1. Caring for the Diabetic
Client
N331 Health Maintenance & Restoration
2. Diabetes Statistics
* Total: 29.1 million children and adults in the United
States—9.3 % of the population—have diabetes.
* Diagnosed: 21.0 million people
* Undiagnosed: 8.1 million people
* Prediabetes: 86 million people
* New Cases: 1.7 million new cases of diabetes are
diagnosed in people aged 20 years and older in 2012.
American Diabetes Association National Diabetes Statistics Report, 2014
3. Diabetes by Race/Ethnicity
* 7.6% of non-Hispanic whites
* 9.0% of Asian Americans
* 12.8% of Hispanics
* 13.2% of non-Hispanic blacks
* 15.9% of American Indians/Alaskan Natives
American Diabetes Association National Diabetes Statistics Report, 2014
4. Cost of Diabetes
* $245 billion: Total costs of diagnosed diabetes
in the United States in 2012
* $176 billion for direct medical costs
* $69 billion in reduced productivity
* Average medical expenditures among people
with diagnosed diabetes were 2.3 times
higher than what expenditures would be in
the absence of diabetes.
American Diabetes Association National Diabetes Statistics Report, 2014
5. U.S. Diabetes Facts
NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2011
Source: 2005–2008 National Health and Nutrition Examination Survey
6. Age-Adjusted Prevalence of Obesity and Diagnosed
Diabetes Among U.S. Adults Aged 18 Years or older
Obesity (BMI ≥30 kg/m2)
Diabetes
1994
2010
No Data <14.0% 14.0-17.9% 18.0-21.9% 22.0-25.9%
>26.0%
1994
2000
2000
No Data <4.5% 4.5-5.9% 6.0-7.4% 7.5-8.9%
>9.0%
CDC’s Division of Diabetes Translation. National Diabetes Surveillance System available at
http://www.cdc.gov/diabetes/statistics
2010
7. Risk Factors
* Age
* Ethnicity and family history
* Body weight
* Hypertension
* Dyslipidemia
* Metabolic Syndrome
* History gestational diabetes or delivered baby > 9 lb
* Polycystic ovary syndrome
* Prediabetes (Impaired glucose tolerance/Impaired fasting glucose)
8. ↵*Criteria for testing for diabetes in
asymptomatic adult individuals
• Testing should be considered in all adults who are overweight (BMI ≥25 kg/m2*) and have additional risk
factors:
• physical inactivity
• first-degree relative with diabetes
• high-risk race/ethnicity (e.g., African American, Latino, Native American, Asian American, Pacific Islander)
• women who delivered a baby weighing >9 lb or were diagnosed with GDM
• hypertension (≥140/90 mmHg or on therapy for hypertension)
• HDL cholesterol level <35 mg/dl (0.90 mmol/l) and/or a triglyceride level >250 mg/dl (2.82 mmol/l)
• women with polycystic ovarian syndrome (PCOS)
• A1C ≥5.7%, IGT, or IFG on previous testing
• other clinical conditions associated with insulin resistance (e.g., severe obesity, acanthosis nigricans)
• history of CVD
_____________________________________________________________________________________________
_
• In the absence of the above criteria, testing for diabetes should begin at age 45 years.
_____________________________________________________________________________________________
_
• If results are normal, testing should be repeated at least at 3-year intervals, with consideration of more
frequent testing depending on initial results and risk status.
9. Normal Physiology
Ingestion of meal
Increased
plasma glucose
Increased plasma
Amino acids
Insulin Secreted
Glycogen
synthesis
Amino acid uptake
+ protein synthesis
FFA + glycerol
Transport +
TGL synthesis
Glucose uptake
into muscle
cells & adipocytes
10. Normal Insulin Secretion
Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise
rapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward
preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate
absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low
and fairly constant, with a slight increase at dawn.
11. Pathophysiology of Diabetes
Decreased insulin
Supply/use
Glycogen catabolism
In liver & muscle
Decreased transport of glucose into cells
Protein catabolism
&
gluconeogenesis
Fat catabolism
FFA + glycerol
produced
Cellular starvation
Ketones
Produced by-product
of fat metabolism
Cortisol
Epinephrine
Growth hormone
Hyperglycemia
12. Major Classifications
* Type 1 diabetes
* Type 2 diabetes
* Gestational diabetes
* Prediabetes
* Impaired glucose tolerance
* Impaired fasting glucose
13. Pathophysiology
* Type 1:
* Autoimmune
destruction of
pancreatic beta
cells thought to
major cause.
* Leads to absolute
insulin deficiency
* 5-10% of diabetics
* Type 2:
* Insulin resistance
* Decreased insulin
receptors or inability
to bind to muscle and
adipose cells leading
to inability to
transport glucose
into cell
* Defect in pancreatic
beta cell secretion
* 90-95% of diabetics
15. Common Clinical Manifestations
* Type 1: Acute onset
* 3 P’s
* Hyperglycemia, ketonuria
* Weight loss, weakness, fatigue, dizziness
* Type 2: Onset may be slow
* Blurry vision, skin infections, vaginitis
* Hyperglycemia
* Target organ damage may already be present
16. Natural Progression of Type 2 Diabetes
Postprandial glucose
-20 -10 0 10 20 30
Years of Diabetes
Plasma
Glucose
Relative
b-Cell
Function
Insulin resistance
Insulin secretion
126 mg/dL
Fasting glucose
Prior to diagnosis After diagnosis
Adapted from Bergenstal et al. 2000; International Diabetes Center.
17. The Changing Face of Diabetes
* Rapid rise of type 2 DM
in minority populations.
* Increased rate of type 2
DM among children and
adolescents.
* Increased recognition
of type 1 DM in adults.
* Atypical forms.
<10 years 10–19 years
Source: SEARCH for Diabetes in Youth Study
NHW=non-Hispanic whites; NHB=non-Hispanic blacks; H=Hispanics; API=Asians/Pacific Islanders; AI=American Indians
18. Diagnosing Diabetes
Fasting Plasma Casual Plasma Oral Glucose A1C
Glucose (FPG)* Glucose * Tolerance Test*
(Preferred Test)
________________________________________________________________________________________
Diabetes FPG >126 mg/dl Casual plasma Two-hour plasma > 6.5 %
glucose >200 mg/dl glucose (2hPG)
>200 mg/dl
_______________________________________________________________________________________
Prediabetes
Impaired Impaired Fasting Impaired Glucose 5.7-6.4 %
Glucose Glucose (IFG)=FPG Tolerance (IGT) =
Homeostasis 100 -125 mg/dl 2hPG >140 and
<199 mg/dl
_______________________________________________________________________________________
Non-Diabetic FPG <100 mg/dl 2hPG <140 mg/dl < 6.5 %
*In the absence of unequivocal hyperglycemia, these need to be repeated on the second day
19. Diagnostic Tests Used to Assess
and Manage Diabetes
* Blood glucose – random, fasting,
postprandial, capillary blood glucose
* Glucose tolerance test
* HbgA1C or A1C
* Glycosylated albumin
* Ketonuria
* Proteinuria:albuminuria, microalbuminuria
* BUN, creatinine, GFR
20. Knowledge Check…
A patient screened for diabetes at a clinic has a fasting
plasma glucose of 120 mg/dL (6.7 mmol/L). The nurse
explains to the patient that this value:
1. Is diagnostic for diabetes.
2. Is normal, and diabetes is not a problem.
3. Reflects impaired glucose tolerance, which is an early
stage of diabetes.
