Chapter 4b Diabetes Mellitus and Wound Care
Transcript of 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
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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.
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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.
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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
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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
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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.