chapter 4b diabetes mellitus and wound care

8/2/2019 Chapter 4b Diabetes Mellitus and Wound Care

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4.2 Diabetes Mellitus And Wound CareNabil Fahim, DPM

Mark G. Mandato, DPM

Diabetes Mellitus can be thought of as a group of metabolic disorders characterized by hyperglycemia thatresults from defects in insulin secretion, insulin action, or both. It was described in the Egyptian Papyrus around

1500 BC. The Greek physician Cappadocia named the disorder diabetes because the condition was characterized by

the passage of large volumes of urine. Willis added the word mellitus, meaning honey, in 1604, in recognition of

the presencof sugar in the urine.1 Diabetes affects nearly 16 million Americans (approximately 6% of the US popu-

lation) and almost half of these are undiagnosed. Diabetes takes many forms with the most common being Type 1,

Type 2, Gestational, and Impaired Glucose Metabolism. Themajority of diagnosed cases are of the Type 2 variety.

Diabetes is the 6th leading cause of death in US and the leading cause of End Stage Renal Disease (ESRD), amputa-

tions & blindness. As of 1993, it is estimated that over $100 billion will be spent treating diabetes in United States

each year.

Diagnosis of Diabetes MellitusScreening Tests

Certain groups of patients must be screened as they are at a higher risk for developing diabetes mellitus. These

include:

Family history of diabetes

Obesity (> 120 % desired body weight)

Women with babies > 9 lbs. at birth (or prior gestational diabetes)

Pregnant women at risk for diabetes

Hypertension and or hyperlipidemia

Members of a high-risk group

African Americans, Native Americans and Hispanics

The Fasting Plasma Glucose Test (FBS) is the screening test of choice in children and non-pregnant adults.Fasting is defined as no food or beverage except water at least eight hours before testing. The test is positive if the

result is greater than 115mg/dl in the non-pregnant adult or greater than 130mg/dl in the child.

After the screening test is completed, the diagnosis of diabetes is made by the following confirmatory regimen: Any

one of these three tests confirmed on a different day by, again, any one of these three tests:

Random plasma glucose > 200 mg/dL with classic signs and symptoms

FBS 126 mg/dL

Oral Glucose Tolerance Test* (75 gram load) in which the 2 hour level 200 mg/dL

The Oral Glucose Tolerance Test is NOT necessary for the diagnosis of diabetes as was previously

thought, but a modified version of this test is currently used to diagnose gestational diabetes. The test is per-

formed by administration of a 75-gram glucose load with serum glucose levels taken every 30 minutes for a

total of two hours. This test should be performed in the morning after a 10-14 hour fast, with the discontinu-

ation of all medication for three days prior to the test. It is also important to have the patient consume 150

grams of carbohydrate each day for three days prior to the administration of the exam.

Patients are to be excluded from this test if they are:

Malnourished

At bed rest

On a restricted carbohydrate in-take diet

Acutely ill

Medicine | Diabetes Mellitus and Wound Care 255


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Types of Diabetes

Diabetes is thought of as a heterogeneous group of diseases with the common factor of sustained periods of

hyperglycemia. It has been classified into a number of types: Type 1, Type 2, Gestational Diabetes, Secondary

Causes and Impaired Glucose Metabolism. Each of these disorders has certain characteristics and treatment proto-

cols that should be followed in order to adequately maintain glucose homeostasis.

Type 1 Diabetes Mellitus

Characteristics

10 % of all diabetics

Onset at any age (75 % before age 18)

Autoimmune destruction of islet ? cells

Abrupt onset

Requires insulin

Type 1 diabetes mellitus results from an absolute insulin deficit and accounts for approximately 5-10 % of all

cases of diabetes in the United States. Its highest incidence can be found in the age group of 10-14, but can occur at

any age. It is the most common chronic disease of children under the age of 16. It has its highest incidence in

Caucasians, with a lower incidence in the African American, Hispanic and Asian populations. The estimated risk fordevelopment of the disease is 0.3% if no one in a family has diabetes and will jump to 3 % if one parent or sibling

has Type 1 diabetes. In monozygotic twins, the risk elevates up to 25-50%

Clinical Presentation

The diagnosis is often made after 90 % of the ? cells have been destroyed and significant fasting hyperglycemia

is present (plasma glucose > 180 mg/dL). The patients may present with the classic signs of polyuria, polydipsia,

polyphagia, weight loss and fatigue. This clinical presentation varies from minimal symptoms to coma.

Pathogenesis

Genetic predisposition:

Genetic factors alone are inadequate to cause type 1 diabetes mellitus

90 % of all Type 1 diabetics have certain HLA types: DR 3 and/or DR 4 loci

Events that trigger islet ? cell destruction in Type 1 diabetes are unknownThe progressive autoimmune destruction of the ? cells occurs over time and results in the loss of the 1st phase

insulin response to IV glucose (initial postprandial bolus of insulin) that leads to progressive impairment in total

insulin response, which ultimately leads to clinically detected hyperglycemia.