4. Indicates an intermediate stage between normal
glucose use and diabetes.
22. Preventing Diabetes Complications
Treatment
*Glucose control
*Diet
*Exercise
*Weight loss – Bariatric surgery
*Diabetes medications – Oral, Insulin
*Blood pressure control – ACE inhibitors or ARB’s
*Blood lipid control – Statins
*Preventive care practices for eyes, kidneys, feet, teeth
and gums
*Aspirin as directed by physician
NIDDK, National Diabetes Statistics fact sheet. HHS, NIH, 2005.
23. Nursing Role
* Know therapeutic management plan
* Assess client’s knowledge and self management
ability
* Assessment and management of complications
* Client education
24. Evidenced-Based Practice
* Diabetes Control & Complications Trial (DCCT)
* Compared intensive treatment to standard treatment in 1,441 people with type 1 diabetes
* 60% reduction in risk between intensively treated group and standard group for retinopathy,
nephropathy, neuropathy (New England Journal of Medicine, 1993).
* Strict glucose control in type 1 diabetes reduces the risk of atherosclerosis (New England Journal of
Medicine, 2003).
* Hyperglycemia is an independent marker of in-hospital mortality in patients with
undiagnosed diabetes (Guillermo et. al.,2002).
* Patients who are encouraged to become actively involved in managing their
diabetes and feel they are competent to do so tend to be less depressed, more
satisfied and have lower blood sugar levels (Williams et al., 2005).
* NICE-SUGAR study
25. Blood Glucose Monitoring
* Plasma glucose (venous)
* Capillary blood glucose – some meters
have a 15% difference between capillary
and venous blood. Capillary blood glucose
is lower.
* Continuous blood glucose monitoring –
subcutaneous sensor
* Testing new non-invasive
methods,eg.wristband.
26. Goals for Glycemic Control
A1C* < 7.0%** Only 43%
achieve goal
Pre- Prandial
glucose
90-130 mg/dl
Postprandial
plasma glucose
< 180 mg/dl
*For non-pregnant individuals
** goal for patients in general; <6% for individual patients if feasible/safe
Diabetes Care: Supp.1. 2011
27. Correlation of A1C with Average Glucose
A1C (%)
Mean plasma
glucose
mg/dl mmol/l
6 126 7.0
7 154 8.6
8 183 10.2
9 212 11.8
10 240 13.4
11 269 14.9
12 298 16.5
These estimates are based on ADAG data of
∼2,700 glucose measurements over 3 months per
A1C measurement in 507 adults with type 1, type 2,
and no diabetes. The correlation between A1C and
average glucose was 0.92 (51). A calculator for
converting A1C results into estimated average
glucose (eAG), in either mg/dl or mmol/l, is available
at http://professional.diabetes.org/eAG.
28. 28
Management Principles for Older Adults
with Complex Illness/Frailty
* Overall treatment goals need to be individualized
8%
* Potential for hypoglycemic to occur from over aggressive treatment or
from undesired adverse effects of medications or inadequate meal plans
* In the case of frail older adults, where the risk of hypoglycemia exceed
benefit from tight control, the HgbA1c value can be used as a means of
monitoring treatment without a target goal
*Used with permission from AACN GNEC Institute
HgbA1c 6.5% to 7%
levels
higher functioning older
persons with diabetes
frail older adults with
functional impairment and
limited life expectancy
29. Inpatient Glycemic Targets
* Critically ill patients:
- glucose results 140-180 mg/dl
- tighter control for some populations (CABG)
* Non-critically ill patients:
- glucose results < 180 mg/dl
Diabetes Care 2011
30. 30
ADA Recommendations: Hospital Care
* Identify in record as having DM and have order for blood
glucose monitoring
* Sliding scale insulin NOT recommended
* Hypoglycemia plan established and episodes racked
* HbA1c drawn if none available form previous 2-3 months
* Education plan and follow-up developed
* New hyperglycemia - plans for follow-up testing documented
* Assess: Pneumococcal and yearly influenza
31. Non-pharmacological Medical Therapy for
Type 2 Diabetes
Consistent carbohydrate intake
Optimize BG Control
Improve blood lipids
Control blood pressure
Monitor blood glucose to
adjust therapy
Moderate weight loss –
Bariatric surgery
Increase physical activity
Modify fat and
calorie content
Space meals
32. Nutritional Management: Goals
* Improve glucose and lipid levels
* Consistent day-to-day food intake.
* Weight management.
* Provide adequate nutrition across lifespan.
33. Macronutrient Recommendations
* CHO 40-60%
* Protein 15-20% (reduced if client has renal disease)
* Fat 30% or less
* Less than 7% saturated fat
* No transfats
* Vitamin & mineral requirements are the same as
general population.
34. Calories, Carbohydrates and Fat
* Carbohydrate counting
* Calorie control diet, e.g.
* 1800 kcal ADA diet
* Choose My Plate
35. Example: Carbohydrate Counting
* Fruits, vegetables, fruit juice
* Breads, cereals, grains, pastries, starchy vegetables.
* Milk and yogurt
* If carbohydrate counting, 1 portion = 15 gm CHO
* Typical meal = 4-5 portions (60-75 gm) CHO
* Carb counting activity
* Breakfast 45g CHO
* Lunch 60g CHO
* Dinner 60g CHO
36. Focus on Type of Fat
* Saturated (butter, hydrogenated fats)
* Polyunsaturated (vegetable oil)
* Monounsaturated- olive, canola
* Transfatty acids – in processed foods, e.g. partially
hydrogenated . .
* Omega 3 fatty acids – cold water fish, walnuts
38. Exercise Readiness Assessment:
* Cardiovascular evaluation prior.
* Eye exam to r/o risk for retinal detachment or
vitreous hemorrhage with exercise.
* Assess for safety concerns related to
peripheral neuropathy.
* Monitor CBG & B/P pre and post exercise.
* Consistency
39. Nursing Role: Exercise
* Be knowledgeable regarding exercise plan.
* Monitor for safety hazards.
* Pre/post exercise assessment to monitor tolerance of
activity.
* If BG < 100 snack prior;100-150 snack after; > 250 +
ketones, no exercise.
41. Where do hypoglycemic agents
Diabetic State
interact?
CHO Intake
Intestinal
absorption
Decreased insulin
secretion
Increased
hepatic
glucose output Decreased peripheral
glucose uptake
42. Oral Medications
Class Mechanism of Action
Sulfonylureas
glipizide (Glucotrol), glyburide (Micronase,
Diabeta) , glimepride (Amaryl)
Secretagogue: stimulates insulin secretion from beta
cell
Meglitinides
repaglinide (Prandin), nateglinide (Starlix)
Stimulate a rapid and short lived release of insulin
from the pancreas
Biguanide
metformin (Glucophage), metformin ER (Glumetza)
Reduces hepatic glucose production; Sensitizer:
increases insulin sensitivity to peripheral uptake, may
cause lactic acidosis if kidneys are not functioning
properly
Thiazolidineodione
pioglitazone (Actos), rosiglitazone (Avandia)
Sensitizer: increases insulin sensitivity to peripheral
uptake, causes edema, weight gain, not for heart
failure pts.
a-glucosidase inhibitor
acarbose (Precose), miglitol (Glyset)
Slows absorption of glucose, slows postprandial
hyperglycemia
DPP-4 Inhibitors
sitagliptin (Januvia), saxagliptin (Onglyza),
linagliptin (Tradjenta)
Enhances the incretin system, stimulates release of
insulin from pancreatic B cells.
