Diabetes and Wound Care Flashcards
What is prediabetes?
Fasting BS between 100-125
What is diabetes?
Fasting BS of 126 and above
Which type of wounds are affected with diabetes?
All types of wounds are affected including acute traumatic, surgical wounds, burns, foot ulcers, venous insufficiency, pressure ulcers.
How does hyperglycemia affect wound healing?
Hyperglycemia:
- represents a catabolic state which means: protein breakdown
- there is a starvation status at a cellular level
- causes an altered host response so it is more difficult to fight off infection
- Toxic to cellular elements
- Patient is at greater susceptibility to infection
How many patients have complications at the time of diagnosis of diabetes?
50% of patients have complications at the time of their diagnosis of diabetes:
- Peripheral arterial disease
- Neuropathy
- Foot deformities
- Diabetic neuropathic foot ulcers
- Gangrene
- Charcot foot disease
- Amputations
What are the general physiologic effects of hyperglycemia?
- Microvascular issues
- Macrovascular impairments
- Thickening of basement membrane
- Extracellular and intracellular dehydration
- Bone cell apoptosis
Which stages of wound healing does hyperglycemia interfere?
All 4 stages of wound healing:
- Hemostasis
- Inflammation
- Proliferation
- Remodeling
Advanced Glycation End-products (AGEs)
Advanced glycation end products are proteins or lipids that became glycated as a result of exposure to sugars. They affect nearly every type of cell and molecules in the body and are thought to be one factor in aging and in some age-related chronic diseases. They are also believed to play a causative role in the vascular complications of diabetes.
In the context of cardiovascular disease, AGEs can induce cross-linking of collagen which can cause vascular stiffening and entrapment of low-density lipoprotein particles in the artery wall. AGEs can also cause glycation of LDL which can promote its oxidation. Oxidized LDL is one of the major factors in the development of atherosclerosis. Finally, AGEs can bind to RAGE (receptor for advanced glycation end-products) and cause oxidative stress as well as activation of inflammatory pathways in vascular endothelial cells.
What is glycated hemoglobin or HbA1C?
A form of hemoglobin that is measured primarily to identify the three-month average plasma glucose concentration.
In diabetes mellitus, higher amounts of glycated hemoglobin have been associated with cardiovascular disease, nephropathy, neuropathy, and retinopathy.
Classification of diabaetic neuropathies
5 types:
- Radiculopathy
- Mononeuropathy
- Polyneuropathy
- Diabetic amyotrophy
- Autonomic neuropathy
How is microvascular disease a factor in the development of diabetic neuropathy?
Narrowing of the blood vessels, causes neuronal dysfunction.
How are AGEs related to diabetic neuropathy?
Elevated levels of glucose within cells cause a non-enzymatic covalent bonding with proteins, which alters their structure and inhibits their function. Some of these glycosylated proteins have been implicated in the pathology of diabetic neuropathy and other long-term complications of diabetes.
How is Sensorimotor polyneuropathy related to diabetic neuropathy?
Longer nerve fibers are affected to a greater degree than shorter ones because nerve conduction is slowed in proportion to a nerve’s length. In this syndrome, decreased sensation and loss of reflexes occurs first in the toes on each foot, then extends upward. Loss of proprioception, the sense of where a limb is in space, is affected early.
What are some autonomic neuropathies of diabetic neuropathy?
Orthostatic hypotension, respiratory sinus arrhythmia, gastroparesis, diarrhea, dysmotility in the small bowel, urinary incontinence..
What are some cranial neuropathies associated with diabetes?
Neuropathies of the oculomotor neruve (cranial nerve # 3) are most common. Symptoms maybe frontal or periorbital pain and then diplopia. Diabetics have a higher incidence of entrapment neuropathies such as carpal tunnel syndrome.
What is the most important risk factor leading to ulceration and is present in more than 80% of diabetic patients with foot ulcerations?
Neuropathy.
The pathology MOST responsible for diabetic foot ulcer is distal sensory neuropathy, peripheral sensory neuropathy.
What are signs and symptoms of peripheral neuropathy?
Paresthesia, hyper or hypoesthesia, loss of deep tendon reflex, loss of sensation, anhydrosis, callus formation, muscle atrophy
Diabetic foot ulcers prognosis
If ulcer size fails to reduce by half over the first 4 weeks of treatment, it is unlikely to heal at 12 weeks
Advanced therapies can be initiated at 4 weeks if 50% of wound closure has not occurred
There is a 5 times increase in the risk of infection in wounds that progress beyond 4 weeks of therapy
155 times greater risk of amputation once infection develops.
What are 11 disorders producing Charcot Joint?
- Diabetes
- Tabes Dorsalis
- Leprosy
- Syringomyelia
- Spina Bifida
- Meningomyelocele
- Congenital insensitivity to pain
- Chronic alcoholism
- Spinal cord injury
- Peripheral nerve injuries
- Rheumatoid arthritis
What is Charcot Joint?
Neuropathic arthropathy or neuropathic osteoarthropathy: a progressive degeneration of a weight-bearing joint, marked by bony destruction, bone resorption, and eventual deformity due to loss of sensation.
Underlying mechanisms:
There are 2 primary theories:
1. Neurotrauma: loss of peripheral sensation and proprioception leads to repetitive microtrauma to the joint; this damage goes unnoticed by the neuropathic patient and the resultant inflammatory resorption of traumatized bone renders that region weak and susceptible to further trauma.
2. Neurovascular: neuropathic patients have dysregulated autonomic nervous system reflexes, and de-sensitized joints receive significantly greater blood flow. The resulting hyperemia leads to increased osteoclastic resorption of bone and this, in concert with mechanical stress, leads to bony destruction.
What is the treatment for a Charcot joint?
- in the acute stage: offloading
2. later on: surgery?
Wagner Ulcer Grade Classification
0 – Preulcerative lesions, healed ulcers, neuropathy, the presence of bony deformity
1 – Superficial ulcer without subcutaneous tissue involvement, not infected
2 – Penetration through the subcutaneous tissue; may expose bone, tendon, ligament or joint capsule
3 – Extensive ulceration with exposed bone and/or deep infection
4 – gangrene of toes or forefoot
5 – gangrene of the whole foot requiring disarticulation
University of Texas DFU grading scale
Stages: A -- no infection or ischemia B -- infection C -- ischemia D -- infection and ischemia Grading: 0 -- epithelialized wound 1 -- superficial wound 2 -- wound penetrates to tendon or capsule 3 -- wound penetrates to bone or joint
Statistics with regards to diabetic amputations
25% - 68% incidence of a contralateral amputation within 3-5 years
50% three-year mortality rate for diabetic amputee
Semmes-Weinstein monofilament test
Absence of protective sensation:
5.07 size filament
Bends on 10 g pressure
Diabetic foot ulcer infections
Most common bacteria: Streptococcux, E Coli, Proteus, and Pseudomonas
Therapies to improve healing in people with diabetes
Blood glucose control
Wound bed preparation
Dressings
Adjunctive technologies
Established treatment methods:
1. offloading
Treatment of Charcot
- Initial treatment: rest, TCC
2. Follow-up treatment: orthotics, molded shoes, bracing, EBO Model 1200 or FLX bone stimulator
