Pathophysiology And Management Of Diabetic Foot Ulcer In Type 2 Diabetes

Pathophysiology of Diabetic Foot Ulcer

Diabetes type 2 is the conditions in which the body cells are unable to use blood-sugar or glucose effectively to produce energy. This is caused when the cells become insensitive the insulin and blood sugar increases (Eckel et al., 2011). Diabetes type two is more common than diabetes type 1. There are nearly 27 million people are affected particularly in the United States (Centers for Disease Control and Prevention, 2011). Mrs. Lowe has a history of this health condition and developed foot ulcer with fluid coming out of it. She has been prescribed antibiotics to deal with the arterial flow.  However, her diabetes problem is not controlled well. The main purpose of this essay is to discuss the disease pathophysiology of diabetic neuropathic foot ulcer and the impact of uncontrolled glycaemia on wound healing and susceptibility to the infection. The impact of local pressure like footwear on healing process and five possible medical to manage the condition will also be discussed in this report.  

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Pathophysiology of patient’s diabetic foot ulcer is caused by several components that added together to cause ulcerations of the foot such as neuropathy, vasculopathy, and Immunopathy. In hyperglycaemia, the production of enzymes like reductase and sorbitol dehydrogenase is increased. Glucose has been converted into sorbitol and fructose by these enzymes. The accumulation of the sugar products leads to a reduction in synthesis of nerve cells myoinositol and affects the nerve conduction. When the nerve gets hurt, the diseased person is at risk of developing an injury that becomes ulcer over time. Hyperglycaemia may also cause dysfunction of endothelial and abnormalities of soft cells in the peripheral arteries. Endothelial cells synthesize nitric oxide which secures the blood vessels in any endogenous wound (Tesfaye, & Selvarajah, 2012). In hyperglycaemia, the physiological properties of nitric oxide-like antioxidant capacity, leukocyte adhesion, anticoagulation, and endothelial homeostasis has been impaired. This may further lead to atherosclerosis and constriction of blood vessels that ultimately leads to ischemia. The microcirculation also impaired by arterial venular shunting which reduces the circulation of blood in that particular area of need. The immune system of a diabetic patient is not similar as the healthy people. Therefore infection of foot in a diabetic patient is the limb threatening and a debilitating condition (Syafril, 2018). The hyperglycemia condition may cause increased pro-inflammatory cytokinesis and abnormal polymorphonuclear function of the cells like chemotaxis, phagocytosis, adherence, and the intracellular killing. The reduced activity of leukocyte leads to the compromised immune system. Decrease chemotaxis of the growth factors and cytokinesis leads to elevation of metalloproteinase and impairment of normal wound healing process by creating an inflammatory state. The fasting hyperglycemia and open wound may develop a catabolic state. The patient with diabetes issues poorly tolerates infection and the infection adversely impact diabetic control (Clayton, & Elasy, 2009).

Impact of Uncontrolled Glycemia on Wound Healing and Susceptibility to Infection

The normal wound healing process includes hemostasis, inflammation, the proliferation of cells, and maturation in which wound contraction, closure, and remodeling takes place. Hemostasis is the first step in the wound healing process. Following skin damage and blood vessel disruption, vasoconstriction and finally coagulation with the platelet plug. If there is poor blood supply in that area it leads to delayed wound healing (Guo, & DiPietro, 2010). Hypoxia plays may occur due to the vascular changes and affect the ability of neutrophils and macrophages functioning and allow the infection to spread. It also plays a key role in the formation of new blood vessels. If the oxygen levels are not improved by new blood vessels this may cause a decrease in the production of collagen form fibroblast, which ultimately leads to impaired healing. In people with the diabetes problems, the inflammatory phase of wound healing is impaired as a result of a decreased number of leukocytes at the site of the wound due to narrowed blood vessels. In the proliferation phase, the new vascular tissues are produced by angiogenesis in a normal wound healing. But in a patient with diabetes this proliferation of the tissues has been compromised due to the cytokinesis profile is changed in diabetes. Hyperglycaemia is the condition that causes the development of the wound infection in people with diabetes. The microorganism (bacteria) thrives on the high glucose level present in the bloodstream, and the high glucose concentration stops neutrophil activity which leads to a multiplication of bacteria and infection. The sloughy tissues and necrosis are commonly impaired in diabetic condition, with the debridement important in wounds. This availability of debris may act as a reservoir for the bacteria and increase the risk of wound infection (Sharp, & Clark, 2011).

