Risk Factors for Diabetic Foot Complications

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The development of diabetic foot complication is multifactorial and rarely due to one factor. A number of these factors can theoretically increase the risk for developing complications of the foot in those with diabetes. However multivariate prospective studies have not necessarily shown that all the factors play a role :

Higher risk in those with increasing age

Duration of diabetes
Several studies have linked duration of diabetes to increased risk for foot ulcers , but it was not linked to diabetic foot ulcers in a multivariate prospective study .
Type 2 subjects treated with insulin appear to be at greater risk than those treated with oral agents

Males are at greater risk than females (could be behavioural or biochemical)

Tudiver & Talbot (1999) used focus groups of family physicians to investigate why men do not access the health care system for medical problems as readily. Three key themes were identified:
Support: Men appear to get most of their support for health concerns from their female partners, little from their male friends. Their pattern of seeking support tends to be indirect rather than straightforward
Help seeking: Perceived vulnerability, fear and denial are important influences on whether men seek help. They look for specific problems rather than for more general health concerns
Barriers: Personal barriers involved factors related to a man’s traditional social role characteristics – a sense of immunity and immortality; difficulty relinquishing control; a belief that seeking help is unacceptable; and believing men are not interested in prevention.

Fitzgerald et al (1995) showed differences between males and females in their attitudes towards their diabetes. Men with type 1 were more likely to agree that patients should do what they are told and less likely to agree that diabetes has a significant negative impact on their lives. Men with type 1 were less likely to be adherent in self monitoring of blood glucose. Most of the differences found suggest that men are more passive in their diabetes care.

Body weight
Higher risk associated with greater weight .
Evidence on body weight and plantar pressures is inconsistent

Some ethnic groups are at greater risk (may be due to pathophysiological differences or socioeconomic factors and access to health care)
Not linked to diabetic foot ulcers in a multivariate prospective study .
Ethnic and geographic variations in amputation rates and risk factors .

Social situation
Those living alone and less socially connected are at greater risk

Glycaemic control
Poor glycaemic control increases risk for neuropathy
A univariate link between blood glucose control and foot ulcers has been shown, but in a multivariate model the effect was diminished . This is assumed to be due to the relationship between glycaemic control and its consequences (eg neuropathy) that a multivariate model would adjust for.

Smoking status
Not linked to diabetic foot ulcers in a multivariate prospective study .

Self care/management
Lack of patient self-management increases risk
Negligent self care was considered to contribute to subsequent LEA in 24%

Psychosocial/Behavioural factors
Lack of perceived vulnerability

Psychosocial factors influence quality of life in those with ulcers

Precipitating event/Predisposing environmental event
Precipitating events (eg new shoes, accidents) are common causes
81% of LEA’s preceded by minor trauma

Thermal trauma


Can be precipitating.

Loss of protective sensation (sensory neuropathy):
Loss of protective sensation from sensory neuropathy is central to the development of foot complication – unable to detect tissue damage.
Young et al (1994) showed that those with a vibration perception threshold above 25 volts were 8 times more likely to develop a foot ulcer compared to those with a threshold of less than 15 volts.

Motor Neuropathy
Motor neuropathy affects muscle balance and foot structure/function

Autonomic neuropathy
Autonomic neuropathy affects control of the microcirculation  dry skin (predisposes to cracking of skin), increased AV shunting (may lead to inadequate nutrition of tissues). Has been shown to be related to foot ulcers in several cross sectional studies and one prospective study .

Peripheral vascular disease (PVD)
Peripheral vascular disease is 4-5x more common in those with diabetes – it puts the tissues at risk due to ischaemia. In isolation, PVD is rarely a cause of ulceration – it is its combination with minor trauma that leads to ulceration

In diabetes, the medium sized arteries are more affected, especially at the popliteal trifurcation. Prediction for small arteries before knee. The distal foot arteries tend not to be affected.

Symptoms of PVA (ischemic pain) may be masked by neuropathy

Generally assumed that macrovascular disease is not a strong risk factor for the development of a foot ulcer, but is a powerful risk factor for the nonhealing of an ulcer once it has occurred.

Mixed results from predictive studies using different measures of vascular status and prediction of foot ulcer. Poor vascular status may be a more important factor in lower extremity amputations compared to foot ulcers.

Vascular components of the clinical examination have been shown to be the best predictors of healing in those who develop a foot ulcer .

Microvascular dysfunction
Microvascular dysfunction  poor response to tissue damage
These functional abnormalities are present prior to or early after he diagnosis of diabetes .