Treatment

The Glucose Hypothesis:

Treatment that normalizes glucose levels will prevent or delay the long-term complications of diabetes mellitus

The above statement is based upon the results of the Diabetes Control and Complications Trial (DCCT) that was

conducted for a period of 10 years. This study was conducted with 1440 Type 1 diabetic patients in 29 centers. 90%

of the study participants completed the study and the results indicated a 50-75 % reduction in risk of development

or progression of diabetic complications. Similar findings were observed in the United Kingdom Prospective

Diabetes Study (UKPDS) in Type 2 diabetics.

256 The 2005 Podiatry Study Guide


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The patients were divided into two groups. The first group was termed the Conventional Therapy group and the

second group was termed the Intensive Therapy group.

The table below summarizes the characteristics of each group.

Conventional Therapy Group Intensive Therapy Group

1 or 2 injections per day 3 Daily injections or insulin pump

Daily self-monitoring 4 or more blood glucose tests daily

Quarterly HbA1c Hospitalization for initiation to help

Pregnant women treated intensively Frequent dietary instruction to help achieve goals

Quarterly visits Monthly clinic visits

Based upon the above study, the results were as follows:

Based upon these results, the Diabetes Control and Complications Trial makes the following recommendations:

1. Intensive therapy, with the goal of achieving normoglycemia, should be employed in most type 1 patients

in whom the likely benefits outweigh the risks.2. Intensive therapy may not be appropriate for patients with recurrent severe hypoglycemia or with hyp

glycemic unawareness.

3. Intensive therapy may not be appropriate in patients with far advanced complications, such as renal failure or

laser treated proliferative retinopathy.

4. Intensive therapy may not be appropriate for patients with coronary artery or cerebrovascular disease.

5. Intensive therapy may not be appropriate in children younger than 13.

6. Intensive therapy should be implemented in centers with the requisite nursing, dietary behavioral and

clinical expertise to ensure safe and effective therapy.

Conclusion of the DCCT:

The majority of Type 1 patients should be treated with intensive therapy with the expectation that their long-term outcome will be measurably improved.


Intensive therapy reduced:

Clinically meaningful retinopathy 35 to 74%

Proliferative retinopathy and laser therapy 45%

First appearance of any retinopathy 27%

Intensive therapy reduced the development of:

Microalbuminaria 35%

Clinical grade albuminuria 56%

Clinical neuropathy 60%


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Insulin Preparations

These are the most common forms of insulin preparation on the market today. They are marketed as U-100 or

100 units/ml.

Lispro: rDNA origin, human insulin analog

Regular: Crystalline Zinc Insulin

NPH: Neutral Protamine Hagedorn

Lente family: Semilente

Lente

Ultralente

Lispro

Soluble and rapidly absorbed

Onset 15 minutes

Peak 30-70 minutes

Duration two to three hours. Not approved for insulin pump use

Regular

Soluble and rapidly absorbed

Onset < 1 hour

Peak two to three hours

Duration three to six hours

Available in buffered form

For insulin pump use

NPH

Altered to slow absorption: precipitated with protamine

Onset 2-4 hours

Peak 4-10 hours

Duration 10-16 hours for human NPH Available as 70/30 and 50/50 premixedReduces error but limits flexibility

Lente Family

Altered to slow absorption

Peak and duration similar to NPH

More likely to interact with regular insulin when mixed

Available in long-acting form (Ultralente), which can be used as basal with pre-meal regular insulin

Premixed insulin:

70/30 70% NPH with 30% Regular

75/25 75% NPL with 25% Lispro premixed (Humalog insulin Pen)



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Insulin Requirements

Provide basal amount and then peaks after each meal

Starting dose = 0.2 m - 0.3 m per kg/day

Average dose = 0.5 m - 1.0 m per kg/day

Pediatric dose = up to 1.0 m to 1.5 m per kg/day

The daily insulin requirement may be administered from one to multiple injections per day or throughContinuous Subcutaneous Insulin Infusion (CSII). More than three daily insulin injections and CCSII constitute

intensive therapy.

