NEUROPATHIC ULCERATION




PATIENT STORY



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A 58-year-old overweight diabetic man presented with bloody drainage from a callous on the plantar aspect of the right first metatarsophalangeal joint (MPJ) for approximately 1 week (Figure 93-1). He has a history of bilateral plantar first MPJ ulcers that healed with conservative treatment. He is a truck driver and wears custom-molded accommodative orthotics that are approximately 1-year old within work boots (Figure 93-2).




FIGURE 93-1


Bleeding callous on plantar aspect of first metatarsophalangeal joint (MPJ).






FIGURE 93-2


Multilaminate custom-molded accommodative foot orthotic.





On physical examination, pedal pulses are palpable. The feet are warm and of equal temperature. Protective sensation is plantarly absent on testing with a 10-g monofilament. He has a planus (flat) foot type with limited first MPJ range of motion and mallet toe deformity (flexion contracture of the hallux interphalangeal joint) (Figure 93-3). Following debridement of hyperkeratotic tissue and cutaneous sanguinous drainage from the plantar aspect of the right first MPJ, a small surface area, full-thickness skin ulceration is identified (Figure 93-4). The wound base is granular and healthy with no signs of active infection. Treatment includes topical use of a hydrogel with silver (to address surface contaminants and facilitate moist wound healing) and a prescription for new orthotic devices. Due to the recurrent callous despite use of the orthotics, routine visits are recommended every 10 to 12 weeks for callous debridement and diabetic foot care. He is not interested in surgical correction of the abnormal mechanics in the forefoot (hallux malleus correction).




FIGURE 93-3


Lateral view of foot demonstrates severe flatfoot deformity with plantar callous and digital contracture.






FIGURE 93-4


Neuropathic ulceration identified following debridement of all hyperkeratotic tissue and sanguinous drainage.






EPIDEMIOLOGY



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  • The incidence of diabetic ulcers in the United States is approximately 1.5 million1 and this is expected to increase as diabetes increases.



  • There are currently nearly 800,000 new cases of diabetes diagnosed every year, affecting approximately 6% of the population.1



  • Approximately 60% of all nontraumatic lower extremity amputations occur in diabetics.2



  • Approximately 85% of diabetic lower extremity amputations are preceded by a foot ulcer.2



  • Within 5 years of amputation, 28% to 51% of diabetic amputees undergo contralateral leg amputation.2



  • 5-year mortality following bilateral amputation: 39% to 68%.2



  • The direct cost of treating noninfected diabetic foot ulcers is more than $6 billion annually.3





ETIOLOGY AND PATHOPHYSIOLOGY



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  • Neuropathic ulceration is typically the result of repetitive, moderate soft tissue trauma in the setting of peripheral sensory neuropathy and abnormal foot mechanics.



  • The most common causes of peripheral neuropathy include




    • Diabetes



    • Alcoholism



    • Nutritional deficiencies



    • Guillain-Barré syndrome



    • Toxicities (heavy metals)



    • Hereditary



    • Endocrine



    • Rheumatologic (SLE)



    • Amyloidosis



    • Pressure neuropathy



    • Idiopathic



    • Sarcoidosis



    • Hypothyroidism



  • Diabetes mellitus is the most common cause of neuropathic ulceration.



  • Diabetic peripheral neuropathy often occurs in a stocking or glove and “dying back” (distal to proximal) distribution. It includes sensory, motor, and autonomic components. Sensory neuropathy is the most common component4 and is defined as the absence of protective sensation (inability to distinguish a 10-g monofilament). Motor neuropathy results in mechanical imbalance between opposing muscle groups (flexors or extensors) and can affect both large muscle groups as well as the intrinsic musculature of the foot. This can lead to foot deformities such as foot drop, equinus, hammertoes, and prominent metatarsal heads.5 Autonomic neuropathy often results in dry, cracked skin creating potential portals of entry for infection. Sympathetic denervation, arteriovenous shunting, and microvascular dysfunction impair tissue perfusion and normal response to injury. These autonomic dysfunctions combined with motor and sensory components are implicated in the pathogenesis of ulceration.6



  • Trauma to the neuropathic foot plays a key role in the development of ulceration. Beyond overt trauma such as that of puncture wounds or blunt trauma, moderate repetitive stress associated with walking and day-to-day activity is most commonly associated with ulceration. Further, variability in activity level or periodic bursts of increased activity can precipitate ulceration.7,8



  • It is widely accepted that there is a strong association between neuropathic foot ulceration and increased plantar pressures.9 Glycosylation of collagen (as a result of long-standing diabetes) may lead to stiffening of capsular and ligamentous structures.10 Subsequently, limited ranges of motion at the ankle, subtalar, and MPJs lead to increased plantar pressures.11 These abnormal plantar pressures often manifest clinically as calluses, corns, blisters, or skin fissures. The locations are specific to the underlying structural deformities. In the absence of adequate off-loading mechanisms, neuropathic ulceration may occur.4



  • Other factors frequently associated with increased risk for neuropathic ulceration include poor glycemic control, duration of diabetes, peripheral arterial disease, nephropathy, visual impairment, advanced age, and prior foot surgery.12


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Jan 13, 2019 | Posted by in CARDIOLOGY | Comments Off on NEUROPATHIC ULCERATION
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