Introduction

DIABETES - A PROBLEM FOR SOCIETY

  • Diabetes mellitus is a growing problem, by the year 2030 its global prevalence will predicted to increase to 10%. It is characterised by a state of hyperglycaemia which is caused by an inability to produce insulin or a lack of insulin sensitivity. It includes a number of conditions including type 1 diabetes mellitus (which typically occurs in children and adolescents) and type 2 diabetes ( associated with obesity, however a genetic predisposition for this form of diabetes also exists.) 
  • Some of the archetypal symptoms of diabetes include polydipsia (excessive thirst), polyuria (excessive urination) and unexplained, rapid weight lost. The progression of these symptoms is typically dependent on the type of diabetes presented in a patient (the progression of these symptoms can be weeks or months in type 1 diabetics however individuals with type 2 diabetes typically experience their symptoms at a slower rate.)

 

 

For more information about diabetes see: http://www.fastbleep.com/medical-notes/endocrine-and-breast/23/63/398

 

 

 



Pathophysiology

Many diabetic individuals will experience diabetic neuropathy (DN). This can be defined as a set of symptoms caused by dysfunction of the peripheral nervous system. Patients with DN experience pain as well as sensory loss and paraesthesia (a pins and needles like sensation in the limbs.) Approximately half of the people living with diabetes will develop DN to some degree. Peripheral neuropathy causes a lack of protective sensations in the feet as well as reduced joint mobility and foot deformities. These symptoms cause increased plantar pressure and the development of calluses on the feet association with diabetic foot ulcers.

Ulceration of the feet occurs from a variety of contributing factors. These include:

  • Nitric Oxide Blocking
  • Maillard Reaction

 

Nitric Oxide Blocking

Hyperglycaemic conditions in diabetic individuals can result in the formation of reactive oxygen species. The inhibition of nitric oxide production (due to high blood sugar levels) can cause the formation of superoxide free radicals which bind to the vasodilatory molecule, nitric oxide. This results in the production of peroxynitrite which causes reduced endothelium-regulated vascular function, inflammation as well as platelet aggregation.

 

Maillard Reaction

The Maillard reaction results in production of advanced glycation endproducts which are associated with a variety of diabetic complications. This resultant problems linked to this reaction include decreased antioxidant production and the increased production of reactive oxygen species. The altered production of these products mediates some of the complications associated with diabetes.

 

 



Prevention and Management

PATIENT EDUCATION

Foot ulcers precede amputation in 85% of diabetic individuals, therefore successful management of this condition is vital. When patients and their physicians are able to recognise the initial signs of foot ulcer the risk of amputation is significantly reduced.

From 2010-2011, the treatment and management of diabetic foot ulcers as well as amputation cost the NHS £662 million. This cost could potentially be reduced through the education of diabetic patients who are at risk of developing this condition. In the USA the potential savings that could be made through detailed patient education amount to $1.1 billion.

 

CLASSIFICATION

Megitt-Wagner classification is the most widely used system for the detection of diabetic foot ulcer and consists of six grades of lesions. Each grade describes the severity of the condition based on the depth of the lesions found on the patient’s feet. The final two grades refer to the extent of gangrenous foot experienced by the patient.

Diabetic foot ulcers are typically managed using one of the following methods:

  • Wound debridement
  • Offloading and redistributing plantar pressure
  • Controlling the onset of infection

 

WOUND DEBRIDEMENT

Wound debridement is the removal of damaged, non-viable tissue (this includes calluses, bacterial biofilms, abnormal keratinocytes as well as unresponsive cells) from the ulcerated foot to allow for the healing of wounds. Immediately after this process, the wounds are thoroughly irrigated with saline solution and are dressed to prevent the desiccation of the remaining viable tissue.

 

OFFLOADING AND REDISTRIBUTING PLANTAR PRESSURE

It is often essential for patients with diabetic foot ulcers to redistribute and offload pressure from the soles of their feet. Total contact casts (TCC) are commonly used as a means of offloading plantar pressure however studies over the last decade have shown that their usage is associated with the development of new ulcers. Therefore the use of walkers, wheelchairs, crutches and therapeutic shoes (which redistribute an individual’s weight at high pressure areas of the feet) are more viable options as they are not linked to the negative side effects like TCCs.

However for some patients these methods of management are less efficacious than surgery to restore some of their joint mobility. Physicians will make informed decisions and individualise the form management used which best suits their patient’s therapeutic needs.

 

CONTROLLING THE ONSET OF INFECTION

Aerobic bacteria like Staphylococcus aureus, streptococci and enterobacteriaceae have the ability to cause the initial infection experienced by patients with diabetic foot ulcer. Typically for mild to moderate infections; a course of antibiotics is prescribed (for average duration of two weeks.) Clinicians assess the individual symptoms of each patient to determine the length of their treatment. Hospitalisation of individiauls with severe and/or life-threating infections is essential for their recovery. In the cases antibiotics are administered intravenously.

 

Megitt-Wagner classification

References

Alavi, A., Sibbald, R. G., Mayer, D., Goodman, L., Botros, M., Armstrong, D. G., Woo, K., Boeni, T., Ayello, E. A. & Kirsner, R. S. 2014a. Diabetic foot ulcers: Part I. Pathophysiology and prevention. Journal of the American Academy of Dermatology, 70, 1.e1-1.e18.

Alavi, A., Sibbald, R. G., Mayer, D., Goodman, L., Botros, M., Armstrong, D. G., Woo, K., Boeni, T., Ayello, E. A. & Kirsner, R. S. 2014b. Diabetic foot ulcers: Part II. Management. Journal of the American Academy of Dermatology, 70, 21.e1-21.e24.

Karthikesalingam, A., Holt, P. J. E., Moxey, P., Jones, K. G., Thompson, M. M. & Hinchliffe, R. J. 2010. A systematic review of scoring systems for diabetic foot ulcers. Diabetic Medicine, 27, 544-549.

Kruse, I. & Edelman, S. 2006. Evaluation and Treatment of Diabetic Foot Ulcers. Clinical Diabetes, 24, 91-93.

NHS Diabetes. 2012. Foot care for people with diabetes in the NHS in England: The economic case for change [Online]. NHS. Available: https://www.diabetes.org.uk/upload/News/Factsheet%20Footcare%20for%20people%20with%20diabetes.pdf [Accessed 14/06/2015].

 

Advertisement

Fastbleep © 2019.