Assessment and Management of Patients with
Diabetes
Mellitus
Growing problem
Estimated 7% of US population is diabetic
Twice that many have prediabetes
21% of those over 60 have diabetes
45% of new diagnoses are being made in
children and adolescents
Diabetes
Type I—beta cells destroyed by autoimmune
process
Type 2—decreased insulin production and
decreased sensitivity to insulin
Type 1 Diabetes Mellitus
Genetic susceptibility
Autoimmune
Glycosuria
Fat breakdown
DKA
Type 2 Diabetes Mellitus
Resistance
Decreased production
Generally no fat breakdown
HHNS
Type 2 Diabetes Mellitus
Exercise enhances action of insulin
Weight loss is cornerstone of treatment
Gestational Diabetes
Glucose intolerance during pregnancy
Placental hormones contributes to insulin
resistance
High risk:
glycosuria, family history, marked obesity
Native Americans, African Americans, Hispanics
and Pacific Islanders
Gestational Diabetes
Women of average risk tested between 24-28
weeks of gestation
Goals for glucose levels during pregnancy are
105 or less before meals; 130 or less after meals
Will have greater risk of developing Type 2 DM
later in life if weight not controlled
Clinical Manifestations
Polyuria
Polydipsia
Polyphagia
Fatigue, tingling or numbness in hands, slow
healing wounds and recurrent infections
Diagnostic findings
Fasting plasma glucose—125 mg/dL
Random sugar >200mg/dL
According to text, OGTT and IV glucose
tolerance test no longer used routinely—see latest guidelines
Gerontologic Considerations
Elevated blood glucose levels are also age
related
Increase with advancing age
Causes may be: increased fat tissue, decreased
insulin production, physical inactivity, decrease in lean body mass
Management
Nutritional
Exercise
Monitoring
Pharmacologic
Education
Dietary Management
Carbohydrate 45-65% total daily calories
Protein-15-20% total daily calories
Fats—less than 30% total calories, saturated
fats only 10% of total calories
Fiber—lowers cholesterol; soluble—legumes,
oats, fruits Insoluble—whole grain breads, cereals and some vegetables.
Both increase satiety. Slowing absorption time seems to lower glycemic index.
Dietary Management
Consistent, well-balanced small meals several
times per day
Exchange system or counting carbohydrates
Exercise and Diabetes
Exercise increases uptake of glucose by
muscles and improves utilization, alters lipid levels, increases HDL and
decreases TG and TC
If on insulin, eat 15g snack before beginning
Check BS before, during and after exercising
if the exercise is prolonged
Exercise and Diabetes
Avoid trauma to the feet
Avoid pounding activities that could cause
vitreous hemorrhage
Caution if CAD
Baseline stress test may be indicated
(especially in those older than 30 and with 2 or more risk factors for CAD)
Glucose monitoring
Patients on insulin should check sugars 2-4
times per day
Not on insulin, two or three times per week
(according to text)
Should check before meals and 2 hours after
meals
Parameters from physician very important
Continuous glucose monitoring
Subcutaneous sensor in abdomen
Download data q72h
Evaluates trends and efficacy of treatment
over 24h period
HGB A1C
Measures blood levels over 2-3 months (per
text)
High levels of glucose will attach to
hemoglobin
Helps to ensure that the patient’s glucometer
is accurate
Ketones
Check in pregnancy
During illness
If BS >240
Insulin therapy
Rapid acting—lispro (Humalog) and insulin
aspart (Novolog) onset 15’, peak 60-90’ and last from 2-4 hours
Short acting—regular. Onset is 30-60’, peak in
2-3h and last for 4-6 hours. Regular insulin is only kind for IV use.
Insulin Therapy
Intermediate insulins—NPH or Lente. Onset
3-4h, peak 4-12 hours and lst 16-20 hours. Names include Humulin N, Novolin N,
Humulin L, Novolin L
Long acting—Humulin Ultralente. Onset 6-8h,
peak 12-16 h and lasts 20-30h.