• Arteriovenous shunting
• Impaired autoregulation

Insulin is a vasoactive hormone, causing a dose dependant endothelial vasodilation. In insulin resistant states there is impaired vasodilation .

In type 2 diabetes and polyneuropathy there has been shown to be reduced capillary blood flow, enhanced reduction in skin blood flux and impaired filtration after sitting up . These abnormalities were more severe in those with a history of foot ulceration.

Haemorheologic abnormalities

Reduced erythrocyte deformability  decreased ability to pass through capillary wall.
Leukocytes show reduced velocity of passage through capillary wall.

Limited joint mobility
Limited joint mobility restricts movement of key joints in the foot
Not linked to diabetic foot ulcers in a multivariate prospective study .
Has been related to higher plantar pressures but not found by Caselli et a l (2002).

Plantar soft tissue characteristics:

Heel pad in those with diabetes has been shown to have poorer rebound properties compared to controls . The collagen fibrils in the sample from the diabetic subjects were ruptured with unclear striations and an uneven distribution.

The presence of a callus/hyperkeratosis increase the risk for ulceration 70 fold

Plantar pressure
Plantar pressures are higher in those with diabetes. Plantar ulcers occur at the areas of highest pressure . Each individual is likely to have their own threshold of pressure at which tissue breakdown is likely to occur at, but Armstrong et al (1998) suggest that 700Kpa as being a good compromise between sensitivity and specificity – this will be very dependent on activity levels (more in Cavanagh in Bowker).

Toe loads in those with diabetes are reduced with metatarsal head pressure increased.

Caselli et al (2002) – ratio of forefoot to rearfoot pressures increased in severe neuropathy (both areas increased in pressure, but the forefoot increased more). The forefoot pressures and the forefoot/rearfoot ratio were prospectively related to the development of foot ulcers.

Possible causes of increased pressures:
• Bony deformity (eg bony prominence in Charcot’s neuroarthropathy)
• Soft tissue thickness
• Alteration of soft tissue properties (eg AGE’s)
• Clawing of toes (common in neuropathy)
• Hyperkeratosis
• Functional factors
• Limited joint mobility
• Muscle strength (weakness as a result of the peripheral neuropathy)
• Previous ulceration (alteration in properties of soft tissues from wound repair)
• Body weight (type 2 have higher BMI’s; 14% of variance in plantar pressures explained by body weight

Theories about how pressure causes tissue damage:
• Tissue ischaemia – pressure induces an ischaemia in the tissues
• Microstructural damage
• Tissue dissolution (microhaemorrhage)
• Wrinkled carpet effect
• Cellular mechanism (Landsman)

Foot structure
Foot structure is altered (eg intrinsic minus foot; claw toes) in those with diabetes
Pre-existing structural deformity (eg HAV) can results in increased focal areas of pressure – most ulcers occur over areas of bony prominence.

The deformity associated with Charcot’s neuroarthropathy increased the risk for foot ulcers.


Gait changes – often due to development of a safer more stable gait pattern in presence of reduced sensory input.

Diminished dynamic ankle joint range of motion  smaller gait cadence, velocities, shorter stride length

EMG studies of tibialis anterior muscle, show onset is delayed in those with diabetic neuropathy  foot is in midstance sooner and forefoot is in contact with the ground longer  pressures present for longer period of time

Kwon et al (2003) showed that, compared to controls, those with diabetic neuropathy had less ankle mobility, slower walking speeds, longer stance phases and lower peak ankle dorsiflexion

Immune/defence function (deficient response to infection):
Infection is more common in those with diabetes

Activity level

Previous ulceration
Strongest risk factor for ulceration is a history if a previous ulcer.

Connor & Mahdi (2004) – showed increased risk for repetitive ulceration in those with neuropathy were neuroarthropathy; high mean HbA1c; males who lived alone; poor compliance with footwear, footcare and with non-foot aspects of diabetes care; higher non-attendance rates; and delay in reporting new foot problems.

Interaction of risk factors:

Causal pathways are the assembly of essential component factors and events that act together to result in a particular outcome. Pecoraro et al (1990) defined the causal pathways that predispose the limb to those with diabetes to amputation. An identifiable minor trauma event preceded most amputations

Boyko et al (1999):
“In conclusion, this study demonstrated that multiple mechanisms contribute to the development of diabetic foot ulcer. Because of the interrelatedness of many diabetic complications and associated factors, it may be misleading to consider individual potential risk factors for foot ulcer in future research, as demonstrated in this study, many predictors in univariate analysis will not be shown to have independent effects on ulcer risk”

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