2 Injection Regimen

NPH and regular insulin given together before breakfast and the evening meal

Initially 40% NPH and 15 % regular in the morning then 30 % NPH and 15 % regular in the evening

Limitations: Poor peaking of noon insulin and excess insulin during the night

3 Injection Regimen

NPH and regular insulin given together before breakfast, regular before the evening meal, and NPH at

bedtime

Limitations: Poor peaking of insulin for noon meal

4 Injection Regimen

Regular insulin before each meal, NPH, Lente or Ultralente at bedtime

Limitations: Meals must be no more than five hours apart

Continuous Subcutaneous Insulin Infusion

Continually delivers phosphate-buffered regular insulin through a mechanically operated syringe and

subcutaneous soft canula

Increased risk of ketoacidosis versus multiple injections

More closely reproduces endogenous insulin release with more predictable insulin absorption and fewer

dosage errors

Provides both basal insulin release and adjustable pre-meal bolus release

Indications

Inability to optimize plasma glucose using two or more injections

Pregnancy or pre-conception

Recurrent major hypoglycemia due to hypoglycemic unawareness, loss of counter-regulatory mechanisms,

or variable absorption of modified insulin

Patient preference

Contra-indications

Reluctance to monitor glucose 4x/day

Intellectual or emotional inability to take responsibility for self-care

Lack of financial resources to pay for pump and pump supplies

Children and adolescents

Goals of Treatment:The goals treatment in the type 1 diabetic are the normalization of blood glucose and the prevention of compli-

cations from the disease process as well as achieve normal blood pressure. Also, to maintain lipids near normal (cho-

lesterol < 200; triglycerides


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Prevent ketoacidosis or severe hypoglycemi

Increase frequency of self monitoring when

Patient is under stress

There are major changes in the patients eating, sleeping or exercise routines

Periodic accuracy testing of monitor with laboratory testing

The following table can be used as a guideline for treatment goals.

Self Monitoring Blood Glucose Levels

Type 1 Diabetes

Insulin dose adjustments for all regimens are based on daily glucose levels and on the peak effect of a given insulin

dose.

Glycosylated Hemoglobin

Non enzymatic glycosylation of hemoglobin direct exposure of the hemoglobin in the erythrocyte to

glucose

Measures the average plasma glucose in the preceding 6-10 weeks

Every three months in type 1

Ideal is within 1% of high end of normal

Fructosamine

Non enzymatic glycosylation of albumin

Measures mean glucose levels of the preceding 1-3 weeks

Interference from increase serum bilirubin

Not affected by HbF or RBC turnover

Adjunctive measures must be utilized to maintain glucose homeostasis in the type 1 diabetic patient. Diet

should be advocated to the patient. Diet recommendations are often the most difficult to adhere to but should be

reinforced at every patient visit. The following diet guideline can be utilized:

Carbohydrate: 55-60

%Protein: 15-20 %

decrease to approximately 10% with onset of nephropathy

Fat: < 30 % (Of this < 10 % saturated fat)

Cholesterol: < 300 mg/day

Sodium: < 3 grams/day

Fiber: 20-35 grams/day


Biochemical index Goal Take Action at

Preprandial glucose 80-120 mg/dL 140

Bedtime glucose 100-140 mg/dL >140 or 8%


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Complications of Type 1 Diabetes

Hypoglycemia

May be due to a number of factors:

Defective counterregulation

Hypoglycemic unawareness

Insulin dosage errors Excess alcohol intake

May also be a consequence of the treatment regimen

Signs and Symptoms

When plasma glucose is < 50 mg/dL: Impaired mentation (decreased cognitive function, confusion)

Adrenergic warning signs: Anxiety, palpitations, diaphoresis

Seizures and/or coma

Treatment:

If conscious:

10-15 grams oral glucose

e.g.: 2 glucose tablets, 5 Lifesavers, or 4 oz juice

repeat in 15-20 minutes if hypoglycemia persists

If next meal is more than 1-2 hours away, the patient should eat an extra snack

If unable to safely swallow:

25 - 50 ml of 50 % dextrose if IV in place

1 mg Glucagon SQ or IM

Patient and family should be trained to recognize and treat hypoglycemia.

All insulin treated diabetics should have Glucagon available. Family, friends, co-workers, etc. should be taught how

to administer it. Wear ID bracelet!



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Diabetic Ketoacidosis

Diabetic ketoacidosis (DKA) represents a decompensation in diabetic control. Three major factors contribute to

the pathophysiology of DKA:

Insulin deficiency

Dehydration

Increase in counter-regulatory hormonesSigns

Acidosis: (pH < 7.2 or bicarbonate < 15)

Increased anion gap: [(Na+ + K+) - (Cl + HCO3) > 20 mEq/L

Ketosis

Hyperglycemia: BG > 250 mg/dL

Dehydration

History of polyuria, polydipsia and weight loss

Abdominal pain: vomiting

Hyperpnea: Kussmaul respiration

Coma: (in severe cases < 20 %)

Fruity odor on breath: (acetone)Initial Workup

History and physical

Electrolytes and CBC

Urinalysis and urine culture

Serum ketones

Blood gasses, pH and blood cultures

EKG

Chest x-ray

Treatment

Fluid Replacement

0.9 % saline @ 1L/hr for first 2 hours then.

