Why people with diabetes suffer foot ulceration
Author Julie Vuolo, BA, DipHE, RN, is senior lecturer, tissue viability, University of Hertfordshire, Hatfield.
Abstract Vuolo, J. (2007) Why people with diabetes suffer foot ulceration. Nursing Times; 103: 15, 44–46.
Many people with diabetes (15–20%) develop foot-related complications (Boulton et al, 1999). These complications result from a number of pathophysiological changes that occur as part of the chronic disease process and that bring with them a significantly increased risk of foot ulceration and lower-limb amputation. Julie Vuolo explains what these changes are.
Diabetes is a group of disorders with a number of characteristics in common, of which raised blood glucose is the most evident. It carries a high risk of serious complications (NICE, 2007) such as renal impairment, urologic dysfunction and gastroparesis (delayed stomach emptying). The chronic, often debilitating, nature of the disease can also have a significant impact on quality of life particularly if complications occur (Jacobson et al, 1994). Management of the disease and its complications also consumes a large amount of the NHS’s expenditure (Currie et al, 1997), costs which are predicted to escalate in the coming years due to the increasing prevalence of the disease (Department of Health, 2007).
Foot-related complications can present in type 1 and type 2 diabetes due to a number of pathophysiological changes that occur in relation to the condition. These take place over a period of time and lead to a substantially increased risk of foot ulceration.
Foot ulceration (any break in the skin including cracks and fissures) on the foot of a patient with diabetes tends to be far more problematic than ulceration on a healthy foot, again due to the changes brought about by the disease process. These include changes in the circulation, in metabolic function and also in the peripheral nervous system – all of which are exacerbated by poor glycaemic control (NICE, 2002; The Diabetes Control and Complications Trial Research Group, 1995).
Microvascular effects of diabetes include nephropathy (kidney disease) and retinopathy (disease of the retina). Both of these are significant as nephropathy is a leading cause of kidney failure (EdREN, 2006) and retinopathy a leading cause of blindness (NICE, 2002). Macrovascular effects include diseases of the coronary and peripheral arteries. The high prevalence of macrovascular disease in diabetes relates to the presence of many risk factors including:
- Abnormalities in lipoprotein components;
- Abnormal haemostatic function;
- Vascular structural disorders (Boulton et al, 1999).
These abnormalities can lead to the development of atherosclerosis, which results in decreased blood flow to tissues. The effects of this are listed in Box 1.
The significance of microvascular disease is that retinopathy-related sight loss impairs the patient’s ability to inspect her or his feet for skin damage, while the significance of macrovascular disease is the development of peripheral arterial disease (PAD) leading to reduced blood flow in the foot. The patient is very vulnerable to skin injury, the wound is slow to heal and has a high risk of infection.
Impaired metabolic dysfunction caused by diabetes leads to hyperglycaemia, reduced leucocyte (white blood cell) function and impaired collagen synthesis. Brownlee et al (1988) suggested that hyperglycaemia can cause both endothelial cell and extracellular matrix dysfunction, resulting in increased permeability of blood vessels and an inelastic vessel wall. These changes result in a diminished blood flow. The patient with poor blood flow to the skin tissues will be less able to cope with injuries related to tissue hypoxia such as those caused by pressure or shearing forces.
Granulocyte (a type of white blood cell) function has also been shown to be impaired in a hyperglycaemic environment (Wall et al, 2003). Defective phagocytosis can impede the inflammatory response resulting in the accumulation of debris in the wound bed that, in turn, prevents the formation of granulation tissue during the proliferative phase of healing (Lioupis, 2005). This, and a reduced neutrophil efficacy, puts people with diabetes at a higher risk of delayed healing and infection than people who do not have the condition.
Fibroblast activity (fibroblasts produce collagen) and collagen (the main protein of connective tissue) formation are both thought to be affected by diabetes and, in particular, hyperglycaemia (Loots et al, 1999; Nissen et al, 1998). Effects include delayed collagen production, decreased collagen strength and impaired neovasculature (growth of new blood vessels).
Clinically this may be seen as wounds that are slow to repair and that remain vulnerable, even when healed, to relapse.
Neuropathy (nerve damage or dysfunction) is the most common complication of diabetes and affects up to 50% of all patients who have the condition. Neuropathy increases with age and the length of time the patient has had diabetes (Boulton et al, 1999). It is also considered to be one of the most important factors in the development of diabetic foot ulcers (Laing, 1998). Neuropathy presents in three forms: motor, sensory and autonomic, each of which has significance in relation to foot ulceration.
The motor nerves are responsible for all voluntary movement. Damage to the motor nerves can result in either paralysis or weakness of the muscles controlled by the affected nerve(s). Classic signs of motor-nerve paralysis in the diabetic foot are high medial longitudinal arches and claw toes. These deformities of foot shape can lead to the development of new pressure points for example, across prominent metatarsal heads, and to changes in gait.
