Ulcers Flashcards
What is the usual location for venous ulcers?
Medial malleolus
Why is the medial malleolus the most common location for venous ulcers?
Cockett’s perforating veins in that area
What physical exam findings should be documented in an ulcer?
Location, size, depth, description of the base (yellow, fibrinous, purulent, eschar, etc), the surrounding sidewalls (rolled, indurated, undermined, color), and the surrounding skin (erythema, color change, livido, puprua, stasis changes? etc)
What physical exam findings might tip you off that an ulcer is from venous origin?
Look for a background of venous stasis (brown hemosiderin deposits, pinpoint purpura, edema lipodermatosclerosis, and varicosities.
What is the common appearance of a venous ulcer?
Tend to occur on the medial malleolus and tend to have irregular borders and yellow fibrinous base. Though these can be big they tend to be shallow w/ granulation tissue evident after debridement.
What is the treatment for a venous ulcers?
Wound care that promotes moist wound bed/occlusion, the elevation of the legs, compression.
NOTE before doing compression therapy coexistent arterial insufficiency and or heart failure need to be exluded
When should patients be counseled to apply stockings for compression in the setting of venous ulcers of edema?
In the morning, before even getting out of bed if possible as legs will be at their smallest size
What level of compression at the ankle is needed for edema in aiding in the healing of venous ulcers?
30-40mmHg at the ankle
What is elephantiasis nostras verrucosa?
Chronic lymphedema of the feet/legs that leads to fibrosis of the dermis and subcutis leading to verrucous, hyperkeratosis, cobblestone-like lesions w/ a papillomatous appearance
What are 3 causes of primary lymphedema?
Nonne-Milroy dz, Meige dz, lymphedema tarda
How do you distinguish between Nonne-Milroy dz, Meige dz, lymphedema tarda?
Milroy= unilateral lower extremity lymphedema +/- hydrocele. Due to mutations in VEGFR-3/FLT4 (AD). Onset is early
Meige disease: AD, FOXC2 gene, most common form of primary lymphedema, usually causes lymphedema of the legs but other areas can occur. Unlike Milroy’s this one usually starts at puberty
Lymphedema tarda: Presents after age 35, usually 2/2 to developmental abnormality being preciptated by some insult
What are some secondary causes of lymphedema that could lead to ulcer?
Lymph node dissection, recurrent cellulitis, obesity, filariasis
What are some risk factors for arterial ulcer?
Tobacco use, DM2, HTN, hyperhomocysteinemia, HLD
What is the presentation of arterial ulcer?
Painful ulcer w/ well-defined borders with round punched out, dry, necrotic base
What is the classical location for ulcer?
Lateral malleolus as well as first and with metatarsal heads
What clues in the surrounding skin may tip you off to arterial ulcer?
Atrophic skin, no hair
How are arterial ulcers diagnosed?
ABI’s are key in dx, but can consider other vascular imaging such as CTA, MRA, or angiography
What treatments must be avoided in ulcer?
Must avoid sharp debridement or vac treatments
What are some physical exam findings which may lead you to suspect arterial ulcer?
Cool extremities, weak or absent pulses, prolonged capillary refill time, pallor or pain with leg elevation (left to 45 degrees for 1 minute), and dependent rubor after lowering.
What should be considered if a violaceous plaque in an area of vascular change (large breasts, lower legs, etc)
Think about diffuse dermal angiomatosis
What should be considered if one sees a violaceous plaque on the lower medial extremity that looks like KS?
Should also think about acroangiodermatitis (pseudo-Kaposi’s sarcoma).
What is the classic presentation of diabetic/neuropathic ulcers?
These often have a moist base with a punched out base and callused borders
What are the most common locations of diabetic/neuropathic ulcers?
Pressure points (metatarsal heads, great toes, heels)
What is the mechanism of diabetic or neuropathic ulcers?
Neuropathy leads to unrecognized foot trauma and motor neuropathy leads to altered biomechanics and structural deformities, and autonomic abnormalities lead to arterio-venous shunting and then that decreases perfusion and reduces sweating all of which leads to dryness, injury, and fissuring