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
What important condition should be ruled out with a diabetic ulcer and how can it be assessed?
Osteomyelitis can occur in the setting of ulcers and should be r/o with MRI ideally. If suspected, antibx should be held until bone bx can be done ideally
Treatments for diabetic ulcers?
Off-loading measures are the mainstay (shoes, etc), debridement, treatment of infection, negative pressure therapy, etc
What are the 4 stages of decubitus ulcers?
- Non-blanchable erythema with induration and warmth
- Irregular shallow ulceration; loss of epidermis, dermis or both with erythema, induration and warmth
- Deep ulceration with decrotitic base
- Deep ulceration reaching the underlying bone
If bottom not visualized or eschar is covering ulcer may be unstageable
Most common areas of decubitus ulcer?
Sacrum, heel, ischial tuberosities, greater trochanters, heels, lateral malleolus (lateral > medial)
If a stage III decubitus ulcer begins to heal and becomes only apparent with erythema and induration what stage would this be?
Still a stage III, once it has been classified at it’s worse that stage sticks
What is the treatment for stage IV decubitus ulcers?
Surgical management
Treatment in general for decubitus ulcers?
Frequent rotation/minimization of pressure on sites, good wound care with occlusive dressing
What risk factors are strongly associated with diffuse dermal angiomatosis?
Smoking and vascular atherosclerosis
What are the most common sites for diffuse dermal angiomatosis?
Legs, breasts, forearms (breasts often used as an example on test)
What is the clinical presentation of an arteriosclerotic ulcer of Martorell?
These start as a painful red blister that then progresses to a blue purpuric lesion and then ulceration.
The ulcer is usually superficial w/ necrotic base and violaceous-erythematous edges, but may be deep or enlarging too
What is the most common location of an arteriosclerotic ulcer of Martorell?
On the anterior or medial lower leg
What are arteriosclerotic ulcers of Martorell associated with?
Severe HTN
What is the histology of an arteriosclerotic ulcer of Martorell?
Thickening of arteriole media and intima sometimes with hyalinosis/calcinosis of media.
What is the treatment of arteriosclerotic ulcer of Martorell?
Controlling HTN, compression stockings, and good wound care
What are some hematologic causes of ulcers?
- Hemoglobinopathies (sickle cell for example)
- Clotting abnormalities: vactor V Leiden def, protein C/S deficiency, anti-phospholipid syndrome, etc
- Ulcers related to hematologic malignancy: Pyoderma gangrenosum, vasculitis, type I cryoglobinulemia
What are some inflammatory causes of ulcer?
PAN, RA/Felty’s syndrome, pyoderma gangrenosum, necrobiosis lipoidica, Behcet’s, ulcerative LP, ulcerative sarcoid, lividoid vasculopathy, panniculitis (see respective sections for further discussion of these
What are 3 examples of angioinvasive fungi?
Zygomycosis, fusarium, aspergillosis
What cancers can cause ulceration?
Almost any, SCC most common, BCC, lymphomas, Kaposi’s, angiosarcoma.
What metabolic conditions can cause ulcer?
Depositional things can cause ulcer (calcinosis cutis, gout) adjacent to joints, if you see necrotic ulcer in areas with more fat content can consider calciphylaxis
What are some genetic forms of ulcers?
Adams-Oliver syndrome: aplasia congenita cutis (scalp most often)
Prolidase deficiency: hallmark of disease is severe, chronic, recalcitrant, painful skin ulcers mostly located on the lower extremities, especially the feet. These occur early in life (as early as 6 months) or as late as 30
Familial tumor calcinosis: the eruption of rapid small acrally located calcified nodules leading to ulceration. Pain is bad
Werner syndrome (leg ulcers): Also known as progeria, causes pre-mature aging and increased risk of cancer and other diseases. Signs usually manifest in teenage years or childhood
Flynn-Aird syndrome: AD, skin atrophy and ulcers cataracts and multiple neural issues (retinitis pigmentosa, sensorineural hearing loss, ataxia, peripheral neuritis, epilepsy, dementia
Klinefelter syndrome (leg ulcers): low testosterone leads to elevated PAI-1 and increased activity of this is implicated in causing ulceration (leg ulcers, can be presenting sx)
What medications are implicated in causing ulcers?
Hydroxyurea (common): malleolus, tibial crest, painful
Interferon (injection sites)
Methotrexate in psoriasis
Anticoagulants: warfarin (secondary to acquired protein C deficiency) and heparin necrosis (secondary to HIT)