Calluses occur more commonly and built up faster on the foot of an individual with diabetes. This is because there are increased pressure areas under the foot. This may lead to slow healing of the wound. These calluses if not treated, get thicker, breakdown and change into ulcers or slows down the healing process of ulcers already present on the foot (Cavanagh, & Bus, 2010). People with diabetes are commonly suffered from nerve damage or peripheral neuropathy in the foot area. There is a lack of sensation in that area. If the patient wears footwear that is too tight on the foot or uncomfortable, may face issues like blisters or sore that may further lead to serious infections. The shoes or other footwear’s that tight fitted may cause increase pressure at the wounded are does not allow it to heal properly. Improper footwear’s are the most common reason for trauma inpatient suffers from diabetes. Wound healing is described as the complex process that can be achieved with various contributing factors like proper blood supply to that area, decreasing the pressure and caring with clinical treatments. This may be altered if uncomfortable shoes are being used by the patient; the shoes that are tight on the foot decrease the proper blood supply to the infected wound and slowing down the process of healing. The pressure exerted by tight shoes on the wound site may also lead to secretion of blood from the affected area this may also cause slow healing and increasing the infection. Wearing footwear that approximate fit according to the size and shape of the foot rather than for patient’s foot to take on the shape of the footwear, will improve the chances of healing and reduces the pressure on the wound (Bus et al., 2013).

Impact of Local Pressure on Wound Healing Process

As discussed in the case study Mrs. Lowe has an infected the wound, therefore it needs to be cleaned on a regular basis. The faster healing of ulcer can be achieved by cleaning the wound as the devitalized tissues prevent cell migration and prohibit healing process. In this process, the debris, dead necrotic tissues, foreign material, particular matter are removed and bacterial load has been reduced. One conventional way is to apply a scalpel to remove all the unwanted debris such as eschar and callus (Yazdanpanah, Nasiri, & Adarvishi, 2015).

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There are different types of dressing can be used in case of Mrs. Lowe such as moisture retaining dressing and saline moistened gauze dressings and antiseptic dressings like silver dressings. These dressings can provide an autolytic and physical debridement (Moura, Dias, Carvalho, & de Sousa, 2013).

To offload the pressure on the wounded foot removable cast walkers, total contact cast (TCC), half shoes, custom shoes, padded socks, soft heel shoes, wheelchairs, and crutches can be used. The removal cast walkers like air cast walker and half shoes in the patients with foot ulcers found to be effective (Vuorisalo, Venermo, & Lepäntalo, 2009).

The glycaemic control needs to be maintained by following the diabetic diet, insulin, and oral hypoglycemic agents. Appropriate antibiotics can be used to treat the infection issue in the case of Mrs. Lowe. The preferred route of administration of antibiotic is intravenous. Some of the most commonly used antibiotics are gabapentin and pregabalin that provide relief from pain (Lázaro-Martínez, J, Aragón-Sánchez, & García-Morales, 2014).

Hyperbaric oxygen is the oxygen can be used as an adjunctive treatment therapy for a diabetic foot ulcer. This therapy is associated with reducing amputation rates. These strategies target defective ECM ( extracellular matrix) in Diabetic foot ulcer including the skin substitute that is formed from growing skin cells of the autologous ort the allogeneic sources onto the collagen (Yazdanpanah, Nasiri, & Adarvishi, 2015).

