Nurse Teachings on Complications of Diabetic Foot Ulcers

Nurse educated the patient/caregiver upon the complications of diabetic foot ulcers as follows:

1. Diabetic foot ulcer usually is an ulcer with full-thickness skin loss and a circular punched out appearance. The ulcer site is surrounded by hard callus, which is thickened and hardened portion of the skin. Due to the neuropathy in poorly managed diabetics, individuals often have poor sensation at the ulcer site, which contributes to the painless nature of the wound. As these wounds are mostly painless, it is often delayed by the time these wounds are realized. Patients, secondary to poorly controlled neuropathy, can as well present with burning, altered/tingling sensation, or numbness in the feet.
2. Secondary infections at the wound site can result in swelling around the wound site, local elevation of temperature, and foul smelling drainage. Patients can as well present with fever and chills, secondary to infection, but can often be absent.
3. Poorly controlled neuropathy in the foot during later stages can also result in compromised nerve supply to the numerous small intrinsic muscles in the foot, which control the action of toes and maintain the shape & arches of the foot. Poor nerve supply to the intrinsic muscles of the foot leads to progressive atrophy of these muscles, resulting in stiffness & contractures of the toes and compromised arches of the foot. Altered shape of the foot in individuals with neuropathy can further lead to increased exposure of the foot to mechanical factors, such as, friction, pressure, and shearing stress. This can increase the risk for development of new pressure points and calluses on the foot with potential to progress in future towards development of new diabetic foot ulcers.
4. Development of dead tissue at the ulcer site can lead to necrosis & gangrene, giving the wound site a black discoloration.
5. Progressive worsening of the diabetic wound with development of repeated infections and necrotic tissue could result in development of deeper and complicated wound. This can worsen the wound on the staging and grading scale, making it a wound difficult to heal.
6. Uncontrolled and poorly treated infection of diabetic foot ulcer can eventually lead to spread of bacteria to deeper tissues, such as, muscle and bone. Involvement of bone along the path of infection can result in inflammation of bone, bone pain, and osteomyelitis. Poorly controlled bone infection in later stages could lead to demineralization & weakening of bones, risk for easy fractures, necrosis & gangrene of the bone tissue. An attempt at saving the uninvolved healthy bone could necessitate an amputation of the limb to the extent involved.
7. Stiffness & contractures of the toes and compromised foot arches in individuals with active or history of diabetic foot ulcers can alter the gait pattern, impair balance during ambulation, and increase dependence on assistive device, thus contributing towards increased risk for falls and accidents.
8. The neuropathy could affect the sweat glands of the feet, resulting in reduced sweat production. Poor sweating in the feet can lead to dry and cracked skin, predisposing the individual to risk for skin breakdown and increased risk for skin infections.
9. Also, as these individuals could be walking and moving around without realizing the wounds on the feet, these wound sites are increasingly exposed to risk for further friction & pressure and risk for infections. This can lead to worsening of the wounds due to complications, such as, bacterial infection and dead tissue formation, before the wounds are even realized.
10. Poorly managed diabetics could also present with compromised blood circulation in the distal lower extremities, which can result in diminished blood supply to the ulcer site. Rich blood supply delivering fair amounts of oxygen and nutrients is needed for healing of the ulcer site. Continued compromised blood supply to the feet in poorly managed diabetics also leads to increased risk for delayed healing at the ulcer site, development of secondary bacterial infections, and dead tissue formation.