Peakless insulins: determir and glargine
Complications of Insulin Therapy
Local allergic reactions
Systemic allergic reactions
Insulin lipodystrophy (lipoatrophy or
lipohypertrophy)
Insulin resistance
Morning hyperglycemia—Dawn phenomenon
(nocturnal surges of growth hormone) so give dose at HS not before dinner
Complications of Insulin Therapy
Somogyi effect—nocturnal hypoglycemia followed
by rebound hyperglycemia-decrease evening dose of insulin
To determine cause, test at HS, 3am and upon
awakening
Methods of Insulin Delivery
Pens
Jet injectors
Insulin pumps—insulin is delivered at .5-2
units/hour. Most common risk of insulin pump therapy is ketoacidosis.
Implantable devices
Transplantation of pancreatic cells
Oral antidiabetic agents
Sulfonylureas—glipizide, glyburide and
glimepiride. Hypoglycemia
Biguanides—metformin. Lactic acidosis.
Alpha-glucosidase inhibitors—acarbose. Delay
absorption of CHO
Oral Agents
Non-sulfonylurea secretagogues—repaglinide.
Cause secretion of insulin.
Thiazolidinediones—pioglitazone and
rosiglitazone. Sensitize. Weight gain.Fertility. Liver.
Pramlintide (Symlin). Analogue of amylin. Used
with insulin. Injection.
Exanatide (Byetta). Incretin mimetic. Causes
satiety. Wt loss.
Januvia.
Teaching Plan
Education is critical
Simple pathophysiology
Treatment modalities
Recognition, treatment and prevention of acute
complications
When to call the doctor
Foot care, eye care, general hygiene, risk
factor management
Teaching patients to administer insulin
Storing insulin (may not refrigerate if used
within one month). Prefilled syringes should be stored standing up.
Syringes
Concentrations of insulin
Mixing insulins
Do not rotate area to area, use same anatomic
area
No need to aspirate
Acute Complications of Diabetes
Hypoglycemia—50-60 or less
DKA
HHNS
Hypoglycemia
Caused by too much insulin or oral agents, too
little food or excessive physical activity
Surge in epinephrine and norepinephrine
results in sweating, tremors, tachycardia, palpitations, nervousness and hunger
Hypoglycemia
CNS effects—inability to concentrate,
headache, lightheadedness, confusion, memory problems, slurred speech,
incoordination, double vision, seizures and even loss of consciousness.
Hypoglycemic unawareness
Related to autonomic neuropathy
Will not experience the sympathetic surge—with
sweating, shakiness, HA, etc.
Treatment for hypoglycemia
2-3 tsp. of sugar or honey
6-10 hard candies
4-6oz. of fruit juice or soda
3-4 commercially prepared glucose tablets
Recheck BS 15 minutes, same s/s, repeat
treatment. After improvement, then cheese and crackers or milk.
Extreme situations, give glucagon. (can cause
n/v). D50W.
Diabetic Ketoacidosis
Clinical features are:
1. Hyperglycemia
2. Dehydration and
electrolyte loss
3. acidosis
DKA
Three main causes: illness, undiagnosed and
untreated and decreased insulin
Other causes: patient error, intentional
skipping of insulin
Presentation of DKA
3 P’s
Orthostatic hypotension
Ketosis
GI s/s
Acetone breath
hyperventilation
Diagnostic Findings of DKA
BS between 300-800
Acidosis
Electrolyte abnormalities
Elevated BUN, creatinine and hct r/t
dehydration
Medical Management of DKA
Rehydrate with normal saline, then follow with
.45% NaCl then D5.45NS (or other)
Restore electrolytes
ECGs
Hourly blood sugars
IV insulin
Avoid bicarbonate as can affect serum K+
Nursing Management
Administer fluids
Insulin
Prevent fluid overload
Strict I&O
Follow lytes
ECG monitoring
Vital signs
Monitor patient responses to treatments
Hyperglycemic Hyperosmolar Nonketotic Syndrome
Predominated by hyperosmolarity and
hyperglycemia
Minimal ketosis
Osmotic diuresis
Glycosuria and increased osmolarity
Occurs over time
Blood sugar is usually over 600
HHNS
Occurs more often in older people
Type 2 diabetes mellitus
No ketosis
Do not usually have the concomitant n/v
Hyperglycemia, dehydration and hyperosmolarity
may be more severe than in DKA
Medical Management
Similar treatment as seen in DKA
Watch fluid resuscitation if history of heart
failure
ECG
Lytes monitoring
Fluids with potassium replacement
Nursing Management of HHNS
Monitor neurologically
Monitor ECG
Monitor vital signs
Labs
Hourly blood glucose monitoring
Insulin IV
Cautious correction of hyperglycemia to avoid
cerebral edema
Long term complications of Diabetes
Increasing numbers of deaths from
cardiovascular and renal complications
Renal (microvascular) disease is more common
in type 1 diabetics
Cardiovascular disease (macrovascular)
complications are more common in type 2 diabetics
Diabetic Vascular Diseases
Chronic hyperglycemia causes irreversible
structural changes in the basement membranes of vessels. Result is thickening
and organ damage.
