓ Thickening and Narrowing of Lumen ↓ Reduced Blood Flow ↓ Ischemia

Clinical features

History questions that matter

• Pain characteristics: Clarify the site of discomfort (buttock, thigh, or calf). Ask if it is brought on by a fixed walking distance, rapidly relieved within minutes of rest, and reproducible on resuming exertion (intermittent claudication). Ask if pain occurs at rest, especially at night when supine, forcing the patient to hang the leg over the edge of the bed (ischaemic rest pain, signifying critical limb-threatening ischaemia [CLTI]).
• Acuteness of onset: Inquire whether pain began suddenly over hours ("6 Ps": pain, pallor, pulselessness, perishing cold, paraesthesia, paralysis) suggesting acute arterial embolism, or progressed insidiously over months, pointing to chronic atherosclerotic occlusion.
• Tissue loss and healing: Ask about non-healing ulcers on pressure points or toes, minor trauma leading to gangrene, or delayed wound healing.
• Systemic and local risk factors: Document tobacco use (quantity and duration), diabetes mellitus, hypertension, and dyslipidaemia. Ask about antiretroviral therapy (especially protease inhibitors causing dyslipidaemia), sickle cell disease (vaso-occlusive crises, leg ulcers), and prior transient ischaemic attacks or angina.
• Erectile dysfunction: In young or middle-aged men with bilateral buttock claudication, screen for impotence (Leriche syndrome: aortoiliac occlusion).

Examination findings and why each occurs

• Decreased or absent peripheral pulses: Palpate the abdominal aorta, femoral, popliteal, posterior tibial, and dorsalis pedis pulses. Mechanism: Fixed luminal narrowing or thromboembolic occlusion dampens or abolishes the pulse wave distal to the obstruction.
• Arterial bruits: Auscultate over the iliac, femoral, and popliteal arteries. Mechanism: Turbulent blood flow generated as blood is forced through a stenotic, non-compliant arterial segment.
• Trophic skin changes: Dry, shiny skin, loss of distal hair, and brittle, thickened toenails. Mechanism: Chronic microvascular hypoperfusion starves the dermal appendages (hair follicles, sebaceous glands, and nail matrix) of oxygen and nutrients.
• Pallor on elevation and dependent rubor (Buerger’s test): Elevate the limbs to 45 degrees for 1 to 2 minutes, then have the patient sit up and hang legs over the bed. Mechanism: Elevation exceeds perfusion pressure, draining blood and causing rapid pallor; dependency prompts gravity-assisted filling into chronically dilated, paralysed distal arterioles, creating an intense dark red flush.
• Prolonged capillary refill time (> 2–3 seconds): Assessed at the digital pulp. Mechanism: Inadequate arterial inflow delays the restoration of microcirculatory blood volume after compression.
• Cool, pale, or cyanotic extremity: Compared directly with the contralateral limb. Mechanism: Reduced warm, oxygenated arterial inflow shifts tissue perfusion toward hypothermia and increases localized deoxygenated haemoglobin.
• Arterial ulcers and gangrene: Punched-out, deep, exquisitely painful ulcers on distal tips of digits, lateral malleolus, or heel base, with pale, sloughy bases and minimal granulation. Mechanism: Complete local microcirculatory failure results in full-thickness coagulative tissue necrosis.
• Neuromotor deficits (paraesthesia, reduced light touch, weakness): Mechanism: Ischaemic injury to peripheral sensory and motor nerve fibres; highly sensitive indicators of impending, non-viable limb loss.

Differential diagnosis

Investigations

Diagnosis and severity

Diagnostic synthesis

A clinical diagnosis of peripheral vascular disease is established through characteristic exertional limb symptoms, physical evidence of arterial insufficiency (reduced pulses, prolonged capillary refill, trophic changes), and confirmed objectively by an ABPI < 0.90 or duplex ultrasound demonstration of flow-limiting stenosis.

Clinical staging and severity

Severity is stratified using two established systems to guide limb-salvage urgency:

• Fontaine Classification:
  • Stage I: Asymptomatic (demonstrable disease on imaging/ABPI without clinical limitation).
  • Stage IIa: Mild intermittent claudication (claudication distance > 200 metres).
  • Stage IIb: Moderate-to-severe intermittent claudication (claudication distance < 200 metres).
  • Stage III: Ischaemic rest pain (persistent pain in the forefoot/toes requiring dependency).
  • Stage IV: Trophic lesions, arterial ulceration, or gangrene.