0.45% saline @ 150-250 ml/hr

Add D5W when BG is < 300 mg/dL

Insulin Replacement

Use continuous IV @ 3-7 units/hr with variable rate based on hourly bedside BG

and continue until patient is eating and SQ insulin is started

Potassium replacement

Bicarbonate: if pH < 7

Phosphate



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Type 2 Diabetes Mellitus

Type 2 diabetes mellitus is a heterogeneous disorder with defects in both insulin secretion and action. It is a

chronic disease syndrome associated with insulin resistance and accounts for most of the cases of diabetes in the

United States. It has its highest incidence in the African American, Hispanic and Asian populations with a lower

incidence in Caucasians. The estimated risk for development of the disease in monozygotic twins is 60-90% versus

25-50 % in Type 1 diabetics.Pathogenesis

Most patients have a genetic defect in insulin action resulting from abnormalities in glycogen synthesis or in

glucose transport.

Insulin resistance in these patients leads to hyperinsulinemia.

Hyperinsulinemia further aggravates insulin resistance.

Acquired factors such as obesity and sedentary lifestyle can contribute to insulin resistance

The following lead to the development of insulin resistance:

Aging

Obesity

Genetics

Insulin resistance is associated with: Acromegaly

Cushings syndrome

Medications

Unknown mechanism of pancreatic exhaustion leads to:

Impaired Glucose Metabolism

Diabetes

May be related to effects of glucose toxicity in a genetically predisposed pancreatic cell

Liver - increased gluconeogenesis (patients with fasting hyperglycemia)

Decreased beta cell function leads to increased alpha cell secretion of glucagon

Skeletal muscle is insulin resistant due to receptor and post receptor defects

Characteristics

When fasting glucose is > 115 mg/dL:

The early insulin response to glucose is lost

When fasting glucose is > 180 mg/dL:

All phases of insulin secretion are markedly impaired

Patients will first present to a physician years after developing diabetes

There is detectable hyperglycemia 9-12 years before diagnosis is made

Treatment Goals

Reverse underlying insulin resistance and impaired cell function by:

Normalizing plasma glucose

Achieving and maintaining desirable body weight through a diet and exercise program

Achieve normal glycemic control, blood pressure and serum lipid levels

Cholesterol < 200 mg/dL

Triglycerides < 200 mg/dL

Prevent macrovascular and microvascular complications



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Self Monitoring of Blood Glucose

The following table indicates the level of glycemic control in the Type 2 diabetic.

Exercise

Benefits

Improves insulin sensitivity and glucose tolerance

Promotes weight loss

Decreases cardiac risk factors

Increase HDL

Decrease Hyperinsulinemia

May reduce or eliminate the need for insulin or oral hypoglycemic medications.

Improves sense of well being and quality of life

Improves strength and endurance for conduct of daily activities

Risks

Potentiate the hypoglycemic effects of insulin and oral agents

Further compromises poor metabolic control in severely insulin-deficient patients

May precipitate arrhythmia or MI in patients with cardiovascular disease

May hasten foot and joint problems

May cause acute vitreous hemorrhage in patients with proliferative retinopathyDiet

Must be individualized best left to Certified Diabetes Educator, nutritionist or dietitian

Initial weight loss is simple

maintenance is difficult

Decreases hepatic glucose production

Improves insulin sensitivity

May improve beta cell secretion


Normal Good Poor

FBS 115 140 >2002 hr PP 140 200 >235

HbA1c 6% 8% >10%


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Oral Hypoglycemic Agents

The oral agents used to treat diabetes should be used as adjunct to diet and exercise not as a substitute. They

should be used when diet and exercise fail to keep plasma glucose in an acceptable range. There are 5 different class-

es of oral drugs used to treat diabetes.

Classes of Oral Hypoglycemic Agents

Sulfonylureas Biguanides

Alpha-glucosidase inhibitors

Thiazolidinediones

Meglitinides

Sulfonylureas:

Four 1st and three 2nd generation agents available

They differ in potency, pharmacokinetics and cost.

Stimulate insulin secretion by blocking the K+ channel of the cell.

Secondary effects:

Decrease hepatic glucose production and may improve insulin sensitivity at the receptor and post rece

tor levels

Clinical Uses of Sulfonylureas

Use when diet and exercise fail to keep plasma glucose in acceptable range

Most effective when plasma glucose is mildly elevated and diabetes onset is recent

Start with the lowest dose and titrate q 1-2 weeks

Initial satisfactory response occurs in 60-70 % of patients but secondary failure occurs at a rate of 5 % per

year

Absolute Contraindications

Type 1 diabetes

Pregnancy

Allergy to sulfonylureasRelative Contraindications

Avoid long acting agents such as Chlorpropamide in elderly patients prone to

hypoglycemia



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Agents

First Generation

TolbutamideOrinase

ChlorpropamideDiabinese

AcetohexamideDymelor

TolazamideTolinaseSecond Generation

Glipizide- Glucotrol

Glimepiride- Amaryl

Glyburide- Diabeta, Micronase, Glynase

Selection of Agents: Second generation agents are more potent, on a weight basis, with less drug interaction.

