Diabetes and Wound Care

Question 1

What is prediabetes?

Answer 1

Fasting BS between 100-125

Question 2

What is diabetes?

Answer 2

Fasting BS of 126 and above

Question 3

Which type of wounds are affected with diabetes?

Answer 3

All types of wounds are affected including acute traumatic, surgical wounds, burns, foot ulcers, venous insufficiency, pressure ulcers.

Question 4

How does hyperglycemia affect wound healing?

Answer 4

Hyperglycemia:

1. represents a catabolic state which means: protein breakdown
2. there is a starvation status at a cellular level
3. causes an altered host response so it is more difficult to fight off infection
4. Toxic to cellular elements
5. Patient is at greater susceptibility to infection

Question 5

How many patients have complications at the time of diagnosis of diabetes?

Answer 5

50% of patients have complications at the time of their diagnosis of diabetes:

1. Peripheral arterial disease
2. Neuropathy
3. Foot deformities
4. Diabetic neuropathic foot ulcers
5. Gangrene
6. Charcot foot disease
7. Amputations

Question 6

What are the general physiologic effects of hyperglycemia?

Answer 6

1. Microvascular issues
2. Macrovascular impairments
3. Thickening of basement membrane
4. Extracellular and intracellular dehydration
5. Bone cell apoptosis

Question 7

Which stages of wound healing does hyperglycemia interfere?

Answer 7

All 4 stages of wound healing:

1. Hemostasis
2. Inflammation
3. Proliferation
4. Remodeling

Question 8

Advanced Glycation End-products (AGEs)

Answer 8

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.

Question 9

What is glycated hemoglobin or HbA1C?

Answer 9

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.

Question 10

Classification of diabaetic neuropathies

Answer 10

5 types:

1. Radiculopathy
2. Mononeuropathy
3. Polyneuropathy
4. Diabetic amyotrophy
5. Autonomic neuropathy

Question 11

How is microvascular disease a factor in the development of diabetic neuropathy?

Answer 11

Narrowing of the blood vessels, causes neuronal dysfunction.

Question 12

How are AGEs related to diabetic neuropathy?

Answer 12

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.

Question 13

How is Sensorimotor polyneuropathy related to diabetic neuropathy?

Answer 13

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.

Question 14

What are some autonomic neuropathies of diabetic neuropathy?

Answer 14

Orthostatic hypotension, respiratory sinus arrhythmia, gastroparesis, diarrhea, dysmotility in the small bowel, urinary incontinence..

Question 15

What are some cranial neuropathies associated with diabetes?

Answer 15

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.

Question 16

What is the most important risk factor leading to ulceration and is present in more than 80% of diabetic patients with foot ulcerations?

Answer 16

Neuropathy.

The pathology MOST responsible for diabetic foot ulcer is distal sensory neuropathy, peripheral sensory neuropathy.

Question 17

What are signs and symptoms of peripheral neuropathy?

Answer 17

Paresthesia, hyper or hypoesthesia, loss of deep tendon reflex, loss of sensation, anhydrosis, callus formation, muscle atrophy

Question 18

Diabetic foot ulcers prognosis

Answer 18

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.

Question 19

What are 11 disorders producing Charcot Joint?

Answer 19

1. Diabetes
2. Tabes Dorsalis
3. Leprosy
4. Syringomyelia
5. Spina Bifida
6. Meningomyelocele
7. Congenital insensitivity to pain
8. Chronic alcoholism
9. Spinal cord injury
10. Peripheral nerve injuries
11. Rheumatoid arthritis

Question 20

What is Charcot Joint?

Answer 20

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.

Question 21

What is the treatment for a Charcot joint?

Answer 21

1. in the acute stage: offloading

2. later on: surgery?

Question 22

Wagner Ulcer Grade Classification

Answer 22

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

Question 23

University of Texas DFU grading scale

Answer 23

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

Question 24

Statistics with regards to diabetic amputations

Answer 24

25% - 68% incidence of a contralateral amputation within 3-5 years
50% three-year mortality rate for diabetic amputee

Question 25

Semmes-Weinstein monofilament test

Answer 25

Absence of protective sensation:
5.07 size filament
Bends on 10 g pressure

Question 26

Diabetic foot ulcer infections

Answer 26

Most common bacteria: Streptococcux, E Coli, Proteus, and Pseudomonas

Question 27

Therapies to improve healing in people with diabetes

Answer 27

Blood glucose control
Wound bed preparation
Dressings
Adjunctive technologies

Established treatment methods:
1. offloading

Question 28

Treatment of Charcot

Answer 28

1. Initial treatment: rest, TCC

2. Follow-up treatment: orthotics, molded shoes, bracing, EBO Model 1200 or FLX bone stimulator