SGLT2 Inhibitors
Canagliflozin (Invokana)
dapagliflozin (Farxiga)
Sodium-glucose transporter 2 (SGLT2) works in the
kidney to reabsorb glucose, and this new class of
43. Therapeutic Agents for Diabetes
Class Mechanism of Action
Bile Acid Sequestrant
(BAS)
colesevelam (Welchol)
A cholesterol-lowering medication that also reduces
blood glucose levels in patients with diabetes
Dopamine Receptor
Agonist
Bromocitine (Cycloset)
Increases CNS dopamine receptor activity, increases
insulin sensitivity and decreases A1C by improving
postprandial hepatic glucose metabolism and
increasing glucose uptake
Incretins
Exenatide (Byetta)
Exenatide ER once-weekly
(Bydureon)
Liraglutide (Victoza)
Stimulates release of insulin, decrease glucagon
secretion, increase satiety, decrease gastric emptying
Injectable
Amylin Analog
Pramlintide (Symlin)
Decrease gastric emptying, decrease glucagon
secretions and endogenous glucose output from the
liver, increase satiety. For type 1 diabetes.
44. Insulin Therapy in Diabetes
* All patients with type 1 diabetes require insulin.
* Many patients with type 2 diabetes will eventually
need insulin.
* As insulin deficiency progresses, a more physiologic
multi-component insulin regimen will be required to
adequately replace normal insulin secretion.
- Basal insulin
- Meal-Related (prandial, bolus) insulin
47. Basal / Bolus Concept
Can you think like a pancreas ???
48. Review of Basal/Bolus Concept
* The use of two insulins with different characteristics to mimic the
pancreas.
* With the advent of long acting analogs insulin, we can mimic the
pancreas by giving a slow release, virtually peakless, 24 hour
basal insulin.
* Rapid acting analogs are preferred over Regular for meal or
prandial dose to cover carbohydrates consumed at meals.
* The purpose of supplemental insulin (correction algorithm) is to
bring a pre-meal elevated glucose level to target quickly and
safely, used in addition to basal and bolus insulin.
* Blood sugars stay in target due to the basal/bolus insulins.
52. Normal Insulin Secretion
Fig. 49-1. Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise
rapidly in blood and peak at about 1 hour. After meals, insulin concentrations promptly decline toward
preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate
absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low
and fairly constant, with a slight increase at dawn.
53. Critical Thinking Questions…
* Which insulin is the only one that can be given IV?
* Why might different routes be chosen?
* Subc.
* IV
54. Insulin Delivery Devices
* Syringes
* 3/10cc = 30 units
* 1/2cc = 50 units
* 1cc = 100 units
* Insulin pens – prefilled or refillable
* Needle-free technology: Jet injectors
* Insulin pumps
55. Insulin Pump
Fig. 49-7. A, OmniPod Insulin Management System. The Pod holds and delivers insulin. B, The Personal Diabetes
Manager (PDM) wirelessly programs insulin delivery via the Pod. The PDM has a built-in glucose meter.
56. Steps to Successful Insulin
Management
• Monitor CBG at appropriate times based on insulin
dosing, meals and activity
• Assess for hyper and hypoglycemia at appropriate
times: Know when insulins are peaking
• Insulin Storage:
* Should be administered at room temperature.
* Can keep a vial of insulin at room temperature for 28-30
days.
* Avoid temperature extremes; maintain at 36-86 degrees F.
* Unused,unopened vials should be stored in refrigerator
57. Side Effects
* Most serious:
* Side effects related to the injection:
* Other adverse effects:
* Lipodystrophy- happens when injections sites
are not rotated
* Lipoatrophy
* Lipohypertrophy
58. Management of Hypoglycemia
* Potential causes?
* Didn’t eat enough
* Skipped a meal
* Assessment of signs and symptoms
* Mild to severe
* Adrenergic symptoms
* Neuroglycopenic symptoms
* What class of drugs mask S/S?
* Management
59. Acute Complications - Hypoglycemia
Mild
* shaking
* sweating
* fast heartbeat
* dizziness
* hunger
Moderate Severe
* impaired vision seizure
* Headache unresponsive
* Irritable coma
60. Hypoglycemia - Treatment
* Treatment mild-moderate hypoglycemia with 15 grams fast acting
carbohydrate
* glucose tablets
* glucose gel
* 4 oz orange juice
* 8 oz milk
* Test blood sugar in 15 minutes
* Repeat treatment if needed
* Treat moderate-severe hypoglycemia or if NPO
* Glucagon
* D50
* Test blood sugar in 15 minutes
* Repeat treatment if needed
62. Acute Complications
Hyperglycemia: Diabetic Ketoacidosis
(DKA)
Critical Thinking Questions…
*What are some possible causes of DKA?
*Assessment
* What might you expect the BG to be?
* What fluid and electrolyte disturbances may result?
* What might the pH and HCO3 be?
* What clinical signs and symptoms may result?
65. Cardiac monitoring is initiated for a patient in diabetic
ketoacidosis. The nurse recognizes that this measure is
important to identify:
1. Dysrhythmias resulting from hypokalemia.
2. Fluid overload resulting from aggressive fluid
replacement.
3. The presence of hypovolemic shock related to
osmotic diuresis.
4. Cardiovascular collapse resulting from the effects of
excess glucose on cardiac cells.
66. Acute Complications
Hyperosmolar Hyperglycemic Syndrome
(HHNS)
Critical Thinking Questions…
*Severe hyperglycemia without ketosis
*Who is at risk?
*Assessment – what clinical manifestations may occur?
* Blood glucose level?
* Acid/base balance?
* VS
* Other S/S?
68. Sick Day Management
* Blood glucose monitoring
* CHO intake
* Insulin needs
* Ketone testing (Type I diabetes)
* When to notify healthcare personnel
* Prevention
69. A patient with type 1 diabetes calls the clinic with
complaints of nausea, vomiting, and diarrhea. It is most
important that the nurse advise the patient to:
1. Hold the regular dose of insulin.
2. Drink cool fluids with high glucose content.
3. Check the blood glucose level every 2 to 4 hours.
4. Use a less strenuous form of exercise than usual until
the illness resolves.
70. Hyperglycemia May Lead to Long-Term
Complications in Multiple Organs
Microvascular Complications
Neuropathy
Macrovascular Complications
Cerebrovascular
Disease
Diagnosed in 37.2% patients
with diabetes > 35 years old
Peripheral
Vascular Disease
Retinopathy
12 % of all new cases of blindness
Nephropathy
>40% new cases ESRD
Heart Disease
Diabetes Control and Complications Trial Research Group. N Engl J Med. 1993;329:977-986.
Stratton IM et al. BMJ. 2000;321:405-412 with permission from the BMJ Publishing Group
www.cdc.gov.
60-70% have mild to severe
nervous system damage
73. Nursing Management Nephropathy:
Impaired urinary elimination; Risk FVE
* Monitor:
* Intake/output
* Serum electrolytes
* Bun, creatinine, GFR
* Lung sounds, o2 sats, edema
* Monitor need to adjust drug
dosages based on renal
clearance
74. Nursing Management Retinopathy and
Neuropathy: Disturbed sensory perception
* Neuropathy:
* Foot care
* Fall prevention for postural
hypotension
* Prevention of aspiration,
attention to
hyper/hypoglycemia with
gastroparesis
* Prevention of urinary
retention
* Monitor for fixed heart rate
with activity
76. Diabetes & Heart Disease
The risk for development
of coronary artery disease is
2- to 4-fold greater and the
risk of cardiac events of a
lethal nature subsequently
higher when diabetes is
present. Insulin resistance
even without diabetes
increases coronary risk.