Glyburide potentiates basal insulin more and is used for fasting hyperglycemia

Glipizide & Glimepiride potentiate postprandial insulin more and are used for postprandial hyper

glycemia

Meglitinides

Similar action as sulfonylureas:

stimulates insulin secretion by blocking the K+ channel of the ? cell.

- best for postprandial hyperglycemia

However, unlike sulfonylureas:

Insulin release is glucose-dependent and diminishes at low glucose concentrations and should not lead to

pancreatic exhaustion.

Similar indications and contraindications.

Agents

Repaglinide- Prandin



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Alpha-Glucosidase Inhibitors

Delays the digestion of carbohydrates

- Decreases the elevation of postprandial plasma glucose.

Does not enhance insulin secretion

- does not cause hypoglycemia if used alone

- hypoglycemia when used in combination with a sulfonylurea must be treatedwith oral or IV glucose or glucagon injection.

Agents

Acarbose- Precose

Miglitol- Glyset

Warnings:

Acarbose is metabolized entirely in the GI tract and is contraindicated in patients with inflammatory

bowel disease, colonic ulceration, partial or predisposition to intestinal obstruction.

Major side effect is increased intestinal gas formation

Glyset is renally excreted and is contraindicated in patients with a creatinine clearance

of < 25Biguanides

Decrease hepatic glucose production and intestinal absorption of glucose. Increase peripheral glucose

uptake and utilization.

Lowers both basal and postprandial plasma glucose.

- does not cause hypoglycemia if used alone

- does not cause hyperinsulinemia

Decreases mean fasting serum triglycerides, total cholesterol, and LDL

Agents

Metformin- Glucophage

Contraindicated in patients with renal disease or dysfunction (creatinine 1.5 mg/dL)

Also contraindicated in patients undergoing radiological studies with iodinated contrast materials. Also contraindicated in patients with acute or chronic metabolic acidosis

0.03/1000 patient years risk of fatal lactic acidosis

Thiazolidinediones

Decrease insulin resistance at peripheral receptor site.

liver, skeletal muscle and adipose tissue.

Decrease hepatic gluconeogenesis

Increase glucose uptake in skeletal muscle & adipose tissue

Decrease plasma insulin concentration

Indicated for Type 2 diabetics on insulin therapy with poorly controlled hyperglycemia.

Agents

Troglitazone- Rezulin-no longer used Rosiglitazone maleate- Avandia

Pioglitazone hydrochloride- Actos



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Contraindications & Precautions

Type 1 diabetics or treatment of DKA

only active in the presence of insulin.

Pioglitazone may decrease effectiveness of oral contraceptives and enhance the

metabolism of the statins.

Monitor LFTs - Rezulin taken off the market in due to cases of hepatic failure.

monitor every 2 months.

Actos with insulin increased CHF risk (evaluate edema)

Other Agents

Glucovance (Glyburide and Metformin)

Metaglip (Glipizide and Metformin)

Avandamet (Rosiglitazone maleate and Metformin)

same indications and contraindications as the parent drugs.

Starlix (Nateglinide)

derived from phenylalanine

supposed to mimic the bodys natural insulin patterns and restore early insulin secretion. Only works

in the presence of glucose. (Approved 2/01)

Insulin Therapy in Type 2 Diabetes Mellitus

Indications

Treat hyperglycemia (>150 mg/dL) during periods of stress, injury, surgery or infection

When FBS > 180 mg/dL

During pregnancy

2 hr PP > 120 mg/dL or FBS > 105 mg/dL



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Ulcer Care in the Diabetic Patient

Definition: An ulcer is a lesion on the surface of the skin or a mucous surface caused by superficial loss of tis-

sue, usually with inflammation. Ulcerations in the diabetic patient have been called in the literature diabetic ulcera-

tions. This term is incorrect, as an ulceration should be classified by its etiology rather than the population it

affects. Treatment of ulcerations is also based upon etiology rather than the patient population where they exist.

