Lower Extremity Ulcers (D'Costa, 1/22/2020)

Thank you to Dr. D’Costa for 40 years of service to our community AND for an informative Grand Rounds this week on lower extremity ulcers.

I’m sorry for those of you who missed the presentation also missed the photos—what Dr. D’Costa finds “beautiful”, frankly I find a little nauseating. 

Also, thanks to Dr. Grierson (Dr. D’Costa’s new partner) for a bonus presentation on Charcot Foot, which will heretofore be on my ddx for diabetics presenting with a red, hot, swollen foot

Here are a few things to remember from both Dr. D’Costa and Dr. Grierson’s presentations: 

• ~9.4% of US population has diabetes (that is over 30 million people
• 6% of Medicare patients with diabetes develop an ulcer annually
• There is a 19-34% lifetime risk of developing a foot ulcer with diabetes
• Over 50% get infected
• 20% of moderate to severe diabetic foot infections get amputated

There is a 70% mortality at 5 years after an amputation, and 74% mortality at 2 years if on hemodialysis. This rivals 5 year rates of death from colon cancer

3 major types of lower extremity ulcers: neuropathic, vascular (arterial and venous), and “other”

You SHOULD culture an ulcer if you suspect infection: but do a DEEP WOUND CULTURE to avoid normal skin flora, also tissue or bone sample is best

Be on the  lookout for absent hair, atrophic skin or nails, dependent rubor, calf pain with walking

Neuropathic ulcers:

Caused by the combination of insensitivity (sensory loss) and pressure

• As neuropathy progresses, the intrinsic muscles of the foot are more and more affected, leading to claw toes and other deformities, often with  ulcers forming under metatarsal heads
• Usually painless, on plantar surface
• Pressure points: metatarsal head, medial hallux, lateral 5th toe
• Rimmed with callus (which needs to be de-bulked to offload)

Venous ulcers: Incompetent valves allow backflow leading to venous hypertensionà increase in interstitial fluidà mast cell inflammationà edema

Also occur in stasis states (e.g CHF), s/p saphenous vein harvesting for CABG

• Trophic skin changes: thinning of skin, drying of skin, hemosiderin deposition
• Ulcer usually moist and weeping fluid
• Can be present for years/decades
• Prevention includes hydrating skin, diuretics, elevation of limb, elevation of limb above heart at rest, venous pumps
• Treatment: create moist wound environment, but also absorb excessive drainage (calcium alginate, silver-impregnated gauze)
• Abx if needed, also biopsy if no improvement to r/o vasculitis vs. malignancy

Ischemic ulcers: Usually occur due to lack of vascular supply  (e.g. PVD, PAD)

• Poor man’s test: Capillary refill (>4 seconds), absence of DP and TP pulses
• Can be extremely painful

Osteomyelitis: infection of bone due to seeding from outside source

• Requires break in skin (e.g. ulcer) or penetrating wound (e.g. nail or insulin)
• You must r/o hematogenous spread if there is no open lesion on the foot
• Bone biopsy is gold standard to diagnose

Charcot foot: neuropathic arthropathy, under-recognized and underreported

• Acutely presents as RED, HOT, swollen foot (similar to gout, cellulitis, VTE)
• Subacute: foot and ankle deformity
• Have to distinguish between osteo/cellulitis and Charcot—which can be tricky
• MRI is sensitive but not specific
• Bone scan is good non-invasive option
• Otherwise bone bx is diagnostic