77. Foot Care
* Daily foot care and inspection
* Always wear protective shoes/slippers
* Wear good-fitting shoes
* Cotton socks vs nylon socks
* Avoid home remedies for corns,
calluses, ingrown toenails
* Cut nail straight across
* Avoid temperature extremes
* Seek immediate medical attention for
any injury or problem
78. 78
Impact of Comorbidities
* Older adults, over age 65 and in particular, those of
advanced old age, typically experience
* Multiple comorbidities
* Higher rates of physical disabilities functional impairment
* Geriatric syndromes
* Depression
* Cognitive impairment
* Falls
* Urinary incontinence
*Used with permission from AACN GNEC Institute
79. Gerontologic Considerations
* Prevalence increases with age.
* Presence of delayed psychomotor function could
interfere with treating hypoglycemia.
* Must consider patient’s own desire for treatment and
coexisting medical problems
* Recognize limitations in physical activity, manual
dexterity, and visual acuity
* Education based on individual’s needs, using slower
pace
80. 80
Impact of Geriatric Syndromes
Poly-pharmacy
Depression Cognitive
impairment Geriatric
Persistent Syndromes
Injurious fall pain Urinary
incontinence
* These syndromes are included in current screening
recommendations for older adults with a diagnosis of Type 2
Diabetes
* Further screening for these events within three to six months
of a new diagnosis should accompany the initial evaluation
period
*Used with permission from AACN GNEC Institute
81. 81
Atypical Presentation of Clinical
Conditions in Older Adults with
Type 2 Diabetes
Integument Skin infections (examples include non-healing venous stasis
ulcers; non-healing traumatic wounds)
Cardiovascular Chest pain (examples include acute coronary syndromes; de
novo cardiac ischemia) 1
Neurological
Altered level of consciousness with non- focal neurological
signs (examples include stupor associated with no focal
neurological deficits and hyperglycemic, hyperosmolar, non-ketotic
coma) Paresthesia of distal extremities (diabetic
peripheral neuropathy) 1
Gento-urinary Erectile dysfunction; Vaginitis
*Used with permission from AACN GNEC Institute
82. 82
Urinary Incontinence
* Older women with Type 2 Diabetes at increased risk for
urinary incontinence due to chronic hyperglycemia
* Physiologically, excess glucose in the serum causes
hyperosmolarity and shifts in fluid balance
* Chronic hyperglycemia directly effects the genito-urinary
system by causing symptoms of frequency, polyuria, nocturia
and potentially urinary incontinence
* Screen: Urinary incontinence at history taking and review of
systems during the initial evaluation of the older adult with
Type 2 Diabetes
*Used with permission from AACN GNEC Institute
84. 84
Self-Management Education
* Older adults with diabetes have special educational needs
secondary to sensory and other deficits related to the aging
process
* Educational plan:
* Include an assessment of the individual’s priorities
* Use easily read or heard messages and proceed at a slower
pace utilizing significant others and caregivers in
instruction
* Elderly persons with diabetes need assistance with
organization of information so they can slowly adapt it to
their activities of daily living
*Used with permission from AACN GNEC Institute
85. Ideally, the goal of patient diabetes education is to:
1. Make all patients responsible for the management of
their disease.
2. Involve the patient’s family and significant others in
the care of the patient.
3. Enable the patient to become the most active
participant in the management of the diabetes.
4. Provide the patient with as much information as soon
as possible to prevent complications of diabetes.
86. Case Study
* 52-year-old woman was diagnosed with type 2 diabetes 6 years ago.
* Did not follow up with recommendations for care
* She works as a banking executive and gets little exercise.
* She has gained 18 pounds over the past year and eats a high-fat diet.
* Complaining of weakness in her right foot
* Began 1 month ago
* Difficult to dorsiflex and feels numb
* Also complains of an itching rash in her groin area
* Has had rash on and off for many years
* Worse when weather is warm
* Increased thirst and frequent nighttime urination
* Denies other weakness, numbness, changes in vision
* BP 162/98
87. Case Study
* Random glucose test 253 mg/dL
* Hb A1C 9.1%
* Urine dipstick positive for glucose and negative for
protein
* Wet prep of smear from rash consistent with Candida
albicans
* ECG with evidence of early ventricular hypertrophy by
voltage
88. Discussion Questions
1. She wants to know why all of these changes have
been happening to her body. How would you
explain this to her?
2. What is the priority nursing intervention?
3. What teaching should be done with her?
Editor's Notes
Prevalence: In 2012, 29.1 million Americans, or 9.3% of the population, had diabetes.
In 2010 the figures were 25.8 million and 8.3%.
Undiagnosed: Of the 29.1 million, 21.0 million were diagnosed, and 8.1 million were undiagnosed.
In 2010 the figures were 18.8 million and 7.0 million.
Prevalence in Seniors: The percentage of Americans age 65 and older remains high, at 25.9%, or 11.8 million seniors (diagnosed and undiagnosed). Worldwide by 2025, adults over age 60 will comprise two-thirds of the population with diabetes. With an aging population projected to be 70 million individual over age 65 years by 2030, the impact of type 2 diabetes will only intensify. For those with type 2 diabetes, the greatest prevalence will be seen in those over age 80 . diabetes afflicts at least 20 percent of individuals over the age of 65 and nearly 40 percent of those age 65-75 years may be affected by hyperglycemia.
Type 2 diabetes is an important public health problem for all adults, but particularly for older adults over age 65.
New Cases: The incidence of diabetes in 2012 was 1.7 million new diagnoses/year; in 2010 it was 1.9 million.
Prediabetes: In 2012, 86 million Americans age 20 and older had prediabetes; this is up from 79 million in 2010.
Deaths: Diabetes remains the 7th leading cause of death in the United States in 2010, with 69,071 death certificates listing it as the underlying cause of death, and a total of 234,051 death certificates listing diabetes as an underlying or contributing cause of death.
The rates of diagnosed diabetes by race/ethnic background are:
7.6% of non-Hispanic whites
9.0% of Asian Americans
12.8% of Hispanics
13.2% of non-Hispanic blacks
15.9% of American Indians/Alaskan Natives
$245 billion: Total costs of diagnosed diabetes in the United States in 2012
$176 billion for direct medical costs
$69 billion in reduced productivity
After adjusting for population age and sex differences, average medical expenditures among people with diagnosed diabetes were 2.3 times higher than what expenditures would be in the absence of diabetes.
Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood; they peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.
Same process as starvation with one major difference--
Discussion of Type I, Type II and Prediabetes on next slides
GDM will be covered during HMR Families
Medications can also affect blood glucose control - steriods
These graphs show the typical progressive nature of type 2 diabetes in terms of 2 key indices: increasing plasma glucose level (top panel) and decline in relative -cell function as reflected by the drop in endogenous insulin and rise in insulin resistance (lower panel).
In the natural history of type 2 diabetes, insulin resistance rises, insulin secretion falls, and glucose levels begin to rise before diabetes is diagnosed.