Ulcerations typically are of three types: pressure, ischemic, and neuropathic.Pressure Ulcerations:

A pressure ulcer is a localized area of soft-tissue injury resulting from compression between a bony

prominence and external surface

Synonyms include: pressure sores, decubitus ulcers, bedsores and ischemic ulcers

The term pressure ulcer is most appropriate as it denotes the principal etiologic factor

Pathophysiology

Two types of pressure have been determined to cause ulcerations: absolute or vertical pressure,and shear pressure:

Absolute (Vertical) Pressure- When the external vertical pressure exceeds the normal capillary filling pressure of

approximately 32 mm Hg, local vascular occlusion occurs sufficient to produce ischemia and subsequent necro-

sis of skin and subcutaneous tissues. Studies have shown microscopic tissue damage when subjected to pressures of

60mm Hg for as little as one hour

Lying supine in a hospital bed generates heel-to-bed pressures of 50 to 94 mm Hg

and trochanter-to-bed pressures of 50 to 94 mm Hg

Thus, the amount of pressure needed to produce tissue damage and pressure ulcers is

readily present in all patients confined to a bed or chair

Shear Pressure- Defined as the applied force that causes an opposite, parallel sliding motion in the planes of an

object.

A common clinical situation in which a shear force occurs is on the sacrum when

the head of the bed is elevated for an immobilized supine patient

Shear pressure develops Friction, which is defined as superficial mechanical forces

directed against the epidermis resulting in increased susceptibility to ulceration

Friction forces are often manifested clinically by restraints against skin, as well as

repeated dragging of patient across sheets for repositioning



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Factors to Consider

Immobility (Sores very rare in ambulatory patients) Limits ability to reposition

Examples: paralysis, fractures, Parkinsons disease and physical restraints

Sensory Deficit Limited ability to sense need to reposition. Examples: neuropathies, spinal cord lesions,

stroke, coma or chemical restraints Malnutrition In prospective cohorts with multivariate analysis, both lower dietary protein in-take and

the inability to feed oneself have been found to be predictors of pressure ulcer development

Prolonged malnutrition will cause abnormal lab values to include hypoalbuminemia,

hypercholesterolemia and low ascorbic acid levels, hindering wound repair

Incontinence Bowel or bladder

Thin Body Habitus More prone to develop pressure ulcers over bony prominences than obese or ave

age-weight patients

Depression More prone to self-neglect

Age Thinner skin is less resistant to shear forces, diminished barrier function and decreased vascularity

Structural Deformity and Limited Joint Mobility Foot deformities, which are common in diabetic

patients, lead to focal areas of high pressure Most diabetic foot ulcers form over areas of bony prominences, especially when

bunions, calluses, or hammer-toe formations lead to abnormally prominent bony points

Testing Modalities

F-Scan

EMED

Force Plate

Harris Mat

The above noted systems measure the vertical pressure per unit area on a foot. The EMED system and the F-

Scan system are computer-assisted measurement systems that can utilize in-shoe sensors to evaluate the pressure on

a foot while ambulating in shoe gear. The force plate can measure both vertical and shear pressures but needs to be

installed in floor of a large analysis center.Ischemic Ulcerations

Arterial Insufficiency

Peripheral arterial occlusive disease is four times more prevalent in diabetics than in nondiabetics

The arterial occlusion typically involves the tibial and peroneal arteries but spares the dorsalis pedi-

artery

Smoking, hypertension and hyperlipidemia commonly contribute to the increased prevalence of

peripheral arterial occlusive disease in diabetics as well as the general population



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Signs

Claudication,

Pain occurring in the arch or forefoot at rest or during the night

Absent popliteal or posterior tibial pulses

Thinned or shiny skin

Absence of hair on the lower leg and foot, thickened nails

Redness of the affected area when the legs are dependent, or dangled, and pallor when the foot is

elevated

Neuropathic Ulcerations

Distal symmetric polyneuropathy is perhaps the most common complication affecting the lower extrem

ties of patients with diabetes mellitus

Neuropathy, a major etiologic component of most diabetic ulcerations, is present in more than 82 percent

of diabetic patients with foot wounds

This lack of protective sensation, combined with unaccommodated foot deformities, exposes patients to

undue sudden or repetitive stress that leads to eventual ulcer formation with a risk of infection and

possible amputation

Classification Systems

Wagner Classification System

Grade 0 - Pre-ulcerative lesion, healed ulcers, presence of bony deformity

Grade I - Superficial ulcer without subcutaneous tissue involvement

Grade 2 - Penetration through the subcutaneous tissue (may expose bone, tendon, ligament or joint

capsule)

Grade 3 - Osteitis, abscess, or osteomyelitis

Grade 4 - Gangrene of the forefoot

Grade 5 - Gangrene of the entire foot

Figure 1. Gangrene of the Entire Foot



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National Pressure Ulcer Advisory Panel (NPUAP) For Pressure Ulcers

Stage I - Non-blanchable erythema of intact skin, the heralding lesion of skin ulceration. In individual-

swith darker skin, discoloration of the skin, warmth, edema, induration, or hardness may be indicators.

