Week 3 - Leg Ulcers, Arterial, Venous & Lymphatic Disorders Flashcards
What are the differential diagnoses of chronic leg ulcers?
- Venous: varicose veins, thrombophlebitis.
- Arterial: atherosclerosis, diabetes.
- Neuropathic: diabetes.
- Malignancy: BCC, SCC, MM.
- Infections: leprosy, TB, Treponemal (Yaws).
- Others: dermatitis, vasculitis, lymphedema.
Outline leg ulcers.
- Can be divided up into venous and non-venous.
- Venous ulcers are commonly found in the gaiter region whereas non-venous ulcers are more common on the foot.
- Leg ulcers are common because the lower part of the leg has ischaemia - blood pools in lower leg due to inactivity/abnormalities (constant ischaemia).
- Can be simple (infection) or serious (malignancy).
- Venous ulcers are the commonest clinically (80%). Arterial ulcers (10%), all other causes (10%).
- Diabetes can cause many different types of leg ulcers (arterial, neuropathic, infectious) but does not typically cause venous ulcers.
Outline the aetiology of venous ulcers.
- Due to varicose veins (most common - obstruction to venous outflow) or thrombophlebitis (venous inflammation with thrombus formation).
- Ulcer results from stasis and infection.
- Loss of skin surface in drainage area of varicose vein, usually in lower leg.
Explain the pathogenesis of venous ulcers.
- Presence of varicose veins results in venous stasis.
- Venous drainage of the skin becomes too poor to maintain metabolism & promote healing.
- Epidermis dies and is sloughed off leaving a venous ulcer (also be triggered by minor trauma).
- Due to lack of venous drainage - obstruction to outflow.
- Blood enters the tissue but does not exit - block in vein results in accumulation of fluid → tissue will become more wet (more hydrostatic pressure then oncotic pressure - filtration is more).
- Ulcers will be wet - accumulation of fluid and stasis of blood → generalised ischaemia and accumulation of excretory products → area becomes ulcerated, red and oozy.
- Wet, bleeding, dermatitis.
Describe the morphology of venous ulcers.
- Location: gaiter region (lower 1/3 of leg - above medial/lateral malleoli).
- Large, irregular, shallow.
- Wet, oedematous, oozing.
- Moist granulating base - bleeds on touch (arterial supply still intact).
- Surrounding eczematous stasis dermatitis (accumulation of waste material - tissue fluid → inflammation).
- Mild pain, relieved by elevation.
- Compression bandage helps (if veins still patent).
- Additional symptoms: skin is warm and oedema often present, possible infection.
Identify the investigations and management of venous ulcers.
Investigations:
• Ankle pressure brachial index (APBI) using Doppler to exclude an arterial ulcer.
• Microbiology (if an infection is suspected).
• Patch testing (if associated dermatitis).
Management: compression bandage*
• Exudate & slough should be removed with normal saline.
• Antibiotics if signs of infection (as ulcers frequently colonised by bacteria).
• Surrounding eczema treated by corticosteroid.
• Local grafting of patients own healthy epidermis into ulcer with leg elevation.
• Vein surgery may help younger patients.
Outline the aetiology, risk factors and pathogenesis of arterial ulcers.
Aetiology:
• Atherosclerosis (PVD - due to block in artery, no fluid enters → ulcer is dry).
• Diabetes.
Risk factors: • Smoking. • Hypertension. • Diabetes. • Hyperlipidaemia.
Pathogenesis:
• Decreased arterial supply to region of skin → poor metabolism/healing of skin.
• Dry, dark, painful.
Describe the morphology of arterial ulcers.
- Location: distal and dorsal foot or toes (tips of toes). Thin part of skin over toe joints, under heel, over malleoli and anterior shin.
- Cold, pale feet, absent or weak pulses (signs of arterial disease).
- Dry, irregular clear border, grey black necrotic.
- Pale granulation, does not bleed on touch (arteries blocked).
- Painful (nocturnal), partly relieved by dependency - putting legs down.
- Skin: shiny, loss of hairs - suggests atrophy due to chronic ischaemia.
- Angiogram, no compression bandage.
- Complication: infection.
• Death of tissue is due to gangrene. Tips of toes → diabetic gangrene. Blood flow to the leg will be affected. Treatment - extensive amputation.
Identify the investigations and management of arterial ulcers.
Investigations:
• APBI using Doppler, microbiology (<8 indicates arterial insufficiency).
• Angiogram.
Management:
• Do not use a compression bandage as this is dangerous (will further reduce arterial supply and cause larger areas of skin to become necrotic).
