The Diabetic Foot

Understanding the High-Risk Foot

            Diabetes mellitus may result in numerous complications, including those affecting the feet. The attached concept map demonstrates these complications and how they may interact, ultimately leading to a high-risk foot. It is important to note that while the concept map outlines the pathways that may lead to a high-risk foot facing ulceration or amputation, each individual will experience these factors in a unique and complex manner, especially with respect to outcomes and quality of life.

The concept map may be separated into two halves. The top half (shades of purple and blue) addresses wound creation, while the lower half (shades of green, red, orange and yellow) addresses wound healing and ulcer formation. This separation is not intended to indicate there is no crossover between the elements of each; the progression to ulceration is a complex one that involves extensive interactions amongst various risk factors. Rather, the separation into two halves serves to provide a simplified understanding of the progression of events that may ultimately lead to ulceration and amputation.

The concept map begins with diabetes, which may, through various pathways, result in three major risk factors (dark purple boxes) for ulceration including peripheral neuropathy, foot deformities, and trauma (Reiber et al., 1999). Trauma is a critical element in the pathway to ulceration and therefore placed centrally in the concept map. Present in 77% of causal pathways to ulceration, it may be due to internal and/or external factors, either through a one time traumatic incident or repetitive mechanical pressure which creates a wound over time (Reiber et al., 1999; Wrobel & Najafi, 2010).

As demonstrated in the concept map, diabetic peripheral neuropathy (DPN) and/or advanced glycosylation end-products (AGEs) may result in trauma through the creation of foot deformities and consequent alterations in biomechanics and pressure distributions (Wrobel & Najafi, 2010). DPN includes three forms of neuropathy that work in concert to lead to trauma. Motor neuropathy results in muscular changes including weakness and activation delays. These muscular imbalances may result in gait instability and foot deformities, and a reduction in joint range of motion (ROM), ultimately leading to altered biomechanics and increased areas of pressure (Wrobel & Najafi, 2010).  An example includes claw toes due to muscular imbalance between the intrinsic digital flexor and extensor musculature. Claw toes lead to prominent proximal intermetatarsophalangeal joints and apices of the toes. Consequently, these areas are subject to increased pressure, frequently exacerbated by inappropriate footwear (the most common extrinsic risk factor for trauma in western countries) (Reiber, Lipsky, and Gibbons, 1998; Boulton, 2008).

Foot deformities and altered foot function and biomechanics may also be due to AGEs. AGEs lead to skin changes, including increased thickness and hardness, as well as thickened tendons, reduced joint ROM, muscle stiffness and atrophy of fat pads (Wrobel & Najafi, 2010).  Reduced joint ROM is a significant factor in producing increased loading of areas of the foot. For example, reduced ankle joint ROM increases both the absolute pressure and duration of pressure applied to the forefoot. These two factors are directly linked to the likelihood of ulceration, as well as the formation of callus which further increases absolute pressure leading to eventual tissue breakdown (Reiber, Lipsky, and Gibbons, 1998).

Somatic and autonomic neuropathies also result in foot deformities, such as Charcot osteoarthropathy. A Charcot foot begins with acute inflammation, and results in “bone and joint fracture, dislocation, instability and gross deformities”, including a ‘rocker bottom’ foot (Perrin, Gardner, Suhaimi, and Murphy, 2010, pg. 117). The bony prominence(s) due to a Charcot foot cause continuous and repeated loading of the bony prominence(s), which may create a wound, especially when combined with reduced skin integrity caused by autonomic neuropathy (Wrobel & Najafi, 2010).

Trauma, due to the described pathways, does not necessarily lead to the creation of a wound, but the chances of wound formation are increased with the presence of sensory neuropathy. Sensory neuropathy “leads to the loss of protective sensation to pain, pressure and heat” and if not present, the affected person would quickly notice the pain associated with trauma or increased focal points of pressure (Reiber, Lipsky, and Gibbons, 1998, pg. 8S). Subsequently, footwear would be altered or treatment sought to address the source of pain or trauma.

Instead, sensory neuropathy allows the patient to apply pressure to the area, undetected, further aggravating the wound and preventing it from healing, potentially resulting in ulceration and its adverse sequelae (Wrobel & Najafi, 2010). Up to 50% of patients with diabetes experience peripheral neuropathy, and is so integral to the formation of wounds and ulceration, that it is a component cause of 78% of ulcers of the foot in patients with diabetes (Tesfaye & Selvarajah, 2011; Reiber et al., 1999). Further, the interaction between DPN, foot deformities and trauma is critical to the formation of an ulcer. Reiber et al. (1999) found that this triad is present in more than 63% of causal pathways to foot ulceration. 

