Foot Ulcer and Diabetes: Pathophysiology, Impact, and Management Strategies

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This essay discusses the pathophysiology of diabetic neuropathic foot ulcer, impact of uncontrolled glycaemia on wound healing and susceptibility to infection, impact of local pressure, and management strategies to achieve the best outcomes.

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Running head: FOOT ULCER AND DIABETES
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Diabetes related issues
STUDENT NAME
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FOOT ULCER AND DIABETES
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Contents
Introduction...........................................................................................................................................2
Pathophysiology of diabetic neuropathic foot ulcer...........................................................................2
Impact of poor glycaemic control......................................................................................................3
Impact of Local pressure...................................................................................................................4
Conclusion.............................................................................................................................................6
References.............................................................................................................................................8
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Introduction
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.
Pathophysiology of diabetic neuropathic foot ulcer
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
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FOOT ULCER AND DIABETES
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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 poor glycaemic control
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

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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).
Impact of Local pressure
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
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FOOT ULCER AND DIABETES
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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).
Management strategies to achieve the best outcomes
Debridement
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).
Dressing
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).
Offloading
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
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FOOT ULCER AND DIABETES
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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).
Medical treatment
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).
Adjuvant therapy
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 treatment
Surgical treatments like wound closure, revascularization surgery, and amputation can
be used to treat the infected wound in severe cases (Lebrun, TomicCanic, & 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

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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.
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FOOT ULCER AND DIABETES
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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.
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FOOT ULCER AND DIABETES
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Lebrun, E., TomicCanic, 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.
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