Wound Care/Diabetes

DIABETES

Diabetes is a metabolic disease that causes high blood glucose. This occurs either because insulin production is inadequate or because the body’s cells do not respond properly to insulin. Insulin is a hormone produced by the pancreas that moves glucose from the blood into the cells. Nine percent of Americans (30 million people) have diabetes. When monitoring diabetes, it is better to err on the side of hyperglycemia; hypoglycemia can result in permanent neuron destruction.

Three Types of Diabetes

Type I

IDDM

The body does not produce insulin.

Usually develops before age 40, juvenile onset

Accounts for only 10% of diabetics

Requires insulin injections

Type II

NIDDM

The body does not produce enough insulin for proper function, or the cells in the body do not react to insulin.

Can sometimes be controlled with diet, exercise, and weight loss

Overweight people are at greater risk, and the risk also increases with age.

Type III

Gestational diabetes

A type of hyperglycemia that occurs during pregnancy

Occurs in 1% to 3% of women

Disappears in 97% of cases at the end of pregnancy

Type I vs. Type II Diabetes

Type I	Type II
IDDM	NIDDM
Juvenile onset	Adult onset
Prone to ketosis	Ketosis resistant
Onset less than 30 years of age	Onset usually over 40 years of age
Accounts for 10% of diabetic	Accounts for 90% of diabetic
Due to insufficient insulin production	Caused by the body not responding to insulin
Abrupt onset	Slow onset and progression
Must take insulin	Controlled with oral hypoglycemic and diet

Hyperglycemia vs. Hypoglycemia

Hyperglycemia	Hypoglycemia
Polyuria	Diaphoresis/syncope
Polydipsia	Tachycardia/palpitations
Polyphagia	Hunger
Weight loss	Anxiety/irritability
Fatigue	Tremors/seizures/mental confusion
Blurred vision	Weakness

Diagnosing Diabetes

FPG (fasting plasma glucose)

Less than 100 mg per dL is normal.

100 to 125.99 mg per dL is prediabetic.

Greater than 126 mg per dL is positive for diabetes.

OGTT (oral glucose tolerance test)

Less than 140 mg per dL is normal.

140 to 199.9 mg per dL is prediabetic.

200 mg per dL and up means diabetes.

A1C

Less than 5.7% is normal.

Between 5.7% and 5.99% is prediabetic.

6.5% and up is diabetic.

Factors That Put Diabetics at Risk for Foot Ulcers

Immunocompromised

Defective PMN function resulting in an increased risk of infection

Angiopathy

Blood vessels in the diabetic are subject to accelerated atherosclerosis, increased clotting, and thrombosis formation.

Neuropathy

Diabetic peripheral neuropathy is caused by direct metabolic damage to nerves. Diabetic peripheral neuropathy affects all nerves: sensory, motor, and autonomic.

Sensory Neuropathy

Sensory impairment typically precedes motor dysfunction.
Classically it begins in the longest nerves of the body and so affects the feet and later the hands. This is sometimes called the “stocking-glove” pattern. Protective threshold and proprioception (loss of balance) are lost.

Motor Neuropathy

Motor deficit affects the intrinsic muscles of the foot, leading to digital deformities.

Autonomic Neuropathy

Autonomic nerves to the sweat glands are damaged, causing anhidrosis (inability to sweat normally). This results in dry scaly feet, which are prone to fissuring. Other autonomic neuropathic symptoms include a hot, hyperemic foot, increased arteriovenous shunting, reduced capillary flow, bounding pulses.

WOUND CLASSIFICATIONS

Wagner Diabetic Ulcer Classification

Grade 0	Intact skin (cellulitis, erythema)
Grade 1	Superficial ulcer involving the skin (no subQ involvement)
Grade 2	Ulcer extending to tendon capsule or bone (through subQ)
Grade 3	More extensive ulcer with associated abscess, osteomyelitis, or joint sepsis
Grade 4	Local gangrene of the toes or forefoot
Grade 5	Gangrene of entire foot

Knighton Classification

I: Partial-thickness ulcer

Extends through the epidermis and into, but not through, the dermis

II: Full-thickness ulcer

Ulcer extending to subcutaneous tissue only

III: Full-thickness ulcer

Ulcer extending to tendon, ligament, joint, and/or bone

IV: Full-thickness ulcer

Level III ulcer with abscess and/or osteomyelitis

V: Full-thickness ulcer

Level III ulcer with necrotic tissue in wound

VI: Full-thickness ulcer

Level III ulcer with gangrene

University of Texas Wound Classification System (Wound Grade and Stage Classification)

Grade

Grade 0	Pre- or postulcerative site
Grade I	Ulcers are superficial wound through the epidermis or dermis.
Grade II	Wound penetrates to tendon or capsule.
Grade III	Wound penetrates to bone or into a joint.