Based on the natural history, type 2 diabetes is a disease of progressive insulin failure as shown in the graphic model developed by researchers at the International Diabetes Center.1
Before the onset of diabetes, glucose levels start to rise, with a slightly sharper increase in the postprandial value than in fasting glucose. Both postprandial and fasting plasma glucose levels continue to rise if diabetes is left untreated.2
Prior to the diagnosis of diabetes, resistance of cell receptor sites to insulin starts to increase, while insulin secretion by -cells decreases. Insulin resistance reaches a peak and remains constant. Endogenous insulin secretion continues to decline over the course of diabetes.2
References:
1. Kendall DM. Postprandial blood glucose in the management of type 2 diabetes: the emerging role of incretin mimetics. Available at: http://www.medscape.com/viewarticle/515693. Accessed April 21, 2006.
2. Ramlo-Halsted BA, Edelman SV. The natural history of type 2 diabetes: implications for clinical practice. Prim Care. 1999;26:771-789.
There are now four ways to diagnose diabetes: fasting plasma glucose, casual plasma glucose, and the oral glucose tolerance test. And most recently added A1C
There are three stages leading to diabetes: pre-diabetes, impaired fasting glucose, and then diabetes.
Answer: 3
Rationale: Impaired fasting glucose (fasting blood glucose level between 100 and 126 mg/dL) and impaired glucose tolerance (2-hour plasma glucose level between 140 and 199 mg/dL) represent an intermediate stage between normal glucose homeostasis and diabetes. This stage is called prediabetes.
Leading cause of adult blindness
Results in 2- to 4-fold increase in cardiovascular risk
Nearly double the rates of diagnosed depression
People with diabetes and their health care providers can reduce the occurrence of diabetes complications by controlling the levels of blood glucose, blood pressure, and blood lipids, and by receiving other preventive care practices in a timely manner.
Studies have found that improved glycemic control benefits people with either type 1 or type 2 diabetes. In general, every percentage point drop in A1C blood test results (i.e., from 8.0% to 7.0%) reduces the risk of microvascular complications—like eye, kidney, and nerve diseases—by 40%.
Blood pressure control reduces the risk of heart disease or stroke among persons with diabetes by 33% to 50%, and the risk of microvascular complications by about 33%.
Improved cholesterol or blood lipids control (for example, HDL, LDL, and triglycerides) can reduce cardiovascular complications by 20% to 50%.
Detecting and treating diabetic eye disease with laser therapy can reduce the development of severe vision loss by an estimated 50% to 60%.
Comprehensive foot care programs can reduce amputation rates by 45% to 85%.
Treating early diabetic kidney disease by lowering blood pressure can reduce the decline in kidney function by 30% to 70%.
Studies have shown that an aspirin a day can help prevent diabetes complications.
Reference
National Institute of Diabetes and Digestive and Kidney Diseases. National Diabetes Statistics fact sheet: general information and national estimates on diabetes in the United States, 2005. Bethesda, MD: U.S. Department of Health and Human Services, National Institutes of Health, 2005.
The largest study to date, NICE-SUGAR, a multicenter, multinational RCT, compared the effect of intensive glycemic control (target 81–108 mg/dl, mean blood glucose attained 115 mg/dl) to standard glycemic control (target 144–180 mg/dl, mean blood glucose attained 144 mg/dl) on outcomes among 6,104 critically ill participants, the majority of whom (&gt;95%) required mechanical ventilation (354). Ninety-day mortality was significantly higher in the intensive versus the conventional group (78 more deaths; 27.5% vs. 24.9%, P = 0.02) in both surgical and medical patients. Mortality from cardiovascular causes was more common in the intensive group (76 more deaths; 41.6% vs. 35.8%; P = 0.02). Severe hypoglycemia was also more common in the intensively treated group (6.8% vs. 0.5%; P &lt; 0.001). The precise reason for the increased mortality in the tightly controlled group is unknown. The results of this study lie in stark contrast to a famous 2001 single-center study that reported a 42% relative reduction in intensive-care unit (ICU) mortality in critically ill surgical patients treated to a target blood glucose of 80–110 mg/dl (350). Importantly, the control group in NICE-SUGAR had reasonably good blood glucose management maintained at a mean glucose of 144 mg/dl, only 29 mg/dl above the intensively managed patients. Accordingly, this study&apos;s findings do not disprove the notion that glycemic control in the ICU is important. However, they do strongly suggest that it is not necessary to target blood glucose values &lt;140 mg/dl, and that a highly stringent target of &lt;110 mg/dl may actually be dangerous.
Unfortunately, many individuals with diabetes do not achieve goals for glycemic control.
If testing and diagnosis occur earlier it may make it easier for the patient to keep their A1C low.
Summary of glycemic recommendations for many nonpregnant adults with diabetes
A1C&lt;7.0%*Preprandial capillary plasma glucose70–130 mg/dl* (3.9–7.2 mmol/l)Peak postprandial capillary plasma glucose† Goals should be individualized based on*:
duration of diabetes
age/life expectancy
comorbid conditions
known CVD or advanced microvascular complications
hypoglycemia unawareness
individual patient considerations
More or less stringent glycemic goals may be appropriate for individual patients.
Postprandial glucose may be targeted if A1C goals are not met despite reaching preprandial glucose goals.
&lt;180 mg/dl* (&lt;10.0 mmol/l)Postprandial glucose measurements should be made 1–2 h after the beginning of the meal, generally peak levels in patients with diabetes.
The two established goals for HgbA1c levels for adults with diabetes (less than 7.0 percent and 6.5 percent) should be applied to higher functioning older persons with diabetes.
There are no data to support different targets in older adults; however, the AGS guidelines recommend that for frail older adults with functional impairment and limited life expectancy, a more modest goal of hemoglobin A1c of 8 percent is acceptable.
Overall treatment goals need to be individualized.
Of concern is the potential for hypoglycemic to occur from over aggressive treatment or from undesired adverse effects of medications or inadequate meal plans. In the case of frail older adults, where the risk of hypoglycemia exceed benefit from tight control, the HgbA1c value can be used as a means of monitoring treatment without a target goal.
• Goals for blood glucose levels:
◦ Critically ill patients: Insulin therapy should be initiated for treatment of persistent hyperglycemia starting at a threshold of no greater than 180 mg/dl (10 mmol/l). Once insulin therapy is started, a glucose range of 140–180 mg/dl (7.8–10 mmol/l) is recommended for the majority of critically ill patients. (A)
◦ More stringent goals, such as 110–140 mg/dl (6.1–7.8 mmol/l) may be appropriate for selected patients, as long as this can be achieved without significant hypoglycemia. (C)
◦ Critically ill patients require an intravenous insulin protocol that has demonstrated efficacy and safety in achieving the desired glucose range without increasing risk for severe hypoglycemia. (E)
◦ Non–critically ill patients: There is no clear evidence for specific blood glucose goals. If treated with insulin, the premeal blood glucose target should generally be &lt;140 mg/dl (7.8 mmol/l) with random blood glucose &lt;180 mg/dl (10.0 mmol/l), provided these targets can be safely achieved. More stringent targets may be appropriate in stable patients with previous tight glycemic control. Less stringent targets may be appropriate in those with severe comorbidites. (E)
•Diabetes care in the hospital Recommendations
• All patients with diabetes admitted to the hospital should have their diabetes clearly identified in the medical record. (E)
• All patients with diabetes should have an order for blood glucose monitoring, with results available to all members of the health care team. (E)
Scheduled subcutaneous insulin with basal, nutritional, and correction components is the preferred method for achieving and maintaining glucose control in noncritically ill patients. (C) Using correction dose or “supplemental” insulin to correct premeal hyperglycemia in addition to scheduled prandial and basal insulin is recommended. (E)
• Glucose monitoring should be initiated in any patient not known to be diabetic who receives therapy associated with high risk for hyperglycemia, including high-dose glucocorticoid therapy, initiation of enteral or parenteral nutrition, or other medications such as octreotide or immunosuppressive medications. (B) If hyperglycemia is documented and persistent, treatment is necessary. Such patients should be treated to the same glycemic goals as patients with known diabetes. (E)
•A hypoglycemia management protocol should be adopted and implemented by each hospital or hospital system. A plan for treating hypoglycemia should be established for each patient. Episodes of hypoglycemia in the hospital should be documented in the medial record and tracked. (E)
•All patients with diabetes admitted to the hospital should have an A1C obtained if the result of testing in the previous 2–3 months is not available. (E)
•Patients with hyperglycemia in the hospital who do not have a diagnosis of diabetes should have appropriate plans for follow-up testing and care documented at discharge. (E)
Traditional nutrition advice focused on avoiding sugar & losing weight. Therapy now focuses on other lifestyle strategies (as shown here) that can contribute to improvements in metabolic control. No clear answer regarding which of these should be the first priority, rather, the strategy is to individualize therapy & set goals based on what the client chooses to focus on.
