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Diabetes Mellitus And Wound Care

Nabil Fahim, DPM Mark G. Mandato, DPM

Diabetes Mellitus can be thought of as a group of metabolic disorders characterized by hyperglycemia that results 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 population) 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), amputations & blindness. As of 1993, it is estimated that over $100 billion will be spent treating diabetes in United States each year.

Diagnosis of Diabetes Mellitus

Screening 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 performed 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 discontinuation 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

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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 protocols 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 for development 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 unknown The 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.

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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

1 or 2 injections per day Daily self-monitoring Quarterly HbA1c Pregnant women treated intensively Quarterly visits

Intensive Therapy Group

3 Daily injections or insulin pump 4 or more blood glucose tests daily Hospitalization for initiation to help Frequent dietary instruction to help achieve goals Monthly clinic visits

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

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%

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 longterm outcome will be measurably improved.

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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 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 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 70% NPH with 30% Regular 75% NPL with 25% Lispro premixed (Humalog insulin Pen)

NPH

Lente Family

Premixed insulin:
70/30 75/25

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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 through Continuous 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 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 Regular insulin before each meal, NPH, Lente or Ultralente at bedtime Limitations: Meals must be no more than five hours apart 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 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 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

3 Injection Regimen

4 Injection Regimen

Continuous Subcutaneous Insulin Infusion

Indications

Contra-indications

Goals of Treatment:
The goals treatment in the type 1 diabetic are the normalization of blood glucose and the prevention of complications from the disease process as well as achieve normal blood pressure. Also, to maintain lipids near normal (cholesterol < 200; triglycerides <150) and prevent microvascular and macrovascular complications. To these ends, protocols have been developed specific for patients with type 1 diabetes.

Self Monitoring of Blood Glucose

Treatment goal:
Maintain plasma glucose level near normal with frequent (4x/day) monitoring
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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 Biochemical index Preprandial glucose Bedtime glucose Hemoglobin A1C Goal 80-120 mg/dL 100-140 mg/dL < 7% Take Action at <80 or >140 > 8% >140 or <100

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

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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 hormones

Signs
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) History and physical Electrolytes and CBC Urinalysis and urine culture Serum ketones Blood gasses, pH and blood cultures EKG Chest x-ray

Initial Workup

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.

Normal FBS 2 hr PP HbA1c 115 140 6%

Good 140 200 8%

Poor >200 >235 >10%

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 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 retinopathy

Risks

Diet 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

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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 classes of oral drugs used to treat diabetes.

Classes of Oral Hypoglycemic Agents

Sulfonylureas Biguanides Alpha-glucosidase inhibitors Thiazolidinediones Meglitinides 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. Decrease hepatic glucose production and may improve insulin sensitivity at the receptor and post rece tor levels 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 Type 1 diabetes Pregnancy Allergy to sulfonylureas Avoid long acting agents such as Chlorpropamide in elderly patients prone to hypoglycemia

Sulfonylureas:

Secondary effects:

Clinical Uses of Sulfonylureas

Absolute Contraindications

Relative Contraindications

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Agents
First Generation
TolbutamideOrinase ChlorpropamideDiabinese AcetohexamideDymelor TolazamideTolinase Glipizide- Glucotrol Glimepiride- Amaryl Glyburide- Diabeta, Micronase, Glynase

Second Generation

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 treated with oral or IV glucose or glucagon injection. Acarbose- Precose Miglitol- Glyset

Agents

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 < 25 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

Biguanides

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 tissue, usually with inflammation. Ulcerations in the diabetic patient have been called in the literature diabetic ulcerations. 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 necrosis 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 FScan 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 pediartery 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 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

Neuropathic Ulcerations

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 individualswith 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 presents clinically as an abrasion, blister, or shallow center. Stage 3 - Full thickness, skin loss involving damage to or necrosis of subcutaneous tissue that may extenddown 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 penetrate 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) 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 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

Statistic

Treatment Concepts

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 deformity.2-4 Neurological Prevalence: 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 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 ulceration. The ideal dressing also allows for a moist wound environment as this has been determined to decrease the bacterial 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 factors 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 maintenance 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. 2. 3. 4. From Nutrition Today, March, 1999. 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. 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. Brower AC, Allman RM. The Neuropathic Joint: A Neurovascular Bone Disorder. Radiol Clin North Am 1981; 19 :571-80.

Additional Readings
1. 2. 3. Lavery LA, Armstrong DG, Harkless LB. Classification of diabetic foot wounds. J Foot Ankle Surg 1996; 35: 528-31. Armstrong DG, Lavery LA, Harkless LB. Treatment-based Classification System for Assessment and Care of Diabetic feet. J Am Podiatr Med Assoc 1996; 86 : 311-6. 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 Assoc 1993; 83: 685-95. 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. Pecoraro RE, Reiber GE, Burgess EM. Pathways to diabetic limb amputation. Basis for prevention. Diabetes Care 1990; 13: 513-21. 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.

4. 5. 6.

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