Vascular Disorders: Causes, Symptoms and Treatment

Chronic Venous Insufficiency and Varicose Veins

Varicose veins are caused by venous stasis, edema, and congenital weakness of the vein wall collagen. Symptoms are aggravated by prolonged standing, pregnancy, puberty, and heat, and include heaviness, tiredness, edema, induration, pain, and nocturnal cramps. Advanced cases may show trophic changes such as skin discoloration, hair loss, thinning of the skin, nail alterations, and ulcers.

Thrombophlebitis and Venous Thrombosis

Superficial venous thrombosis (thrombophlebitis) is caused by venous stasis, hypercoagulability, endothelial injury, and the consequences of surgery. It is characterized by a painful course, edema, induration, increased skin temperature, redness, and, when infected, bacterial infection with malaise, fever, and leukocytosis.

Treatment: heat, limb elevation, rest, relative compression, and anti-inflammatory drugs.

Deep Vein Thrombosis (DVT)

Deep vein thrombosis involves an occlusive thrombus, wall inflammation, and adherence of the vessel wall with arterial spasm. It is explained by Virchow's triad: endothelial injury, slowed circulation (stasis), and hypercoagulability.

Symptoms include persistent pain that increases with movement, heaviness, tingling, and pain along the course of the vein. Homans' sign may be present. Edema is initially soft and later becomes hard, with cutaneous hyperthermia.

Lymphangitis and Lymphedema

Lymphangitis is caused by staphylococcal or streptococcal bacteria and is associated with superficial phlebitis, pain, hyperthermia, erythema, fever, chills, malaise, leukocytosis, swelling, and painful lymph node enlargement. It may progress to cellulitis with ulceration.

Treatment: rest, immobilization, cool compresses (Burow's solution), betamethasone, and antibiotics.

Extra-aponeurotic lymphedema presents as hard edema without pitting (no fovea), skin tightening, and persistent swelling that does not resolve with elevation.

Treatment: diuretics, exercise, compression dressings, and dietary measures.

Acute Arterial Ischemia (AAI)

Acute arterial ischemia presents with a pulseless, cold, pale limb, sudden pain, paresthesia, and loss of sensation. Muscle necrosis begins within 4 to 6 hours, becomes irreversible at 8 to 12 hours, and results in functional impairment.

Chronic Arterial Ischemia (CAI)

Chronic arterial ischemia is usually arteriosclerotic and presents with a weak pulse, claudication, rest pain, necrosis, ulceration, and infection. The Leriche-Fontaine classification defines four stages: (1) asymptomatic, (2) claudication, (3) rest pain, and (4) ulceration or gangrene.

Raynaud's Phenomenon

Raynaud's phenomenon is triggered by cold and emotional shock, causing vasospasm and ischemia of the digits, which may lead to thinning and decalcification of the phalanges. It progresses through three phases:

• Ischemic phase: pallor and coldness of the digits.
• Asphyxic phase (cyanosis): cyanosis, swelling, and cold.
• Trophic phase: dry skin, brittle nails, and torpid ulcers.

Treatment: vasodilators and avoidance of cold exposure.

Acrocyanosis

Acrocyanosis is caused by arteriolar spasm and increased vasodilation in the extremities, worsened by cold. Differential diagnosis includes arterial stenosis, which is evaluated with arteriography and arterial pulse examination.

Erythromelalgia

Erythromelalgia presents with redness, heat, sweating, hypersensitivity, burning crises, trophic disorders, and bullae.

Treatment: cold baths, vasoconstrictors, and analgesics.

Pernio (Chilblains)

Erythematous pernio presents as red plaques with edema, itching, and lesions on the heels and fingers.

Treatment: avoid cold and heat, contrast therapy, vasodilators, corticosteroids, antihistamines, and topical menthol alcohol.

Thromboangiitis Obliterans (TAO)

Thromboangiitis obliterans is a chronic inflammation of the vessel intima with endothelial proliferation and thrombosis. It affects the limbs bilaterally, with paresthesia, coldness, and cyanosis. It is strongly associated with smoking.

Pretibial Dermopathy and Necrobiosis

Pretibial lesions begin as reddish papules that later become hyperpigmented, brown, atrophic patches. Ulcerated foci may progress to diabetic gangrene.

Necrobiosis lipoidica presents as violaceous macules, plaques, and ulcers.

Idiopathic Bullous Conditions

Idiopathic superficial blisters may progress to hemorrhagic or gangrenous bullae.

Symmetrical Polyneuropathy

Symmetrical polyneuropathy causes nocturnal pain, improvement with walking, coldness, paresthesia, numbness, burning, a crawling sensation, and loss of vibration and tendon reflexes.

Charcot Neuroarthropathy

Charcot neuroarthropathy results from altered nociception, joint destruction, demineralization, dislocations, and osteoconden­sation. Clinical signs include heat, subsidence of the medial longitudinal arch, increased transverse diameter, and a rocker-bottom foot.

Diabetic Foot Assessment

Examination should include:

• Skin inspection
• Vascular evaluation: pulses, Doppler studies, skin color, trophic changes, temperature, and capillary refill.
• Neurological evaluation: Semmes-Weinstein monofilament, tuning fork vibration testing, and light touch sensitivity.
• Biomechanical evaluation