The field trial of NPGs for Type 2 showed evidence of lifestyle changes by 6 weeks to 3 months. At that point, changes in therapy were made.
Consistent carbohydrate intake: Carbohydrate is the macronutrient with the greatest impact on BG levels. Individuals need to be provided with the basic guidelines for the amount of carbohydrate to eat at meals and snacks, e.g., 3 to 4 carbohydrate choices/meal (60 g/meal plus/minus 15 g) and 1-2 carbohydrate choices (15-30 g) at snacks. With the help of BG monitoring, the amount eaten at a particular meal or snack from day to day can be evaluated and adjustments made accordingly to find the tolerable “carbohydrate load”.
Modify calorie and fat content; reduce saturated fat: Calorie and fat content of the diet need to be modified based on individualized treatment goals; due to the increased risk of CVD for those with diabetes, most individuals will benefit by decreasing saturated fat intake
Space meals: This will be discussed more on a subsequent slide. Due to a slowed first phase insulin release, spacing meals and distributing food intake throughtout the day may be beneficial.
Increase physical activity: The benefits of physical activity for those with type 2 diabetes are well documented. Physical activity is known to enhance blood glucose uptake by the muscle during or shortly after the activity and to improve insulin sensitivity. It is recommended that individuals adopt a lifetime activity model : An approach developed by the Centers for Disease Control and American College of Sports Medicine. The 1995 report states that all Americans need 30 minutes daily of moderate intensity activity: walking 3-4 mph, golf (walking), general home cleaning; if light intensity used, needs to be longer duration or couple times/day: walking 1-2 mph, vacuuming, golf (riding cart)
Monitoring blood glucose: Testing BG postprandially provides tangible information to assist the person with diabetes to take a more active role in evaluating food choices and the CHO load tolerable for them at a particular meal. Patients also need to be reminded that while the meal plan has a significant impact on BG, there are several variables which affect BG, and that food is not always the reason for variances.
Recommendations for management of diabetes
Macronutrients in diabetes management
•The best mix of carbohydrate, protein, and fat may be adjusted to meet the metabolic goals and individual preferences of the person with diabetes. (E)
•Monitoring carbohydrate, whether by carbohydrate counting, choices, or experience-based estimation, remains a key strategy in achieving glycemic control. (A)
•For individuals with diabetes, the use of the glycemic index and glycemic load may provide a modest additional benefit for glycemic control over that observed when total carbohydrate is considered alone. (B)
•Saturated fat intake should be &lt;7% of total calories. (A)
•Reducing intake of trans fat lowers LDL cholesterol and increases HDL cholesterol (A), therefore intake of trans fat should be minimized. (E)
Other nutrition recommendations
•If adults with diabetes choose to use alcohol, daily intake should be limited to a moderate amount (one drink per day or less for adult women and two drinks per day or less for adult men). (E)
•Routine supplementation with antioxidants, such as vitamins E and C and carotene, is not advised because of lack of evidence of efficacy and concern related to long-term safety. (A)
•Individualized meal planning should include optimization of food choices to meet recommended dietary allowance (RDA)/dietary reference intake (DRI) for all micronutrients. (E)
Physical activity Recommendations
•People with diabetes should be advised to perform at least 150 min/week of moderate-intensity aerobic physical activity (50–70% of maximum heart rate). (A)
•In the absence of contraindications, people with type 2 diabetes should be encouraged to perform resistance training three times per week. (A)
Exercise in the presence of nonoptimal glycemic control
Hyperglycemia.
When people with type 1 diabetes are deprived of insulin for 12–48 h and are ketotic, exercise can worsen hyperglycemia and ketosis (155); therefore, vigorous activity should be avoided in the presence of ketosis. However, it is not necessary to postpone exercise based simply on hyperglycemia, provided the patient feels well and urine and/or blood ketones are negative.
Hypoglycemia.
In individuals taking insulin and/or insulin secretagogues, physical activity can cause hypoglycemia if medication dose or carbohydrate consumption is not altered. For individuals on these therapies, added carbohydrate should be ingested if pre-exercise glucose levels are &lt;100 mg/dl (5.6 mmol/l). Hypoglycemia is rare in diabetic individuals who are not treated with insulin or insulin secretagogues, and no preventive measures for hypoglycemia are usually advised in these cases.
Slide 6-22
INSULIN TACTICS
Comparison of Human Insulins and Analogs
Insulin has been used therapeutically for more than 70 years. In general, human insulin, synthesized by genetically altered microorganisms, has a more rapid onset of action and a shorter duration of action than previous preparations derived from animal pancreas. Regular human insulin has an onset of action ranging from about 30 to 60 minutes with peak concentrations achieved at between 2 and 4 hours. The “intermediate-acting” insulins NPH has gradual onset and peak effects usually between 4 and 8 hours, and a total duration of 10 to 20 hours.
Short-acting insulin analogs (lispro and aspart) have very desirable action profiles at mealtimes because they have an onset of action ranging from 5 to 15 minutes; the peak of action occurs 1 hour after injection, and the insulin effect practically vanishes 4 hours after administration. Insulin glargine is a long-acting analog insulin that has essentially no peak. Glargine is absorbed within 1 to 2 hours and has a plasma concentration about 50% lower than that observed with NPH, but twice the duration of action.
There are many tools at your disposal. You must decide what is best for your patient. There is no right or wrong; just know what to expect and patient preferences.
Regular insulin acts in 30 min
NPH acts in a couple hours
Insulin is recognized as a high risk medication –
Should be labeled clearly, insulin separated in different locations and double checked by another nurse
There are many tools at your disposal. You must decide what is best for your patient. There is no right or wrong; just know what to expect and patient preferences.
Normal endogenous insulin secretion. In the first hour or two after meals, insulin concentrations rise rapidly in blood; they peak at about 1 hour. After meals, insulin concentrations promptly decline toward preprandial values as carbohydrate absorption from the gastrointestinal tract declines. After carbohydrate absorption from the gastrointestinal tract is complete and during the night, insulin concentrations are low and fairly constant, with a slight increase at dawn.
Regular insulin is the only one allowed to be given via IV
A, OmniPod Insulin Management System. The Pod holds and delivers insulin.
B, The Personal Diabetes Manager (PDM) wirelessly programs insulin delivery via the Pod. The PDM has a built-in glucose meter.