Surgical treatments like wound closure, revascularization surgery, and amputation can be used to treat the infected wound in severe cases (Lebrun, Tomic?Canic, & Kirsner, 2010).

Conclusion

Diabetes type 2 is the health condition which can be caused when the cells are unable to use the blood sugar or glucose effectively to generate energy. It is more common than diabetes type one, estimated 27 million people affected with this health issues in UA. Mrs. Lowe has poorly controlled diabetes and infected foot ulcer.  Various factors associated with the pathophysiology of diabetes type two including neuropathy, vasculopathy, and immunopathy. It was concluded that the poorly controlled glycemia responsible to increase the infection and prevent or slows down the wound healing process by hindering four different phases of wound healing that are hemostasis, inflammation, proliferation, maturation, closure, and remodeling. The footwear increases the pressure on the wound area and reduces the blood supply; this may slow down the wound healing. The five effective management strategies can be used in Mrs. Lowe’s case are debridement, dressings, offloading, antibiotics, adjuvant therapy, and surgery.  

References

Bus, S. A., Waaijman, R., Arts, M., De Haart, M., Busch-Westbroek, T., Van Baal, J., & Nollet, F. (2013). Effect of custom-made footwear on foot ulcer recurrence in diabetes: a multicenter randomized controlled trial. Diabetes care, DC_130996.

Cavanagh, P. R., & Bus, S. A. (2010). Off-loading the diabetic foot for ulcer prevention and healing. Journal of the American Podiatric Medical Association, 100(5), 360-368.

Centers for Disease Control and Prevention. (2011). National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: US department of health and human services, centers for disease control and prevention, 201(1). Retrieved from: https://www.cdc.gov/diabetes/pubs/pdf/ndfs_2011.pdf

Clayton, W., & Elasy, T. A. (2009). A review of the pathophysiology, classification, and treatment of foot ulcers in diabetic patients. Clinical Diabetology, 10(5), 209-216.

Eckel, R. H., Kahn, S. E., Ferrannini, E., Goldfine, A. B., Nathan, D. M., Schwartz, M. W., & Smith, S. R. (2011). Obesity and type 2 diabetes: what can be unified and what needs to be individualized?. The Journal of Clinical Endocrinology & Metabolism, 96(6), 1654-1663.

Guo, S. A., & DiPietro, L. A. (2010). Factors affecting wound healing. Journal of dental research, 89(3), 219-229.

Lázaro-Martínez, J. L., Aragón-Sánchez, J., & García-Morales, E. (2014). Antibiotics versus conservative surgery for treating diabetic foot osteomyelitis: a randomized comparative trial. Diabetes care, 37(3), 789-795.

Lebrun, E., Tomic?Canic, M., & Kirsner, R. S. (2010). The role of surgical debridement in healing of diabetic foot ulcers. Wound repair and regeneration, 18(5), 433-438.

Moura, L. I., Dias, A. M., Carvalho, E., & de Sousa, H. C. (2013). Recent advances on the development of wound dressings for diabetic foot ulcer treatment—a review. Acta biomaterialia, 9(7), 7093-7114.

Sharp, A., & Clark, J. (2011). Diabetes and its effects on wound healing. Nursing Standard (through 2013), 25(45), 41.

Syafril, S. (2018, March). Pathophysiology diabetic foot ulcer. In IOP Conference Series: Earth and Environmental Science, 125 (1), 012161.

Tesfaye, S., & Selvarajah, D. (2012). Advances in the epidemiology, pathogenesis and management of diabetic peripheral neuropathy. Diabetes/metabolism research and reviews, 28(1), 8-14.

Vuorisalo, S., Venermo, M., & Lepäntalo, M. (2009). Treatment of diabetic foot ulcers. Journal of Cardiovascular Surgery, 50(3), 275.

Yazdanpanah, L., Nasiri, M., & Adarvishi, S. (2015). Literature review on the management of diabetic foot ulcer. World journal of diabetes, 6(1), 37.