Neuropathic ulcers form as a result of peripheral neuropathy, typically in diabetic patients. Local paresthesias, or lack of sensation, over pressure points on the foot leads to extended microtrauma, breakdown of overlying tissue, and eventual ulceration. In addition, neuropathy can result in minor scrapes or cuts failing to be properly treated and eventually developing into ulcers.
Typically, peripheral neuropathy affects the sensory nerves responsible for detecting sensations such as temperature or pain; however, it can also affect the motor nerves responsible for the contraction of muscles. Damage to motor nerves can cause minor muscle wasting, resulting in the imbalance of flexor and extensor muscles to cause foot deformities, such as claw toes or prominent metatarsal heads (the end of the long foot bone that is closest to the toe joint). This then provides additional pressure points prone to ulceration. In addition to these irregularities, ulceration frequently occurs at common pressure points on the plantar (bottom) surface of the foot, such as at the hallux (big toe), metatarsophalangeal joint (the aforementioned area between the long bones in the foot and typically the big or pinky toe), or the heel. Ulceration on the side of the foot is typically a result of poor-fitting footwear, whereas ulceration on the dorsum (top) of the foot is typically due to trauma.
The base of neuropathic ulcers will vary based on the patient’s circulation from reddish to brown/black. The wound margins will have a well-defined, punched-out look, and the surrounding skin will often be calloused, with depth of the wound typically depending on the thickness of the callous. Often there will be undermining in the wound, our underlying pockets of infection, which can in turn lead to osteomyelitis (infection of the bone or bone marrow) if left untreated. The combination of pressure-related ischemia (restriction in the blood supply) and neuropathy can allow infection to escalate further before being treated compared to other types of ulcers. The wound itself will typically be painless unless there is also infection or an arterial component to the ulcer. The limb will generally maintain a normal pulse, barring additional circulatory components to the ulcer.
As mentioned above, neuropathic ulcers are caused by repeated stress on feet that have diminished sensation. However, if the neuropathic ulcer is present in an area that suggests trauma and not at a pressure point, there must additionally be vascular impairment to lead to ulceration. For this reason, neuropathy is a common factor in combination ulcers.
Peripheral neuropathy is often a result of:
Some less common conditions that can lead to neuropathic ulcers are chronic leprosy, spina bifida, and syringomyelia.
The wound should be thoroughly debrided down to healthy, bleeding tissue. Often there is infection underneath the superficial layer of necrotic tissue, even extending down into the bone and bone marrow. Debridement allows for better assessment of the ulcer and any underlying infections, as well as providing a better healing environment. Ideally, the wound environment should be moist while healing, but also allowed to breathe. The exact properties of the dressing should be matched to those of the wound.
One of the most essential components to effectively healing neuropathic ulcers is to reduce pressure on the affected area. However, relieving pressure from the wound needs to be balanced with keeping proper circulation to the extremities, so excessive bed rest is not recommended. Contact casts can be used to decrease pressure of the affected area while allowing the patient to remain ambulatory. Therapeutic shoes are also available to serve the same purpose, but are typically used for prevention or to avoid recurrence as opposed to during treatment.
If the ulcer does not resolve after more conservative measures, surgery to correct deformities in the foot may be considered to remove excessive pressure.
The following precautions can help minimize the risk of developing neuropathic ulcers in at-risk patients and to minimize complications in patients already exhibiting symptoms: