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;
Embarrassment and low self-esteem due to stigma
Stress and apprehension
Decline in social activities
Restricted employment, and
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
Human amniotic: Averts the gathering of threatening bacteria and moderates’ pain and damage to fluids and proteins within the body
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
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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