Changes in gait can also result in the development of new pressure points. New pressure points are particularly vulnerable to ulceration either through friction and blistering or as a consequence of callus formation. Callus formation is the rapid layering of skin cells to thicken and protect a vulnerable area. While it serves in the short term to protect soft tissue from pressure damage, it eventually causes additional pressure on the site; consequently ulcer formation beneath the callus is common.
Patients sometimes suggest that the removal of a callus by a podiatrist has caused an ulcer to form when in reality the ulcer was sitting beneath the callus all the time. Failure to remove the callus simply results in a delay in treatment while the pressure exerted by the callus continues to silently exacerbate the problem.
Sensory nerves receive external sensory stimuli and relay them to the central nervous system for interpretation. Sensory nerve damage can present with a range of distressing sensations from stabbing, shooting or burning pain through to tingling (pins and needles), numbness or actual absence of sensation (Gilron et al, 2006).
Pain performs an important warning function, telling us when to remove ourselves from a potentially harmful situation. People with diabetes may be unable to detect painful stimuli and this can have disastrous consequences.
Patients may be unaware that they have sustaining foot trauma caused by ill-fitting footwear or hosiery. Thermal injury may also be caused by sources such as scalding water, hot-water bottles or hot radiators.
Another feature of neuropathic pain is hyperalgesia (an increased pain response to a painful stimulus) or allodynia (a pain response elicited by a non-painful stimulus) (Woolf and Mannion, 1999). Patients with these conditions can be unjustly accused of over-reacting to pain or as having a low pain threshold.
In practice the diverse features of pain in the diabetic foot can present a very confusing clinical picture as well as putting the patient at a higher risk of tissue injury.
The autonomic nerves control involuntary processes such heart-rate contraction, blood-vessel constriction/dilatation and sweating. Autonomic neuropathy as a result of diabetes develops over a number of years and leads to a wide range of complications, the more serious of which include myocardial infarction (often silent), stroke and sudden death (Aaron and Tomris, 2001).
In the diabetic foot, autonomic neuropathy can result in two noticeable changes: a decrease or absence of sweating (anhidrosis) and an increased rate of blood flow.
The decrease in sweat production as a result of disordered capillary function results in very dry skin that can lead to the development of calluses or skin fissures. These can easily open into wounds, which can then become infected through the ingress of micro-organisms.
The faster rate of blood flow, exacerbated by poor glucose control, results in new channels opening up between the arterial and venous systems in the lower leg and foot (arteriovenous shunting). This phenomenon is thought to be aggravated by the rigidity of the smaller arteries in the foot caused by arteriosclerosis and the widely dilated vascular bed caused by autonomic disorder (Ward et al, 1983).
Clinically these changes are seen as the presence of distended veins over the dorsum of the foot and lower leg, and an easily palpable, bounding pulse in the foot. Although these signs could be interpreted as indicators of a good blood supply to the foot, it has been suggested that the fast rate of flow actually fails to fill the smaller vessels of the foot resulting in a reduced distal blood supply (Ward et al, 1983).
Although the foot is warm to the touch with a strong pulse, the autonomic pathology and co-existence of micro and macrovascular disease means the picture of healthy skin and a good pulse is often confused by the presence of localised ischaemia or ulceration.
The Charcot foot is a complication of diabetes that is strongly linked to the presence of long-standing neuropathy (Sommer and Lee, 2001).
The disease takes its name from Jean-Martin Charcot (1825–1893) who was the first to describe the typical pattern of disintegration that occurs to the foot ligaments and joints as a result of the disease process.
In the Charcot foot the muscles lose their ability to support the foot correctly resulting in ligament laxity (slackness), joint dislocation and bone and cartilage damage. Fractures occur readily, often without any associated major trauma. Typically, the warning signs of pain go unnoticed (because of advanced sensory neuropathy) and so the person continues to walk on the foot despite the injury. Persistent damage can lead to foot deformity.
The two classic Charcot foot deformities – rocker bottom deformity and medial convexity deformity – are caused by damage in the tarsometatarsal joints and mid-tarsal joints. Foot deformities are problematic for the patient because they cause abnormal pressure distribution and an increased risk of foot ulceration.
Three factors have been cited in the development of Charcot foot (Jeffcoate et al, 2000):
- Motor neuropathy leading to the development of abnormal forces within the foot and the collapse of supportive structures;
- Osteopenia leading to bone weakness and fracture;
- Progressive damage from continued weight-bearing after injury because the patient has diminished pain sensation.
