Ulcers
(open wounds)

How to distinguish between arterial and venous pain?

Symptoms derived from varicose veins can usually be distinguish from arterial symptoms. Pain associated with arterial disease often disappears at rest and is exacerbated with walking.

Pain associated with varicose veins is dull vague and localized on the inner side of the legs. It is usually relieved with walking.

In addition to the dull aching, varicose veins associated with high venous pressure may produce cramping or painful spasms of the legs and an increase in leg fatigue and Restless legs especially at night.

You can do a diagnostic test to determine if the pain is of venous origin. If your symptoms are alleviated with gradient compression stockings or elevating your legs you need to see a Vein Specialist

Evaluation and Management of Lower-Extremity Ulcers:

Lower-extremity ulcers : 1-2% of USA population. Divided in 2 groups: Leg and foot ulcers. 25-50% leg ulcers and 30% of foot ulcers not healed in 6/12. 70% of leg ulcers caused by venous disease, 20% arterial insufficiency or mixed disease. 85% of foot ulcers caused by peripheral neuropathy, complicated by arterial disease.

Risk factors for venous ulcers:

Advanced age
Female
Family history of venous ulcers
White race
History of deep vein thrombosis or phlebitis.
Prolonged standing
Sedentary lifestyle
Leg injury
Chronic leg edema

Risk factors for arterial ulcers:

Lack of sensation
Limited joint mobility
Anatomical abnormalities
DM
Vascular disease
Repetitive high pressure.

Venous Ulcers:

When valves in leg veins are damaged or dilated retrograde blood flow results in venous hypertension. Sustained ambulatory venous pressure leads to extraction of fluid and protein causes edema and extravasation of red cells results in hemosiderin deposition and pigmentation. Mechanical disruption of endothelial cells and their glycocalyx coating get margination of white cells. Causes persistent inflammation , oxidative stress with expression of multiple cytokines and chemokines. Overexpression of matrix metalloproteinases alters collagen turnover get destruction of the dermal tissue and the ulcer formation. Pericapillary fibrin cuffs trap growth factors disrupt oxygen diffusion causes tissue hypoxia. Results in open draining wounds with surrounding induration.

Diagnosis:

Medial aspect of the leg, between lower calf and malleolus and are associated with edema, pigment deposition(hemosiderin and melanin), venous dermatitis, atrophie blanche(porcelain white scars, telangiectasia, dyspigmentation) and lipodermatosclerosis. Aching, burning pain, and swelling in the leg progress during the day and improve with leg elevation. Can have history of DVT trauma, or surgery. They are swallow and irregularly shaped and contain granulation tissue or yellow fibrin.

Arterial Ulcers:

Impaired tissue perfusion. Intramural restriction of blood flow, extramural strangulation and mural thickness cause reduced perfusion. Causes: Peripheral vascular disease due to atherosclerosis, macro micro vascular due to DM, vasculitis, microthrombi . Reduced perfusion of skin and soft tissues results in ischemia and necrosis.

Diagnosis:

Common among smokers, DM, hyperlipidemia, hypertension. Intermittent claudication, pain at rest , pain worsens when elevated and pain improve when leg in dependent position. Affect toe heels area of trauma, anterior aspect of leg where arterial redundancy is lacking. Ulcers often dry , punched out with well demarcated edges and pale non granulating necrotic base. May be very deep. Foot can feel warm due to arteriovenous shunting. Pale when elevated. Delayed return of blood or prolonged venous filling when leg in a dependent position. ABI< 0.9 indicates arterial insufficiency. Falsely normal or even elevated ABI’s patients with non-compressible vessels, DM patients with glycation of blood vessels and elderly patients with vessel calcification.

Thin shiny skin, reduced air growth, cool skin, absent, weak pulses, delayed capillary filling.

Diabetic Ulcers:

Arterial insufficiency and neuropathy , predisposition to injury an ulcer formation. Loss of protective sensation makes them vulnerable to physical trauma. Deficient sweating and altered perfusion in the foot lead to dry skin and easily injured by minimal trauma. Autonomic neuropathy leads to foot deformity (Charcot foot) result in pressure over prominent areas of the foot. Get also defective white-cell function impair wound healing and lead to perpetuation of ulcers and secondary infection.

Diagnosis:

Neuropathy in patients with DM, and risk factor for foot ulceration. Blood glucose and sensory examination. Areas of trauma, tip of toe, medial side if first metatarsal, phalangeal, or plantar surface foot. Deep surrounded by callus and insensate, dry cracked, calluses. Rx Off load of pressure, and topical growth factors.