Stage 2 - Partial thickness, skin loss involving epidermis, dermis, or both. The ulcer is superficial and pres-

ents clinically as an abrasion, blister, or shallow center.

Stage 3 - Full thickness, skin loss involving damage to or necrosis of subcutaneous tissue that may extend-

down to, but not through underlying fascia. The ulcer presents clinically as a deep crater with or without

undermining of adjacent tissue.

Stage 4 - Full thickness skinloss with extensive destruction, tissue necrosis, or damage to muscle, bone, or

supporting structures (e.g., tendon, joint capsule). Undermining and sinus tracts also may be associated

with Stage 4 pressure ulcers.

The University of Texas San Antonio Diabetic Wound Classification System

The following classification uses a system of wound grade and stage to categorize wounds by severity. Wounds

are graded by depth, infection and ischemia.

Grade 0 represents a pre or postulcerative site.

Grade I ulcers are superficial wounds through the epidermis or epidermis and dermis but do not pene-

trate to tendon, capsule or bone.

Grade II wounds are penetrate to tendon or capsule.

Grade III wounds penetrate to bone or into a joint.

Within each wound grade there are three stages:

Clean wounds (A)

Non-ischemic infected wounds (B), Ischemic wounds (C)

Statistic

Approximately 20 % of patients with diabetes will develop foot ulceration in their lifetime

It has been estimated that for each new foot ulcer, the attributable cost for a middle-aged diabetic man in

the first two years is approximately $30,000

Treatment Concepts

The standard of care recommended by the American Diabetes Association is saline-moistened gauze

The wet-to-dry concept is no longer acceptable because if the gauze becomes dry before the next dres

sing change, it may cause damage to the wound bed and disrupt the healing process

Hydrocolloid dressings and hydrogels can maintain the moist wound environment while providing some

autolytic debridemen

Other dressings are impregnated with collagen, zinc, or other factors that stimulate wound healing

Specific Treatments

Treatment of ulcerations must be based upon the ETIOLOGY of the ulceration. Do NOT treat all ulcerations

the same!



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Ischemic Ulcerations

Begin with non-invasive testing

Transcutaneous oxygen measuremen

The ankle-brachial index (ABI)

The absolute toe systolic pressure

Continue to invasive testing

Arteriogram

Determine level of occlusion

Assess if patients are bypassable

Optimal ulcer healing requires adequate tissue perfusion. Thus, arterial insufficiency should be suspected

if an ulcer fails to heal

Vascular surgery consultation and possible revascularization should be considered when clinical signs of

ischemia are present in the lower extremity of a patient and the results of noninvasive vascular tests or

imaging studies suggest that the patient has peripheral arterial occlusive disease

If the patient is not a candidate for arterial bypass, consider the use of hemorrheologic agents.

Trental (Pentoxifylline)- lowers blood viscosity, and improves erythrocyte flexibility

Pletal (cilostazol)- inhibits cellular phosphodiesterase (PDE), especially PDE III

Ischemic ulcerations should NOT be debrided to bleeding. Wounds should be kept clean and dry with a dry

sterile dressing applied daily. It is important to keep these wounds free of infections as they can be limb and life

threatening. Close monitoring of these ulcerations and referrals to vascular specialists as well as nursing support is

essential to heal these ulcerations.

Neurogenic Ulcerations

In the diabetic foot, autonomic neuropathy has several common manifestations. First, denervation of dermal

structures leads to decreased sweating. This causes dry skin and fissure formation, which predispose the skin to

infection. In vascularly competent patients, this autosympathectomy may lead to increased blood flow, which has

been implicated as one of the primary etiologic factors in the development of Charcots joint and severe foot defor-

mity.2-4

NeurologicalPrevalence:

The prevalence of neuropathy increases with:

Age

Duration of diabetes

Presence of microvascular complications

Poor glycemic control

Neurological Examination

5.07 Semmes-Weinstein monofilament

10 grams of force

Loss of protective sensation Vibratory sensation

Position Sense

Light Touch

Sharp/Dull

These preliminary tests give the examiner an idea as to the level of sensation still present in the patients foot. If

any of these test are found to be abnormal or absent, further testing is required to demonstrate the severity. The

tests customarily ordered are the NCV and the EMG. Recently, Qualitative Sensory Testing performed with the



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Pressure-Specified Sensory Device has identified patients with earlier stages of sensation loss. However, this device

is limited to patients with signs of compression neuropathy as opposed to the distal symmetrical polyneuropathy

frequently encountered.

Patients with neuropathy should have a visual inspection at every visit to a health care provider.

Distal symmetrical polyneuropathy is an important predictor of ulcers and amputations.