• Rutherford Classification:
  • Category 0: Asymptomatic.
  • Category 1: Mild claudication (treadmill completion with minimal symptoms).
  • Category 2: Moderate claudication.
  • Category 3: Severe claudication (inability to complete standard treadmill walk).
  • Category 4: Ischaemic rest pain.
  • Category 5: Minor tissue loss (non-healing ulceration, focal digit gangrene).
  • Category 6: Major tissue loss (extensive gangrene extending above the transmetatarsal level, non-salvageable foot).

Critical Limb-Threatening Ischaemia (CLTI) is defined by the presence of ischaemic rest pain (Fontaine III / Rutherford 4) for more than two weeks, or tissue loss consisting of non-healing ulcers or gangrene (Fontaine IV / Rutherford 5–6), attributable to objectively verified arterial occlusive disease (absolute ankle systolic pressure < 50 mmHg or toe pressure < 30 mmHg). It represents a vascular emergency requiring urgent revascularization to prevent major amputation.

Management

Immediate Stabilisation

• Acute limb-threatening ischaemia (The 6 Ps): Keep the limb dependent to aid gravity perfusion; do not elevate or apply heat. Administer systemic anticoagulation with unfractionated heparin immediately to stop thrombus propagation. Provide adequate intravenous opioid analgesia.
• Infection control: Start empirical broad-spectrum intravenous antibiotics if tissue necrosis, ulcer infection, or wet gangrene is present.
• Systemic resuscitation: Correct dehydration and optimise cardiac output to maintain peripheral perfusion pressure.

Definitive Management

Monitoring and Safety

• Supervised exercise therapy: First-line intervention for claudication; builds collateral vessels.
• Wound and foot care: Daily inspection, avoidance of bare feet, well-fitted footwear, and prompt management of fungal interdigital infections.
• Contraindications: Cilostazol is strictly contraindicated in patients with heart failure of any severity (increases mortality). Compression stockings are contraindicated in significant arterial disease (ABPI < 0.8) as they cause skin necrosis. Unopposed non-cardioselective beta-blockers should be used cautiously if critical limb ischaemia is present.

Complications and Prognosis

• Ischaemic ulcers and non-healing wounds: Located over pressure points or distal toes.
• Wet or dry gangrene: Dry gangrene results from pure ischaemia; wet gangrene represents bacterial superinfection requiring emergency debridement.
• Secondary limb loss: Major amputation (below-knee or above-knee).
• Cardiovascular events: High 5-year mortality, predominantly driven by concomitant coronary artery disease and ischaemic stroke.

High-Yield Exam Points

• The elevation pallor mistake: Elevating a chronically ischaemic leg causes dramatic blanching (Buerger's test); lowering it causes a deep sunset red rubor (reactive hyperaemia). Examiners ask for this differentiation versus cellulitis.
• Compression wrap hazard: Applying compression bandages to an ulcerated leg before checking the ABPI is a critical fail; it converts chronic ischaemia into acute necrosis.
• Spinal vs. vascular claudication: Vascular is relieved simply by standing still; spinal claudication (stenosis) requires lumbar flexion (sitting or leaning forward).
• Bedside palpation trap: Palpating a cold limb with cold hands; examiners expect you to assess skin temperature using the dorsal surface of your fingers, moving symmetrically from proximal to distal.
• HIV-associated vasculopathy: Can present in young non-smokers with advanced aneurysmal or occlusive disease; always review the CD4 count and ART history.

Clinical Case

A 62-year-old male with long-standing type 2 diabetes presents with a 2-month history of severe burning pain in his right forefoot that wakes him at night. Relief is obtained only by dangling the foot over the side of the bed. Examination reveals a pale, cold right foot with absent dorsalis pedis and posterior tibial pulses, sluggish capillary refill of 5 seconds, and a non-healing 1-cm punch-out ulcer over the head of the first metatarsal.

Question 1

What clinical stage of peripheral vascular disease does this presentation represent? Model Answer: Critical limb-threatening ischaemia (Fontaine stage III/IV or Rutherford grade II/III), defined by rest pain lasting more than two weeks, tissue loss/ulceration, and compromised perfusion.