Once a wound forms, it does not automatically turn into an ulcer, rather it must fail to heal. The capability of a wound to heal is decreased by the presence of sensory neuropathy, oedema and peripheral arterial occlusive disease (PAOD), leading us into the second half of the concept map. Oedema contributes to the creation of a wound by predisposing tissues to trauma, but also impairs cutaneous circulation, limiting the ability to heal (Reiber, Lipsky, and Gibbons, 1998).  

PAOD is characterised by the narrowing or occlusion of peripheral arteries, resulting in decreased perfusion to the limbs (Jude, Eleftheriadou, and Tentolouris, 2010). PAOD is a significant factor in the pathway to ulceration, and is found in approximately one-half of patients with diabetic foot ulcers (Brownrigg, Apelqvist, Bakker, Schaper, and Hinchliffe, 2013). PAOD may result from a variety of modifiable and non-modifiable risk factors, but those with diabetes are twice as likely to develop PAOD compared to those without diabetes; again, highlighting its significance in the pathway to ulceration (Peach, Griffin, Jones, Thompson, and Hinchliffe, 2012).

  With respect to wounds, in order for a wound to heal, sufficient blood must reach it, as blood contains oxygen and nutrients that assist in the healing process. As can be seen from the concept map, if perfusion is insufficient (indicated by various measurements in the red ‘impaired healing’ box), wound healing is impaired and an ulcer or chronic ulcer may form (Jude, Eleftheriadou, and Tentolouris, 2010). Impaired healing is exacerbated by the presence of neuropathy, which allows the patient to continue applying pressure to the wound, undetected (Wrobel & Najafi, 2010). Reduced perfusion also increases the risk of infection, and the inability of antibiotics to be carried to the infected site may require amputation. This is reflected in the fact that infection is the most common precipitating event to lower limb amputation (Lipsky, Berendt, Embil, and de Lalla, 2004).

As well as affecting wound healing, decreased perfusion may result in ischaemia. Whether ischaemia is chronic or acute, the outcome may be devastating. Acute ischaemia leads to pain, paralysis, and may ultimately result in tissue necrosis, gangrene and amputation, depending on the degree of occlusion (Callum & Bradbury, 2000). All results serve to reduce functional capabilities, and it is for this reason that PAOD, as well as all other consequences of diabetes, lead to a vicious cycle, perpetuating negative consequences.

Reduction in function from all aspects is not reflected in the concept map because it is a global occurrence that cannot be tied to any one outcome of diabetes. For example, PAOD may result in intermittent claudication, and hence, pain when undertaking exercise. This pain may deter the person with diabetes from undertaking further exercise, thereby causing further deterioration to their cardiovascular health (demonstrated by the double arrow between PAOD and intermittent claudication). As PAOD worsens, so do the outcomes discussed above (Peach, Griffin, Jones, Thompson, and Hinchliffe, 2012).

The final aspects of the concept map - morbidity, mortality and quality of life - further demonstrate this cycle. Ulcers require a significant amount of time and resources on the part of the patient, the patient’s family and friends, and upon society as a whole (Vileikyte, 2001).  Importantly, for a wound or ulcer to heal properly, off-loading and wound dressings are required, leading to a reduction in mobility and function, as well as the requirement that the patient adapt his or her lifestyle (Vileikyte, 2001). In turn, these negatively affect all aspects of life (physical, social, economic and psychological), and in turn increase the possibility of adverse sequelae, denoted by the double arrows (Vileikyte, 2001). For example, decreased mobility through off-loading may threaten a patient’s employment. To negate this, the patient may not comply with off-loading or attend clinic appointments; a possibility heightened if the ulcer is pain-free due to neuropathy (Vileikyte, 2005). Non-compliance impairs healing and increases the possibility of infection, ultimately resulting in amputation, placing further strain on the patient and his/her family. These negative consequences may be long-standing, which is why previous ulceration is a significant risk factor for further ulceration (Boulton, 2008). Further, limb amputation results in increased morbidity, an increased chance of further amputation and a five-year mortality rate of 40% – 60% (Vileikyte, 2001).

These potential outcomes highlight the need for both early intervention and addressing the aetiology of the risk factors (physiological and/or psychosocial). At various points on the concept map, times for interaction are noted with pink boxes. Earlier intervention leads to better outcomes. For example, if perfusion is not impeded, through early modifications in lifestyle or revascularisation, ulcers will heal more easily. A study by Tennvall and Apelqvist (2000) demonstrated that quality of life “was significantly lower in patients with current diabetic foot ulcers that in patients with healed ulcers” (pg. 237). Further, ulcer prevention reduces the likelihood of amputation, demonstrated by the fact that more than 85% of major amputations in patients with diabetes are preceded by foot ulcers (Moulik, Mtonga, and Gill, 2003).