Most serious = hypoglycemia,analphylaxis, hypersensitivity
Local side effects = inflammation andl ocal allergic reactions, tend to decrease over time, less with human insulins, rotate sites, avoid alcohol
Hypoglycemia is the leading limiting factor in the glycemic management of type 1 and insulin-treated type 2 diabetes
Mild hypoglycemia may be inconvenient or frightening to patients with diabetes, and more severe hypoglycemia can cause acute harm to the person with diabetes or others, if it causes falls, motor vehicle accidents, or other injury. A large cohort study suggested that among older adults with type 2 diabetes, a history of severe hypoglycemia was associated with greater risk of dementia.
Severe hypoglycemia (where the individual requires the assistance of another person and cannot be treated with oral carbohydrate due to confusion or unconsciousness) should be treated using emergency glucagon kits, which require a prescription. Those in close contact with, or having custodial care of, people with hypoglycemia-prone diabetes (family members, roommates, school personnel, child care providers, correctional institution staff, or coworkers), should be instructed in use of such kits. An individual does not need to be a health care professional to safely administer glucagon.
•Individuals with hypoglycemia unawareness or one or more episodes of severe hypoglycemia should be advised to raise their glycemic targets to strictly avoid further hypoglycemia for at least several weeks, to partially reverse hypoglycemia unawareness and reduce risk of future episodes.
Hypoglycemia Recommendations
•Glucose (15–20 g) is the preferred treatment for the conscious individual with hypoglycemia, although any form of carbohydrate that contains glucose may be used. If SMBG 15 min after treatment shows continued hypoglycemia, the treatment should be repeated. Once SMBG glucose returns to normal, the individual should consume a meal or snack to prevent recurrence of hypoglycemia.
•Glucagon should be prescribed for all individuals at significant risk of severe hypoglycemia, and caregivers or family members of these individuals should be instructed in its administration. Glucagon administration is not limited to health care professionals.
Treatment of hypoglycemia (plasma glucose &lt;70 mg/dl) requires ingestion of glucose- or carbohydrate-containing foods. The acute glycemic response correlates better with the glucose content than with the carbohydrate content of the food. Although pure glucose is the preferred treatment, any form of carbohydrate that contains glucose will raise blood glucose. Added fat may retard and then prolong the acute glycemic response. Ongoing activity of insulin or insulin secretagogues may lead to recurrence of hypoglycemia unless further food is ingested after recovery.
Somogyi – rebound hyperglycemia following hypoglycemia—normal eveing BG, low during noc, counterreg. Hormones increase BG. Rx with less evening insulin.
Dawn – Increased BG due to 3 am growth hormone secretion –Rx with more bedtime insulin
Happens with type 1 diabetes
Blood sugar between 300-1500
Not taking enough insulin or any
Undiagnosed
Potassium levels go up
S=s
nausea
Vomiting
Dehydrated
Abdominal pain
Impaired conciousness
Acute weight loss
Kussmal respirations
Metabolic events leading to diabetic ketoacidosis and diabetic coma
Take each goal, how will it be achieved?
Answer: 1
Rationale: Electrolytes are depleted in diabetic ketoacidosis. Osmotic diuresis occurs with depletion of sodium, potassium, chloride, magnesium, and phosphate. Hypokalemia may lead to ventricular dysrhythmias such as premature ventricular complexes and bradycardia.
Blood sugar over 2000
Severe dehydrations
No kussmal respirations
Change in LOC \
More common in older adults
Gove fluids more slowly
Immunization Recommendations
•Annually provide an influenza vaccine to all diabetic patients at least 6 months of age.
•Administer pneumococcal polysaccharide vaccine to all diabetic patients ≥2 years of age. A one-time revaccination is recommended for individuals &gt;64 years of age previously immunized when they were &lt;65 years of age if the vaccine was administered &gt;5 years ago. Other indications for repeat vaccination include nephrotic syndrome, chronic renal disease, and other immunocompromised states, such as after transplantation.
Influenza and pneumonia are common, preventable infectious diseases associated with high mortality and morbidity in the elderly and in people with chronic diseases People with diabetes may be at increased risk of the bacteremic form of pneumococcal infection and have been reported to have a high risk of nosocomial bacteremia, which has a mortality rate as high as 50% .
The Centers for Disease Control and Prevention (CDC) Advisory Committee on Immunization Practices recommends influenza and pneumococcal vaccines for all individuals with diabetes (http://www.cdc.gov/vaccines/recs/).
Answer: 3
Rationale: If a person with type 1 diabetes mellitus is ill, he or she should test blood glucose levels at least at 2-to-4-hour intervals to determine the effects of this stressor on the blood glucose level.
Diabetes may lead to long-term complications as a result of injury to the large and small vasculature. Microvascular complications include disorders of the eye (diabetic retinopathy), kidney (nephropathy), and nervous system (neuropathy)1. Injury to the large vessels results in diseases of the cerebrovascular, cardiovascular, and peripheral vascular systems,2 leading to clinical outcomes such as stroke, heart disease, and amputations.
Between 1984 and 2001, the incidence for end stage renal disease (ESRD) attributable to diabetes increased by 388%. The incidence increased from 29.7 to 144.8 per 1,000,000 population.
In 2003, among persons with diabetes age 35 years and older, 38.1% reported being diagnosed with cardiovascular disease (ie, coronary heart disease, stroke, or other heart conditions). In the same year, 22.0% of adults with diabetes age 18 years and older reported visual impairment (ie, trouble seeing even with their glasses or contact lenses).3
Conversely, evidence from the DCCT and UKPDS studies, among others, has shown that treatment to control HbA1C can substantially reduce the risk of end-organ damage.
In the UKPDS, for example, each 1% reduction in mean HbA1C was associated with a reduction in the range of 14% to 30% for macrovascular complications and a reduction in the range of 30% to 40% for microvascular complications.4
References:
1. Nathan, DM. Long-term complications of diabetes . N Eng J Med. 1993;328:1676-1685.
2. American Diabetes Association. Diagnosis and classification of diabetes . Diabetes Care. 2005;28:S37-S42.
3. Centers for Disease Control and Prevention. http://www.cdc.gov/diabetes/statistics/esrd/Fig4.htm; http://www.cdc.gov/diabetes/statistics/visual/fig2.htm; http://www.cdc.gov/diabetes/statistics/cvd/fig3.htm Accessed April 5, 2006.
4. Stratton IM, Adler AI, Neil HAW, et al, on behalf of the UK Prospective Diabetes Study Group. Association of glycaemia with macrovascular and microvascular complications of type 2 diabetes (UKPDS 35): prospective observational study. BMJ. 2000;321:405-412.
Summary of recommendations for glycemic blood pressure and lipid control for most adults with diabetes
A1C &lt;7.0%*
Blood pressure &lt;130/80 mmHg†
Lipids
LDL cholesterol &lt;100 mg/dl (&lt;2.6 mmol/l)‡
•↵*More or less stringent glycemic goals may be appropriate for individual patients. Goals should be individualized based on: duration of diabetes, age/life expectancy, comorbid conditions, known CVD or advanced microvascular complications, hypoglycemia unawareness, and individual patient considerations.
•↵†Based on patient characteristics and response to therapy, higher or lower systolic blood pressure targets may be appropriate.
•↵‡In individuals with overt CVD, a lower LDL cholesterol goal of &lt;70 mg/dl (1.8 mmol/l), using a high dose of a statin, is an option.