Outline the aetiology of neuropathic ulcers.
- Due to nerve damage. Most common cause is diabetes.
- Ulcers due to lack of sensation, nerve fibre damage.
- Clean, caving, callus.
Explain the pathogenesis of neuropathic ulcers.
• Multifactorial. Final common pathway is pressure leading to ischaemia & necrosis.
- Diabetes → damage to vessels (microangiopathy) → reduced blood supply to lower limbs.
- Diabetes → damage to nerves (neuropathy) → patient doesn’t feel damage to skin.
- Bed sores → compression vascular supply → ischaemia → ulcer.
- Usually clean, painless, surrounded by a rim of hard skin. This happens because of constant pressure e.g. footwear, bottom of foot (walking).
- Constant damage for a long time (months-years) due to footwear/walking → gradually causes ulceration because of lack of sensation, protection not there → pain not felt by patient.
- In response to constant damage, the skin becomes harder → corneal layer thickens around ulcer.
Describe the morphology of neuropathic ulcers.
- Location: distal leg, pressure points.
- Clean punched-out ulcers, deep caving.
- Frequently painless, absent or weak pulses.
- Often with surrounding calluses (hyperkeratosis).
- Probing or debriding leads to brisk bleeding (arteries still intact - bleeding but no pain).
- May also have impaired sensation and diminished positional sense or 2-point discrimination in surrounding skin (extensive neural damage, diabetes).
- Complication: infection.
Identify the investigations and management of neuropathic ulcers.
Investigations:
• Glucose tolerance (for diabetes).
• APBI using Doppler to exclude an arterial ulcer.
• Microbiology (if infection suspected).
Management:
• Prevention: Effective management of diabetes and care of feet (e.g. wearing shoes etc.)
• Prevention: For bedridden patients, should roll them or use pressure-relieving mattresses.
Outline malignant ulcers.
- Growth, tumour.
- Cause: UV rays, idiopathic.
- Location: sun exposed.
Features:
• ABCDE*
• Irregular, punched-out, deep, caving with tumour.
• Swelling, extensive ulceration.
• Frequently painless (can be painful).
• Lymph nodes, spreading, metastases, cancer cachexia - weight loss etc.
*EXAM HINT - SCC, BCC, melanoma.
Outline infectious ulcers.
- Multiple - many different types of infection can cause ulcers in the lower leg.
- Common in tropical area, islanders. Respond to penicillin.
- Cause: TB, Treponema (Yaws, Pinta) etc.
- Location: Not particular, usually multiple. Can occur anywhere but more common in legs.
Features:
• Irregular, non-specific.
• Associated with lymphadenitis.
What are the 3 types of arteries?
Arteries (high pressure) are divided into 3 types based on their size and structure:
• Large - e.g. aorta and pulmonary arteries - classified by many elastic fibres which alternate with smooth muscle cells throughout the media (all elastic lamina in between smooth muscles).
• Medium (muscular) - any artery that has a name e.g. coronary, renal - only smooth muscle bundles in media. The media is composed primarily of smooth muscle cells, with elastin limited to the internal and external elastic lamina.
• Small/arterioles - capacitance vessels - hold a major amount of blood. Function - maintenance of BP. The media in these vessels is mostly composed of smooth muscle cells. No elastic lamina.
Identify the diseases of arteries.
Arteriosclerosis: hardening of the arteries (age, diabetes, hypertension). Generic term reflecting arterial wall thickening and loss of elasticity. 3 distinct types:
• Atherosclerosis - large and medium arteries (macroangiopathy).
• Monkeberg medial sclerosis - medium arteries.
• Arteriolosclerosis - small arteries/arterioles (microangiopathy).
Arteritis: vasculitis - inflammation of blood vessels (arteries). 2 groups:
• Immune - ANCA +ve (anti-neutrophil cytoplasmic Ab) - formation of Ab’s that react with cytoplasm of neutrophils. Activated neutrophils cause damage to blood vessels.
- Giant cell arteritis.
- Polyarteritis nodosa.
- Wegener’s granulomatosis.
- Buerger disease.
• Infection - bacteria, virus, fungi, mycotic aneurysm, septicaemia.
Congenital disorders:
• Aneurysms, ectasia, AV malformations.
• Tumours (nevi - excess proliferation of BV), ectasia (birthmark - dilation of BV).
Tumours:
• Haemangioma (benign), angiosarcoma (malignant).
• Tumour like - pyogenic granuloma (complications of wound healing).
Describe Monkeberg medial sclerosis.
- AKA medial calcific sclerosis.
