Pathophysiology, Nursing Priorities and Management of Diabetic Foot Ulcer: A Case Study

Nursing
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Introduction
This is a case study of Mrs. Bacci, a 49 year-old Italian lady. She was admitted to the hospital
two weeks ago after developing a complication from the foot ulcer. She had a partial limp
amputation of the foot including the great toes and first toes under general anesthesia. Mrs. Bacci
is a known type 2 diabetic. She was discharged a week ago from the hospital nut has now
presented to the outpatient department for further assessment of her wound status. This essay
will discuss the underlying pathophysiology of her wound and the status. Nursing priorities of
care will also be addressed and a clear rationale provided. Finally, the safe and appropriate
nursing management at the moment will be discussed
Underlying pathophysiology and causes of Mrs Bacci post-operative wound status
Diabetes is a metabolic disorder that occurs when the blood glucose cannot be controlled
effectively. Majority of diabetic patients usually develop a diabetic foot especially after a
previous lower extremity amputation, anatomic foot deformity, peripheral vascular disease and
history of a foot ulcer. It is mail y caused by loss of glycemic control, peripheral vascular
disease, immunosuppression, and peripheral neuropathy. According to Bakker et.al (2016), a
diabetic foot ulcer develops when there is a combination of different components which show a
base relationship with the hyperglycemic state of diabetes. Some of these components are;
vascular, neuropathic and immune system components. According to Volmer and Lobmann
(2016), neuropathy is caused by the oxidative stress on the nerves by the effects of
hyperglycemia. In addition, further glycosylation of nerve cell proteins leads to ischemia. This
contributes to further nerve dysfunction and therefore its function is impaired too. If this occurs,
there is cellular changer and this can be observed from, sensory, motor and autonomic

components of the diabetic foot. The normal functioning of these reflexes are affected and it can
be clearly seen.
If the autonomic nerves are damaged, then the organs innervated by the nerve cannot
function properly. For example, organs such as sweat glands which are innervated by the
autonomic nerves will fail to produce sweat and therefore decreased the ability to moisturize the
skin. This can be clearly seen as the epidermis may crack or skin breakdown may occur. The
leading causes of diabetic wound or ulcers are high blood sugar levels which stiffen the body’s
arteries and narrow blood vessels reducing blood supply to the tissues, poor blood circulation
due to peripheral arterial disease and nerve damage which can lead to the development of ulcer
without the sensation of pain. Others are immune system issues and infections can also lead to
the development or worsening of a diabetic ulcer.
Moreover, if motor neurons innervating the foot muscles are damaged, then the various
ranges of movements are affected. Muscles’ ability to extend and flex is affected. Skin
ulcerations can also result due to impaired innervation. Moreover, the patient’s peripheral
sensation is decreased. This can make the patient not be able to notice wound development until
it worsens. Lastly, the amount of blood required to heal a diabetic wound is higher than the
amount required by any other wound. From the case study, Mrs. Bacci has a history of peripheral
vascular disease. This disease causes narrowing of arteries especially those supplying the lower
extremities. Since amputation creates a wound that needs to heal, it requires increased blood
supply as the patient is already diabetic. This has greatly contributed to the serious nature of the
wound dehiscence and inflammation of the surgical site. This clearly indicates impaired wound
healing and it can even lead to a chronic diabetic ulcer. Other factors such as endothelial cell
dysfunction causing decreased vasodilation and elevated plasma thromboxane A2 which causes