The cause of the osteopenia in diabetes is not known but it is associated with increased blood flow through the bone (Jeffcoate et al, 2000) (see autonomic neuropathy).
Charcot foot can present as an acute problem, with or without a preceding traumatic event. Typically the foot is reddened in appearance, very warm to touch and oedematous. Clinicians need to be aware of the importance of prompt diagnosis and intervention if disabling consequences including amputation are to be avoided.
The development of foot ulceration associated with diabetes is multifactorial with complications arising from circulatory, metabolic and neuropathic changes. If ulcers do develop they are more likely to become infected and there is a high risk of gangrene, which could lead to auto or surgical amputation. However, screening (Mousley, 2006) and an assessment of foot ulceration risk (NICE, 2004), together with early intervention at the point of ulceration, can all make a significant difference to the outcome for the patient (NICE, 2007).
Aaron, I.V., Tomris, E. (2001) Recognising and treating diabetic autonomic neuropathy. Cleveland Clinic Journal of Medicine;
68: 11, 928–944.
Boulton, A.J. et al (1999) Diabetic foot ulcers: a framework for prevention and care. Wound Repair and Regeneration; 7: 1, 7–16.
Brownlee, M. et al (1988) Advanced glycosylation end products in tissue and the biochemical basis of diabetic complications. New England Journal of Medicine; 199: 20, 1315–1321.
Currie, C.J. et al (1997) NHS acute sector expenditure for diabetes: the present, future, and excess inpatient cost of care. Diabetic Medicine; 14: 8, 686–692.
Department of Health (2007) Diabetes. www.dh.gov.uk/PolicyAndGuidance/HealthAndSocialCareTopics/Diabetes/fs/en.
EdREN (2006) Diabetic Nephropathy. Edinburgh: Royal Infirmary of Edinburgh. http://renux.dmed.ed.ac.uk/edren/EdRenINFObits/Diabetic_nephLong.html.
Gilron, I. et al (2006) Neuropathic pain: a practical guide for the clinician. Canadian Medical Association Journal; 175:
Jacobson, A.M. et al (1994) The evaluation of two measures of quality of life in patients with type I and type II diabetes. Diabetes Care; 17: 4, 267–274.
Jeffcoate, W. et al (2000) The Charcot foot. Diabetic Medicine; 17: 4, 253–258.
Laing, P. (1998) The development and complications of diabetic foot ulcers. American Journal of Surgery; 176: 2A Suppl, 11S–19S.
Lioupis, C. (2005) Effects of diabetes mellitus on wound healing: an update. Journal of Wound Care; 14: 2, 84–86.
Loots, M.A.M et al (1999) Cultured fibroblasts from chronic diabetic wounds on the lower extremity (non-insulin dependent diabetes mellitus) show disturbed proliferation. Archives of Dermatological Research;
291: 2–3, 93–99.
Mousley, M. (2006) Diabetic foot screening: why it is not assessment. The Diabetic Foot; 9: 4, 192–196.
NICE (2007) Scope Type 1 Diabetes: Diagnosis and Management of Type 1 Diabetes in Primary and Secondary Care. www.nice.org.uk/page.aspx?o=30594.
NICE (2004) Type 2 Diabetes – Prevention and Management of Foot Problems. London: NICE.
NICE (2002) Management of Type 2 Diabetes. Retinopathy – Screening and Early Management.
Nissen, N.N. et al (1998) Vascular endothelial growth factors mediates angiogenic activity during the proliferative phase of wound healing. American Journal of Pathology; 152: 6, 1445–1452.
Sommer, T.C., Lee, T.H. (2001) Charcot Foot: the Diagnostic Dilemma. American Family Physician. http://www.aafp.org/afp/20011101/1591.html.
The Diabetes Control and Complications Trial Research Group (1995) The effect of intensive diabetes therapy on the development and progression of neuropathy. Annals Intern Medicine; 122: 561–568.
Tooke, J.E., Brash, P.D. (1996) Microvascular aspects of diabetic foot disease. Diabetic Medicine; 13: Supplement, S26–S29.
Wall, S.J. et al (2003) Elevated matrix metalloproteinases-2 and -3 production from human diabetic dermal fibroblasts. British Journal of Dermatology; 149: 1, 13–16.
Ward, J.D. et al (1983) Venous distension in the diabetic neuropathic foot (physical signs of arteriovenous shunting). Journal of the Royal Society of Medicine; 76: 12, 1011–1014.
Woolf, C.J., Mannion, R.J. (1999) Neuropathic pain: aetiology, symptoms, mechanisms and management. The Lancet; 353: 9168, 1959–1964.
Young, M.J. et al (1993) The diabetic foot: aetiopathogenesis and management. Diabetes Metabolism Reviews; 9: 2, 109–127