- Characterised by the presence of calcific deposits in muscular arteries, typically in persons older than 50. The lesions do not encroach on the vessel lumen and usually are not clinically significant.
- Intima and media fibrosis and calcification - no obstruction* → not many clinical symptoms (except for calcification of arteries on X-ray).
- Fibrosis and calcification of blood vessels. Usually age associated - older age group.
- Dilation, hardening of large artery.
- Dilation and unfolding of aortic arch.
Outline arteriolosclerosis (microangiopathy).
- Hardening and thickening of arterioles and capillaries.
- Common cause of organ failure, organ ischaemia and infarction in all lifestyle disorders - diabetes, hypertension, hypercholesterolaemia, obesity.
- 2 major types - hyaline and hyperplastic.
Describe the 2 types of arteriolosclerosis.
Hyaline:
• Typically in diabetes.
• Deposition of proteins in the wall. Leakage of proteins, proteinuria.
• Is marked by homogenous, pink hyaline thickening of the arteriolar walls, with loss of underlying structural detail and luminal narrowing.
• The lesions stem from leakage of plasma components across injured endothelial cells, into vessel walls and increased ECM production by SMCs in response to chronic haemodynamic stress.
• In diabetes the underlying aetiology is hyperglycaemia-associated endothelial cell dysfunction.
Hyperplastic:
• Typically in hypertension.
• Proliferation of smooth muscle fibres.
• Vessels exhibit concentric, laminated thickening of arteriolar walls and luminal narrowing.
• The laminations consist of SMCs and thickened, reduplicated basement membrane.
• Mixture of both in either condition because diabetes usually associated with hypertension.
Outline vasculitis.
• General term for vessel wall inflammation.
• Besides findings referable to the involved tissue(s), there are usually also signs and symptoms of systemic inflammation such as fever, myalgia, arthralgia and malaise.
• Although several forms of vasculitis have a predilection for relative large vessels (e.g. large or medium arteries), most affect small vessels (arterioles, capillaries and venules).
• 2 types:
- Immune mediated inflammation.
- Direct vascular invasion by infections pathogens. (Infections can also indirectly precipitate immune-mediated vasculitis e.g. by generating immune complexes or triggering cross-reactivity).
• It is critical to distinguish between infectious and immunologic mechanisms because immunosuppressive therapy is appropriate for immune mediated vasculitis but could exacerbate infectious vasculitis.
• Physical and chemical injury including that due to radiation, mechanical trauma and toxins can also cause vasculitis.
Identify the main immunologic mechanisms underlying non-infectious vasculitis.
- Immune complex deposition.
- Anti-neutrophil cytoplasmic antibodies.
- Anti-endothelial cell antibodies.
- Autoreactive T cells.
What are anti-neutrophil cytoplasmic antibodies?
- ANCAs are a heterogeneous group of autoantibodies directed against constituents (mainly enzymes) of neutrophils primary granules, monocyte lysosomes, and endothelial cells.
- Very useful diagnostic markers - their titers generally mirror clinical severity and a rise in titers after periods of quiescence is predictive of disease recurrence.
- ANCAs can directly activate neutrophils, stimulating the release of reactive oxygen species and proteolytic enzymes; in vascular beds, this may lead to endothelial cell injury.
- The ANCA autoantibodies are directed against cellular constituents and do not form circulating immune complexes.
Outline giant cell (temporal) arteritis.
- Typically affects the temporal artery but can effect them all e.g. large aorta and all the medium sized arteries.
- Granulomatous (T cell) inflammation of large and medium arteries leading to fragmentation of internal elastic lamina, giant cells, thrombosis.
- Is associated with polymyalgia rheumatica (pain/stiffness in hip/shoulder).
- Frequently involves the temporal artery (ophthalmic artery - blindness). Ocular symptoms abruptly appear in 50% of patients and range from diplopia to complete vision loss.
- Usually occurs in older patients (>50 yo).
- Associated with HLA - autoimmune?
- Plenty of inflammatory cells - T lymphocytes and giant cells destroying the tunica media and elastic fibres → results in thrombosis of blood vessel.
- Clinically presents as painful, thickened, nodular temporal arteries.
- Segmental/patchy involvement - does not involve whole thickness. Therefore, a biopsy of the artery may be normal but show inflammation elsewhere (negative biopsy does not exclude the diagnosis).
- Aetiology/Pathogenesis: predominantly unknown but thought to involve immune factors.
- Clinical features: painful nodules on skull, headache, fever, fatigue, sudden blindness.
- Histology: inflammation in tunica media and interna with breaks in elastic tissue + presence of giant cells.
- Treatment: corticosteroids or anti-TNF therapy.