Glucose toxicity affects cellular integrity
Chronic ischemia in microcirculatory
brances>>cause connective tissue hypoxia and microischemia
Diabetic Vascular Diseases
Up to 21% of diabetics have retinopathy at
time of diagnosis
Macrovascular Complications
Coronary artery disease
Cerebrovascular disease
Peripheral arterial disease
Management of Macrovascular Diseases
Modify/reduce risk factors
Meds for hypertension and hyperlipidemia
Smoking cessation
Control of blood sugars which will help reduce
TG
Microvascular Complications--Retinopathy
Diabetic retinopathy-leading cause of
blindness in those 20-74
Blood vessel changes—worst case scenario,
proliferative retinopathy. Also an increased incidence of cataracts and
glaucoma in diabetics.
Need regular eye exams
Control BP, control BS and cessation of
smoking can help
Microvascular complications-Nephropathy
Accounts for 50% of patients with ESRD
Earliest clinical sign of nephropathy is microalbuminuria.
Warrants frequent periodic monitoring for
microalbuminuria—if exceeds 30mg/24h on two consecutive random urines, need 24h
urine sample
Nephropathy
Diabetes causes hypertension in renal vessels
which cause leaking glomeruli, deposits in narrow vessels, scarring and
vascular damage
Microvascular disease-Nephropathy
Medical management: control BP (ACE or ARB)
Tx of UTIs
Avoid nephrotoxic agents, contrast dyes
Low sodium diet
Low protein diet
Tight glycemic control
Nephropathy
May require dialysis
May have co-existent retinopathy
Kidney transplantation—success now 75-80% for
5 years
Pancreas transplantation may also be performed
at time of kidney transplantation
Neuropathies
Group of diseases that affect all types of
nerves.
Includes peripheral, autonomic and spinal
nerves.
Prevalence increases with duration of the
disease and degree of glycemic control
Neuropathies
Capillary basement membrane thickening and
capillary closure may be present.
May be demyelination of the nerves, nerve
conduction is disrupted.
Two most common types of neuropathy are:
sensorimotor polyneuropathy and autonomic neuropathy.
Peripheral neuropathy
Manifestations:paresthesias, burning
sensations, numbness, decrease in proprioception.
Charcot foot can result from abnormal weight
distribution on joints secondary to lack of proprioception
Management of Peripheral Neuropathies
Pain management in the form of TCAs, Dilantin,
Tegretol, Neurontin, mexilitene, and TENS. Cymbalta has been recommended. Also,
the drug Lyrica (pregabalin)
Autonomic Neuropathies
Cardiac, gastrointestinal and renal systems
Cardiac—myocardial ischemia may be painless
GI—delayed gastric emptying with early
satiety, nausea, bloating, diarrhea or constipation
Urinary retention—decreased sensation of
bladder, neurogenic bladder
Autonomic neuropathy—hypoglycemia unawareness
No longer feel shakiness, sweating,
nervousness and palpitations associated with hypoglycemia
The inability to detect warning signs of
hypoglycemia can place the patient at very high risk
Autonomic neuropathy-sudomotor neuropathy
Patient will have a decrease or absence of
sweating of the extremities with compensatory increase in upper body sweating.
