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Diabetes Mellitus, Wound Healing & The Dermal Clinician

Wounds and Diabetes Mellitus

The human skin embodies a crucial and imperative barrier against environmental perils, and

what’s more, when cutaneous injury emerges the human body commences a sequence of

coordinated molecular progressions. Though, in some disastrous instances non-healing

chronic wounds may advance where an anatomical and functional outcome is not achieved

within a timely means and the wound remains in a self-perpetuating inflammatory phase.

There are innumerable influences that can delay wound healing, one of the most frequent

being chronic disease, more specifically Diabetes Mellitus. Diabetes Mellitus is one of the

most widespread metabolic disorders worldwide and concerns approximately 383 million

people globally. The World Health organisation delineates Diabetes Mellitus as a chronic

endocrine condition identified by hyperglycaemia consequential of insulin deficiency, insulin

resistance, glucagon secretion, or potentially an aggregation of all three.

Normal cutaneous healing

To entirely comprehend the fundamental mechanisms of chronic wounds associated with

Diabetes Mellitus, a reconsideration of the well-regulated developments of physiological

wound healing is elemental.

Haemostasis: Initially succeeding cutaneous injury, the extra-cellular matrix stimulate and

unite circulating platelets, which then withstand adhesion and accumulation. The impaired

tissue and the aggregated platelets activate coagulation pathways to secure the fibrin

platelet clot, which eventually formulates a framework for the migration and proliferation

of additional participating cells in the wound healing progressions.

Inflammation: The inflammatory phase is a central reaction to anatomical injury and

comprises the cessation of tissue and the clearing of cellular, extra-cellular and pathogen

debris. In standard cutaneous wound healing inflammation is resolute after one to two

weeks, though in chronic wounds, this phase becomes extended and intensified.

Proliferation: Throughout the proliferation stage, re-epithelisation launches as the

keratinocytes and the epithelial cells proliferate and migrate. Simultaneously, angiogenesis

also takes place to postulate oxygen, nutrients and hydrate the matrix for cellular activity.

Remodelling: To finish the developments of normal cutaneous wound healing, contraction

and remodelling undergo, where collagen synthesis and lysis ensue, and collagen fibres are

reorganised in small parallel bundles along tension lines to form a scar. The end of the

wound healing phases is signified by apoptosis of vascular cells and myofibroblasts, finally transfiguring the granulation tissue into a collagen filled scar.

Diabetic Foot Ulcers

Diabetic Foot Ulcers, a chronic wound, are the most disastrous extensive impediment of

Diabetes Mellitus. For the sufferer, Diabetic Foot Ulcers extant with neuropathic pain, skin

discolouration, occasional haemorrhage, reduced mobility, sleep troubles, leakage and

malodour, and in more catastrophic cases, they may lead to amputation or mortality for the

patient. Emergent research has affirmed up to 4% of Diabetics cultivate a Diabetic Foot

Ulcer annually, with at least 25% of Diabetics presenting with one Diabetic Foot Ulcer

throughout their lifespan, these statistics convert to 16 million Diabetic Foot Ulcers per

annum. Even more to this, Australian studies have confirmed one limb is amputated every

three hours due to Diabetic Foot Ulcers, and a total of 8% of all Diabetic fatalities being

credited to Diabetic Foot Ulcers. Furthermore, owing to Diabetic Foot Ulcers necessitating

long-standing wound management and being one of the most common reasons for

hospitalisation they are associated with substantial health care costs and burden, further

indicating the requirement and importance for greater understanding and awareness.

The pathophysiology of Diabetic Foot Ulcers

Diabetic Foot Ulcers are consequential of both ischemia and neuropathy, which

fundamentally deteriorate a patient’s skin integrity and lead to a cascade of consequences,

such as hindered wound healing. Diabetic Foot Ulcers extant due to sensory, motor and autonomic neuropathies associated with Diabetes, devastatingly, this culminates a loss of

protective foot sensation, foot deformity due to abnormal weight bearing, reduced

sweating and amplified skin dehydration, causing hyperkeratosis, also known as callus

formation. Subsequent to this, once a callus has formed, the continual weight bearing

compression causes subcutaneous haemorrhage beneath the callus, and finally, a Diabetic

Foot Ulcer develops. The newly formed Diabetic Foot Ulcer is vulnerable to secondary

infection owing to the Diabetic’s already compromised immune system and the lessened

blood supply to the lower limbs which creates an ischaemic environment.

The damaging effects of Diabetic Foot Ulcers on patients

Both former and developing studies have indicated sufferers of Diabetic Foot Ulcers

regularly display concerning psychological and social issues, such as;

  • Depression

  • Anxiety

  • Mood disorders

  • Embarrassment and low self-esteem due to stigma

  • Isolation

  • Stress and apprehension

  • Decline in social activities

  • Restricted employment, and

  • Financial difficulty

To evade patient non-concordance and provide support for the sufferer’s mental and

physical wellbeing, research endorses the implementation of a patient centred

management plan that encompasses the imparting of knowledge and education to both the

sufferer and their family, caregiver and significant others.

Treatment and management of Diabetic Foot Ulcers

Essentially, although challenging and tedious, the aim of Diabetic Foot Ulcer treatment is

to achieve swift wound closure and prevent catastrophic consequences such as amputation

and fatality. The treatments which are currently available comprise of;

  • Hyperbaric Oxygen Chamber: Heightens the local distribution of oxygen to ischaemic tissues and the site of the wound

  • Debridement: The elimination of whole superficial debris and the peri wound callus necrotic, hyperkeratotic and pestiferous tissues and external bodies to expose healthy feasible tissue that can then heal

  • Wound off-loading: Reduces vertical plantar pressure and plantar shear stress, this can be succeeded through the employment of bed rest, a wheel chair, crutches or via surgical approaches

  • Low Level Laser Therapy (LLLT): Encourages and enables swift wound contraction and healing through stimulation of neovascularization and collagen remodelling

  • Dressings

  • Human amniotic: Averts the gathering of threatening bacteria and moderates’ pain and damage to fluids and proteins within the body

  • Antibiotic Therapy

  • Stem Cell Therapy

  • Revascularisation: Restores blood flow to the foot

  • Human Growth Factors

Further to this, research has also summarised numeral ways for Diabetic Mellitus patients to

inhibit the advancement of Diabetic Foot Ulcers, these include;

  • Regular and systematic screenings and risk assessments

  • Properly controlled blood glucose levels, blood pressure and lipid profile

  • Weight management through a healthy diet and amplified physical activity

  • Smoking cessation

To conclude, it is well acknowledged in medical literature that the treatment of Diabetic

Foot Ulcers is to be approached interprofessionally to extant successful and effective

outcomes. Diabetes Mellitus and Diabetic Foot Ulcers are both multifaceted and complex

inhibitions and their management necessitates collaboration with a range of specialists and

Allied Health Professionals, including the Dermal Clinician.



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