Figure 2. Site Guide for Foot Screening

Complications of Peripheral Neuropathy

Sensory - loss of protective sensation

Pain, pressure, temperature

Motor - atrophy of the intrinsic muscles

flexion deformity

pressure under metatarsal heads and tips of toes

Autonomic - dyshidrosis and dry skin

also AV shunting fi bone and skin perfusion

Altered Biomechanics

Associated with an increased risk of ulceration and amputation.

Increased plantar pressure

Bony prominence

Limited joint mobility

Figure 3.



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Biomechanics - Bony deformity

Motor neuropathy

Atrophy intrinsic muscles

Hammertoe or clawtoe

Increased metatarsal pressure Plantar ulceration

Treatment of Neurogenic Ulcerations:

Debridement of ulcerations is absolutely essential for a number of reasons:

Removal of surrounding hyperkeratosis

Promote the release of growth factors

Provide for more granulation tissue formation

Allow epithelialization to occur without undermining of necrotic tissue

Mechanically remove debris

After adequate debridement has occurred, the choice of dressings is important. Dressings should provide a

protective layer around the ulceration and allow serous drainage to accumulate in the dressing away from the ulcera-

tion. The ideal dressing also allows for a moist wound environment as this has been determined to decrease thebacterial count. There are several commercially available products that are composed of calcium alginate which

were designed to accomplish these goals. The standard of care has been the use of the saline wet to dry dressings.

Today, these dressings have been modified so they do not dry on the ulcerated skin. The newer term is saline wet to

moist dressings. It has been shown that when a wet dressing is allowed to dry on an ulceration, removal of the dry

dressing may destroy the developing epithelium and actually hinder the wound healing process.

Newer Wound Care Products

As more research is being done on the molecular biology of wound healing, products that address specific fac-

tors are coming to the market. Regranex is one such product. It is platelet-derived growth factor that must be

applied once per day. It promotes the in-growth of blood vessels to the ulceration and the epithelialization process.

It requires the patient to perform daily dressing changes. It is applied to the ulcer and then covered for 12 hours.

The dressing is then removed, the wound is then cleansed and a saline dressing is applied for another 12 hours.

Patients selected for this therapy must be able to perform daily dressing changes and patients must be seen on a

weekly basis for debridement.

Orthopedic Biomechanical Devices

Removing or decreasing the absolute vertical pressures surrounding an ulceration must be achieved in order to

heal the ulcer. Use of orthoses, dispersion pads, and possibly a total contact cast all work to achieve this end. The

goal is to limit weight bearing on the area of high pressure and disperse it to another location. If a significant bony

prominence is encountered, which can not be accommodated by paddings and shoes, surgical intervention to

remove these areas of high pressure are recommended.

Finally, once an ulceration is healed, you are half done! The goal is to prevent the ulceration from returning. It

is imperative that the patient be followed closely and constantly educated about proper foot hygiene as well as main-

tenance of good glucose control. Debridement of hyperkeratosis and removal of areas of high pressure by the use of

accommodative orthoses or paddings will work to prevent ulcerations from leading to loss of the foot or lower

extremity.



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References

1. FromNutrition Today, March, 1999.

2. Armstrong DG, Todd WF, Lavery LA, Harkless LB, Bushman TR. The Natural History of Acute Charcots

Arthropathy in a Diabetic Foot Specialty Clinic. Diabet Med, 1997; 14: 357-63.

3. Edmonds ME, Clarke MB, Newton S, Barrett J, Watkins PJ. Increased Uptake of Bone

Radiopharmaceutical in Diabetic Neuropathy. Q J Med 1985; 57: 843-55.4. Brower AC, Allman RM. The Neuropathic Joint: A Neurovascular Bone Disorder. Radiol Clin North Am

1981; 19 :571-80.

Additional Readings

1. Lavery LA, Armstrong DG, Harkless LB.Classification of diabetic foot wounds.J Foot Ankle Surg1996;

35: 528-31.

2. Armstrong DG, Lavery LA, Harkless LB.Treatment-based Classification System for Assessment and Care

of Diabetic feet.J Am Podiatr Med Assoc1996; 86 : 311-6.

3. Orchard TJ, Strandness DE Jr. Assessment of Peripheral Vascular Disease in Diabetes. Report and reco

mendation of an international workshop sponsored by the American Heart Association and the American

Diabetes Association. 1820 September 1992; New Orleans, Louisiana.J Am Podiatr Med Assoc1993; 83:685-95.

4. LoGerfo FW, Coffman JD. Vascular and microvascular disease of the foot in diabetes. Implications for

foot care.N Engl J Med 1984; 311: 1615-9.

5. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention.

Diabetes Care 1990; 13: 513-21.

6. Caputo GM, Cavanagh PR, Ulbrecht JS, Gibbons GW, Karchmer AW. Assessment and Management of

Foot Disease in Patients with Diabetes.N Engl J Med 1994; 331: 854-60.

chapter 4b diabetes mellitus and wound care

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