Over the four weeks in which this concept map was created, it evolved from an outline of some of the factors leading to a high risk foot to a detailed and highly connected and integrated idea of how complications from diabetes may ultimately lead to a high-risk foot. The wealth of information gained from weekly readings and workshops demonstrated just how complex the pathway to ulceration might be, and this information was incorporated into the concept map on a weekly basis.

Further, the concept map came to demonstrate that the pathways are deeply personal and reliant on the support in which the patient receives from self, family, friends, and podiatrist. The realisation that diabetes complications form a vicious cycle, led to the inclusion of double arrows between ulceration and quality of life, amputation and quality of life, as well as morbidity and mortality and ulceration and amputation.

Therefore, preventative steps and support from those in the best position to help the patient are critical at an early stage (Boulton, 2008). While the concept map may suggest that diabetes ultimately results in ulceration, patient education, self-care, and assistance from family and friends for those unable to self-treat have the ability to stop the pathways at their earliest stages. This led to the inclusion of the pink boxes, the final change to the concept map, demonstrating where education and support may come in to stop the diabetic foot from becoming a high-risk foot.

References

Boulton, A.J.M. (2008). The diabetic foot – an update. Foot and Ankle Surgery, 14, 120 – 124. doi: 10.1016/j.fas.2008.05.004

Brownrigg, J.R.W., Apelqvist, J., Bakker, K., Shaper, N.C., & Hinchliffe, R.J. (2013). Evidence-based management of PAD and the diabetic foot. European Journal of Vascular and Endovascular Surgery, 45(6), 673 – 681.

Callum, K., & Bradbury, A. Acute limb ischaemia. British Journal of Medicine, 320, 764 – 767.

Jude, E.B., Eleftheriadou, I., Tentolouris, N. (2010). Peripheral arterial disease in diabetes – a review. Diabetic Medicine, 27, 4 – 14. doi: 10.1111/j.1464-5491.2009.02866.x

Lipsky, B.A., Berendt, A.R., Embil, J., & de Lalla, F. (2004). Diagnosing and treating diabetic foot infections. Diabetes/Metabolism Research and Review, 20(Supp. 1), S56 – S64.

Moulik, P.K., Mtonga, R., & Gill, G.V. (2003). Amputation and mortality in new-onset diabetic foot ulcers stratified by etiology. Diabetes Care, 26(2), 491 – 494.

Peach, G., Griffin, M., Jones, K.G., Thompson, M.M., & HInchliffe, R.J. (2012). Diagnosis and management of peripheral arterial disease. British Journal of Medicine, 345. doi: 10.1136/bmj.e5208

Perrin, B.M., Gardner, M.J., Suhaimi, A., & Murphy, D. (2010). Charcot osteoarthropathy of the foot. Australian Family Physician, 39(3), 117 – 119.

Reiber, G.E., Lipsky, B.A., & Gibbons, G.W. (1998). The burden of diabetic foot ulcers. The American Journal of Surgery, 176(Supp. 2A), 5S – 10S.

Reiber, G.E., Vileikyte, L., Boyko, E.J., del Aguila, M., Smith, D.G., Lavery, L.A., & Boulton, A.J.M. (1999). Causal pathways for incident lower-extremity ulcers in patients with diabetes from two settings.  Diabetes Care, 22(1), 157 – 162.

Tennvall, G.R., & Apelqvist, J. (2000). Health-related quality of life in patients with diabetes mellitus and foot ulcers. Journal of Diabetes Complications, 14, 235 – 241.

Tesfaye, S., & Selvarajah, D. (2012). Advances in the epidemiology, pathogenesis and management of diabetic peripheral neuropathy. Diabetes/Metabolism Research and Reviews, 28(Supp. 1), 8 – 14.

Vileikyte, L. (2001). Diabetic foot ulcers: a quality of life issue. Diabetes/Metabolism Research and Reviews, 17, 246 – 249.

Vileikyte, L. (2005). The psycho-social impact of diabetes foot damage. Diabetes Voice, 50, 11 – 13.

Wrobel, J.S., & Najafi, B. (2010). Diabetic foot biomechanics and gait dysfunction. Journal of Diabetes Science and Technology, 4(4), 833 – 845. 

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