Retinopathy screening and treatment Recommendations
General recommendations
•To reduce the risk or slow the progression of retinopathy, optimize glycemic control.
•To reduce the risk or slow the progression of retinopathy, optimize blood pressure control.
Screening
•Adults and children aged 10 years or older with type 1 diabetes should have an initial dilated and comprehensive eye examination by an ophthalmologist or optometrist within 5 years after the onset of diabetes.
•Patients with type 2 diabetes should have an initial dilated and comprehensive eye examination by an ophthalmologist or optometrist shortly after the diagnosis of diabetes.
•Subsequent examinations for type 1 and type 2 diabetic patients should be repeated annually by an ophthalmologist or optometrist. Less frequent exams (every 2–3 years) may be considered following one or more normal eye exams. Examinations will be required more frequently if retinopathy is progressing.
•High-quality fundus photographs can detect most clinically significant diabetic retinopathy. Interpretation of the images should be performed by a trained eye care provider. While retinal photography may serve as a screening tool for retinopathy, it is not a substitute for a comprehensive eye exam, which should be performed at least initially and at intervals thereafter as recommended by an eye care professional.
•Women with preexisting diabetes who are planning a pregnancy or who have become pregnant should have a comprehensive eye examination and should be counseled on the risk of development and/or progression of diabetic retinopathy. Eye examination should occur in the first trimester with close follow-up throughout pregnancy and for 1 year postpartum.
Nephropathy screening and treatment Recommendations
General recommendations
•To reduce the risk or slow the progression of nephropathy, optimize glucose control.
•To reduce the risk or slow the progression of nephropathy, optimize blood pressure control.
Screening
•Perform an annual test to assess urine albumin excretion in type 1 diabetic patients with diabetes duration of 5 years and in all type 2 diabetic patients starting at diagnosis.
•Measure serum creatinine at least annually in all adults with diabetes regardless of the degree of urine albumin excretion. The serum creatinine should be used to estimate GFR and stage the level of chronic kidney disease (CKD), if present.
Treatment
•In the treatment of the nonpregnant patient with micro- or macroalbuminuria, either ACE inhibitors or ARBs should be used.
•While there are no adequate head-to-head comparisons of ACE inhibitors and ARBs, there is clinical trial support for each of the following statements:
◦In patients with type 1 diabetes, with hypertension and any degree of albuminuria, ACE inhibitors have been shown to delay the progression of nephropathy.
◦In patients with type 2 diabetes, hypertension, and microalbuminuria, both ACE inhibitors and ARBs have been shown to delay the progression to macroalbuminuria.
◦In patients with type 2 diabetes, hypertension, macroalbuminuria, and renal insufficiency (serum creatinine &gt;1.5 mg/dl), ARBs have been shown to delay the progression of nephropathy.
•If one class is not tolerated, the other should be substituted.
•
Reduction of protein intake to 0.8–1.0 g · kg body wt−1 · day−1 in individuals with diabetes and the earlier stages of CKD and to 0.8 g · kg body wt−1 · day−1 in the later stages of CKD may improve measures of renal function (urine albumin excretion rate, GFR) and is recommended. (B)
•
When ACE inhibitors, ARBs, or diuretics are used, monitor serum creatinine and potassium levels for the development of acute kidney disease and hyperkalemia. (E)
•
Continued monitoring of urine albumin excretion to assess both response to therapy and progression of disease is recommended. (E)
•
When eGFR &lt;60 ml/min/1.73 m2, evaluate and manage potential complications of CKD. (E)
•
Consider referral to a physician experienced in the care of kidney disease when there is uncertainty about the etiology of kidney disease (heavy proteinuria, active urine sediment, absence of retinopathy, rapid decline in GFR), difficult management issues, or advanced kidney disease. (B)
Foot care Recommendations
•For all patients with diabetes, perform an annual comprehensive foot examination to identify risk factors predictive of ulcers and amputations. The foot examination should include inspection, assessment of foot pulses, and testing for loss of protective sensation (10-g monofilament plus testing any one of: vibration using 128-Hz tuning fork, pinprick sensation, ankle reflexes, or vibration perception threshold).
•Provide general foot self-care education to all patients with diabetes.
Amputation and foot ulceration, consequences of diabetic neuropathy and/or PAD, are common and major causes of morbidity and disability in people with diabetes. Early recognition and management of risk factors can prevent or delay adverse outcomes.
The risk of ulcers or amputations is increased in people who have the following risk factors:
•Previous amputation
•Past foot ulcer history
•Peripheral neuropathy
•Foot deformity
•Peripheral vascular disease
•Visual impairment
•Diabetic nephropathy (especially patients on dialysis)
•Poor glycemic control
•Cigarette smoking
Older adults over age 65, those of advanced old age, typically experience multiple comorbidities, higher rates of physical disabilities and functional impairment, and/or geriatric syndromes such as depression, cognitive impairment, falls and urinary incontinence than younger cohorts.
A major reason for the increased prevalence is that the process of aging is associated with a reduction in β-cell function, decreased insulin sensitivity, and altered carbohydrate metabolism.
Compounding the challenge, diabetes has been found to contribute to a greater rate of decline in cognitive function.
As with any group, diet and exercise are recommended as therapy for older adult patients with diabetes. This should take into account functional limitations that may interfere with physical activity and the ability to prepare meals.
Current knowledge and evidence-based research surrounding six common geriatric syndromes are presented.
Falls:
Autonomic neuropathy, when it causes orthostatic hypotension commonly plagues the Type 2 Diabetic
Fall occurs: When an older Type 2 Diabetic stands quickly without support and non-existent orthostatic hypotension
Accentuated with anti-hypertensive medications and volume deficit
Screen: Orthostatic blood pressure
Urinary Incontinence:
Older women with Type 2 Diabetes at increased risk for urinary incontinence due to chronic hyperglycemia
Physiologically, excess glucose in the serum causes hyperosmolarity and shifts in fluid balance
Chronic hyperglycemia directly effects the genito-urinary system by causing symptoms of frequency, polyuria, nocturia and potentially urinary incontinence
Screen: Urinary incontinence at history taking and review of systems during the initial evaluation of the older adult with Type 2 Diabetes
Reference: Adapted from: American Association of Diabetes Educators, A Core Curriculum for Diabetes Edition, 5th edition,
Older women with type 2 diabetes are at increased risk for urinary incontinence due to chronic hyperglycemia.
Physiologically, excess glucose in the serum causes hyperosmolarity and shifts in fluid balance.
Chronic hyperglycemia directly effects the gento-urinary system by causing symptoms of frequency, polyuria, nocturia and potentially urinary incontinence.
Screening for urinary incontinence begins with its inclusion in history taking and review of systems during the initial evaluation of the older adult with type 2 diabetes.
Strong evidence exists as to the added value of geriatric focused patient education and patient-oriented interventions on positive health outcomes for the older adult.
Older adults with diabetes have special educational needs secondary to sensory and other deficits related to the aging process.
The educational plan should include an assessment of the individual’s priorities.
Answer: 3
Rationale: The goal of diabetes education is to enable the patient to become the most active participant in his or her own care.
Dawn phenomenon- hormones are released in the morning that effects the release of insulin
Her lack of glucose control has affected multiple other parts of her body, including the nerves in her lower extremities, cardiovascular function, and ability to fight off infection.
Treatment of hyperglycemia, neuropathy, and hypertension, and, more important, patient teaching.
Stress the importance of adhering to her medical regimen and monitoring her blood glucose regularly. Teach her the repercussions if she does not do these things.