Question 2

Why does dangling the foot over the edge of the bed relieve the patient's rest pain? Model Answer: Dependent positioning uses hydrostatic gravity to augment arterial perfusion pressure across high-resistance, stenotic infrapopliteal vessels, temporarily increasing capillary flow to ischaemic sensory nerve endings.

Question 3

What non-invasive bedside investigation must be performed immediately, and what diagnostic pitfall must be anticipated? Model Answer: Ankle-Brachial Pressure Index (ABPI); diabetic patients frequently have medial arterial calcification (Mönckeberg sclerosis), rendering vessels non-compressible and falsely elevating the ABPI (> 1.4), which requires toe-brachial index testing instead.

Practice Questions

Question 1

A 58-year-old male smoker with severe bilateral calf claudication is evaluated. Echocardiography reveals an ejection fraction of 32% secondary to a prior anterior myocardial infarction. Which medication is strictly contraindicated for the management of his claudication symptoms?

A. Atorvastatin B. Cilostazol C. Aspirin D. Enalapril

Answer: B. Cilostazol Explanation: Cilostazol is a phosphodiesterase-3 inhibitor that increases mortality in patients with any degree of congestive heart failure.

Question 2

A 68-year-old woman lies in a medical ward bed with an acutely painful, pale, and cold left leg of 4 hours' duration. The femoral pulse is palpable, but popliteal and pedal pulses are absent. Heart rate is 112 beats per minute and irregularly irregular. What is the most appropriate immediate medical intervention?

A. Immediate application of warm blankets and hot water bottles to the affected foot B. Intravenous unfractionated heparin bolus and infusion C. Elevation of the limb to 45 degrees D. Subcutaneous low-dose aspirin and an oral statin

Answer: B. Intravenous unfractionated heparin bolus and infusion Explanation: This presentation represents acute arterial embolism likely secondary to atrial fibrillation; systemic unfractionated heparin stops ongoing thrombus formation while preparing for emergency revascularisation.

Question 3

A 54-year-old man presents with chronic, bilateral lower leg swelling and a shallow, irregular ulcer above the medial malleolus. The surrounding skin is hyperpigmented. Which finding on clinical assessment definitively argues against using standard high-compression bandage therapy?

A. Presence of superficial varicose veins B. An Ankle-Brachial Pressure Index (ABPI) of 0.55 C. Ulcer base covered in slough D. Fasting blood glucose of 7.8 mmol/L

Answer: B. An Ankle-Brachial Pressure Index (ABPI) of 0.55 Explanation: Compression therapy is contraindicated when significant co-existing arterial disease is present (ABPI < 0.8), as external pressure will occlude arterial flow and cause rapid tissue necrosis.

Question 4

A 45-year-old manual labourer complains of calf pain after walking 200 metres. The pain disappears after standing upright for 3 minutes. Examination shows normal pedal pulses at rest that disappear following 1 minute of repeated tiptoe exercises. What is the mechanism behind the disappearance of pulses?

A. Venous hypertension causing compartment syndrome B. Musculoskeletal entrapment without arterial disease C. Vasodilation in non-ischaemic proximal beds causing distal arterial pressure drop across a fixed stenosis D. Conversion of arterial flow to retrograde collateral flow via perforators

Answer: C. Vasodilation in non-ischaemic proximal beds causing distal arterial pressure drop across a fixed stenosis Explanation: Exercise induces physiological vasodilation; in the presence of a proximal arterial stenosis, flow cannot increase adequately, the pressure gradient steepens, and distal perfusion pressure drops below the threshold needed to palpate pulses.

Question 5

A 34-year-old HIV-positive patient on antiretroviral therapy presents with rapid-onset digital cyanosis and dry necrosis of two toes. Which feature best distinguishes HIV-associated vasculopathy from classic atherosclerotic peripheral arterial disease?

A. Sparing of infrapopliteal vessels B. Absence of traditional cardiovascular risk factors and presence of non-atherosclerotic occlusive aneurysmal remodelling C. Elevated Ankle-Brachial Pressure Index due to heavy medial calcification D. Rapid response to high-intensity statin monotherapy

Answer: B. Absence of traditional cardiovascular risk factors and presence of non-atherosclerotic occlusive aneurysmal remodelling Explanation: HIV vasculopathy often causes necrotising arterial inflammation, thrombosis, and multiple small aneurysms in young patients without standard atherogenic risk profiles.

Drafted with AI assistance from standard references and reviewed for structure. Check details against your lecture notes and the Kenya MoH guideline.