Stage

Stage A	Clean
Stage B	Nonischemic infected
Stage C	Ischemic
Stage D	Infected ischemic

NPUAP Pressure Ulcer Staging System

Stage	Definition
I	Nonblanchable erythema of intact skin
II	Partial-thickness skin loss involving epidermis and/or dermis
III	Full-thickness skin loss involving damage or necrosis of subcutaneous tissue that may extend down to, but not through, underlying fascia
IV	Full-thickness skin loss with extensive destruction, tissue necrosis, or damage to muscle, bone, or supportive structures

ULCER EXAM

Systemic Signs

Rule out sepsis. Assess for fever, chills, sweats, lethargic, general malaise, and elevated pulses. Sepsis is a medical emergency, and patient should be admitted.

Vascular

VENOUS VS. ARTERIAL ULCERS

	ARTERIAL ULCER	VENOUS ULCER
Etiology	Arterial insufficiency	Venous insufficiency
Location	Distal to medial malleolus (dorsal foot, toes, & heels)	Proximal to medial malleolus (medial ankle & lower leg)
Pain	Severe, relieved by dependency	Moderate, relieved by elevation
Drainage	Little	Venous weeping
Edges	Irregular edges	Rounded edges
Appearance	“Punched out”	Shallow, irregular shaped
Associated findings	Trophic changes, absent pulses, trophic skin changes	Stasis dermatitis, hemosiderin deposits, palpable pulses, edema

Establish adequate perfusion. A toe systolic pressure of at least 30 mm Hg is required to heal a foot ulcer.

Neurologic

Establish adequate protective threshold.

Musculoskeletal

Assess bony prominences that may be the cause of ulcers.

Dermatologic

Assessing Ulcer

Depth (probe with Q-tip)

Diameter (measure)

Base (necrotic, granular, beefy red, macerated, fibrotic)

Margins (keratolytic, usually neuropathic in origin)

Drainage (purulent, clear, red, brown)

Odor (fecal smell—anaerobes; fruity smell—pseudomonas)

Assessing Surrounding Tissue

Temperature (warm to touch)

Erythema, note distribution and rate of progression (draw margins of erythema directly on
skin). Rule out cellulitis and necrotizing fasciitis.

Edema, note pitting vs. nonpitting and extent

Lymphangitis/lymphadenopathy

Red streaks up leg

Tender palpable regional lymph nodes

LABS

Blood Tests

CBC with diff

WBC greater than 10,000 indicates an infection.

An acute infection will show an increase in immature leukocytes called a left shift.

Check for anemia, which is often associated with diabetic infection.

ESR and C-reactive protein

Used to follow progression and regression of infection

Hemoglobin A1C

Determine long-term control of diabetes.

Glucose

Hyperglycemia, despite using the normal dose of insulin, may indicate an infection.

Values above 250 mg per dL have a negative effect on wound healing.

Types of Debridement

Surgical Debridement

Sharp or surgical procedure that is mostly selective, causing little or no damage to healthy tissue. Per-formed with a scalpel or curette.

Mechanical Debridement

Nonselective procedure performed by changing wet-to-dry gauze dressings or hydrotherapy. As the gauze is removed, necrotic tissue comes along with it; drainage and debris are stuck to the dressing.

Enzymatic or Chemical Debridement

A process requiring topical agents capable of degrading eschar, protein, and other nucleic agents (collagenase [Santyl])

Autolytic Debridement

The body’s own phagocytic debridement, which is encouraged by a moist occlusive dressing such as Hydrogel

PHASES OF WOUND HEALING

Inflammatory Phase

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