Diabetic Ulcer Case Study

Some of the complications are foot injury, infections, ulcers, damage to nerve and bone, poor circulation, and possible amputation of the limb, and in this case sepsis (Mainhealth, 2018).

The father decided to do the biopsy and they took her back. Studdert removed an inch long ellipse of skin and tissue stretching from the top of the foot to the tendon. Then, he removed some of the muscles at the center of the redness. Both samples were sent to the pathology department where a dermatopathologist had later confirmed their suspicions. When she was taken into surgery, the destruction was obvious and they had questioned the need for an AKA or BKA. However, they decided to trust their guts again and did a debridement and flushed out the muscles. Two hours later, she was transported to another hospital and put in a hyperbaric oxygen chamber for two hours to boost muscle repair. The following day, she was taken back into surgery to remove more of the infected muscle and they decided to increase the oxygen treatment to twice a day for two hours. Twelve days later, she was released from the hospital bacteria free. A patch of skin, about sixty-four-square-inches, had been removed from her thigh and used as a skin

Outcome 1 understand the anatomy and physiology of the skin in relation to pressure area care

Pressure ulcers are; damage to the skin or underlying structures from either inadequate perfusion or tissue compression. (Taber’s Cyclopedic Medical Dictionary, 2009, p. 1889). Those at an increased risk for pressure ulcer formation: older adults, persons with spinal cord injury, surgical patients, obese patients, underweight patients, children and patients at end of life. (Ruth & Nix, 2012, p. 125). The Braden Scale, is a tool used to help identify a patient’s risk of developing a pressure ulcer.

Stage IV pressure ulcers are the most severe type of ulcer in which there is full-thickness tissue loss. Stage IV pressure ulcers are deep and effect muscle and bone causing extensive damage. Stage IV pressure ulcers cause severe damage causing the surrounding tissue to begin necrosis. Stage IV pressure ulcers lead to an increase risk of severe and possibly life threatening infections. Stage IV pressure ulcers are classified as an event that should never occur within acute or long term care

Stage 1- The skin isn’t broke, but it is discolored. The surface may appear red if the person has a light complexion.

The worse possible outcome of a pressure ulcer is death, with an approximation of 60,000 patients dying each year as a direct result of a pressure ulcer (Stotts & Gunningberg, 2007). This is significant to nursing practice because if we can prevent more pressure ulcers from occurring, we can dramatically improve patient outcomes, patient family and satisfaction, and even prevent the death of a loved one.

There are 4 stages of progression for the decubitus ulcer. In the first stage there is no open wound however there will be evidence of discoloration. For those with lighter skin the affected area will appear red, however for those with darker skin the discolored area can appear bluish

These are usually caused by fatty plaque build-up on the arteries, or atherosclerosis. They can also be caused by peripheral artery disease. A small wound or scratch may not heal because of the low blood supply in the area. Cholesterol, which narrow and harden the arteries, resulting in poor circulation. These ulcers are mostly found in the ankle or distal digits. These wounds are very painful.

Williams, 1992 states that pressure ulcer occurs where there is poor level of nursing care for a long term basis but it is also found with hospitals that offer severe care. We know that a sore healing needs conditions of dietary aspects and it can be reversed. There have been several studies made

Arterial and venous ulcers have both similarities and differences when considering etiology, underlying pathology, clinical manifestations, and interventions that are used for management of each. In this paper I will be comparing and contrasting the two ulcerations.

The sore is very deep, reaching into muscle and bone as well as causing extensive damage. Damage to deeper tissue, tendons, and joints may be possible.

Previously known as Pressure Ulcer is now being called Pressure Injury (PI), according to the National Pressure Ulcer Advisory Panel (2016). The name was changed due to the different formation and presentation of PI. What many appear as intact clear skin may actually be deeply damaged within the tissues making it invisible to the naked eye. PI is acquired through ischemia the skin on bony prominences of the body usually from pressure. Pressure to the area within 1-2 hours can cause PI, thus the importance of repositioning our patients every 2 hours is emphasized nationwide. However, other contributing factors also play a major role in the formation of PI, the problems of pressure, shear, friction, immobility worsens the condition and it

There are many issues in the clinical setting that nurses have to be aware of and be educated on preventing and treating. One of those issues that have to be addressed is pressure ulcers. Pressure ulcers can occur over the bony prominences where the body’s tissue has been pressed against for extended periods of time. There are certain factors that put a patient at risk for the development of these pressure ulcers and it’s the nurse’s responsibility to be aware of these risk factors. The most common places that a patient can develop these ulcers are ankles, sacrum and hips. Patients who have impaired mobility and those who aren’t able to ambulate have and increased risk for developing pressure ulcers.

Microorganisms that are cultured from the wounds have two types that exist. Type 1 necrotizing fasciitis is a polymicrobial infection which consist of infection with aerobic and anaerobic bacteria. Which consists of clostridium and bacteroides species, these work synergistically in the progression of necrotizing fasciitis. Type 2 necrotizing fasciitis consists of group A streptococcus and with or without a coexisting staphylococcal infection. The Type 2 also consists of staphylococcus aureus, clostridium perfringens, bacteroides fragilis, and aeromonas hydrophila. The microscopic level would include the laboratory of necrotizing fasciitis the bacteria that is seen with a microscope. “The micrograph of necrotizing fasciitis shows necrosis of the dense connective tissues and fascia interposed between fat lobules”. The gross anatomy is the structures visible to the naked eye, such as the