Autonomic neuropathy—sexual dysfunction
Decreased libido in women
Anorgasmia
ED in men
UTI and vaginitis
Retrograde ejaculations
Management of neuropathies
Early detection, periodic f/u on patient’s
with cardiac disease
Monitor BP frequently for s/s orthostatic
hypotension
Low fat diet, frequent small meals, close BS
monitoring and use of prokinetic medications
Meticulous skin care
Foot and Leg Problems
Sensory loss
Sudomotor neuropathy leads to dry, cracking
feet
PAD—so poor wound healing/gangrene
Lowered resistance to infection
Management of Foot and Leg Problems
Teaching patient foot care-inspect feet and
shoes daily
Examine feet every time goes to doctor
See podiatrist at least annually
Closed toe shoes
Trimming toenails
Good foot hygiene
Glycemic control is the key to preventing
complications
Special issues
Hyperglycemia in the hospital—increased food,
decreased insulin, steroids, IV dextrose,overly vigorous treatment of
hypoglycemia, inappropriate holding of insulin
Hypoglycemia in the hospital—overuse of
sliding scale, lack of insulin change when dietary intake withheld, overzealous
treatment of hyperglycemia, delayed meals after insulin given
Alterations in diet—enteral, TPN and clear
liquid diets
Latest guidelines in diabetes management
according to Clinical Advisor
Risk factors for Diabetes Mellitus
Family history
Cardiovascular disease
Obesity
Sedentary lifestyle
History of impaired fasting glucose or
impaired glucose tolerance
Hypertension
PCOS
Gestational diabetes
Risk Factors continued
Ethnic groups at high risk—Asian Americans,
Native Americans, Latinos, Blacks, Pacific Islanders
Recommended Screening
Fasting glucose levels
Oral glucose tolerance testing using 75g of
Glucola
Fasting glucose of 100-125mg/dL=prediabetes
Fasting level >126 is diagnostic
OGTT>200 is diagnostic
Reducing Risk
Weight reduction
Exercise of 150 minutes per week
Comprehensive diet
education
Controlling blood sugar
Hemoglobin A1C less than or equal to 6.5%
Fasting plasma glucose <110
Two hour postprandial sugar <140
Comprehensive education
Treating Type I Diabetes
Basal bolus insulin and mealtime rapid-acting
insulin analog (lispro, aspart, or glulisine)
Basal insulin should include determir or
glargine
Continuous subcu insulin infusion or pump very
effective
Treating Type I diabetes
Pump is ideal for those with very “brittle
diabetes” or hypoglycemic unawareness
Pump also very useful in pregnant women
Symlin (pramlintide) should be considered to
enhance glycemic control and control weight
Treating Type I diabetes
If poor control—check 2h postprandial and at
2AM
Check urine ketones if BS>250
Type 2 diabetes
Diagnosed 9-12 years after they develop the
condition
HgbA1C 6-7% needs monotherapy
Choices are: thiazolidinedione, metformin,
insulin secretagogue (sulfonylureas, Prandin), alpha glucosidase inhibitor or a
dipeptidyl-peptidase-4 inhibitor (Januvia)
Using insulin in Type 2 DM
Usually will meet patient resistance
May benefit from a 70/30 combination
Requires frequent blood glucose monitoring
Cardiac risk factors
50% of those with Type 2 Diabetes Mellitus
have hypertension, 25% in type 1
Need ARB or ACE inhibitor
Dyslipidemia needs to be addressed—goal of LDL
<100 (<70 if DM and CAD); HDL >40 in men and >50 in women, TG
<150
Cardiac risk factors
Treat with statins, Zetia (ezetimibe) or fibrates if TG
>400***
Nutrition
CHO 45-65% of total calories
Protein 15-20%
Fiber intake 25-50g/day---blunts the glycemic
response
Dietary fat <30% w/saturated fat <10%
and cholesterol <300mg/day
Type 2 diabetes
Evaluate treatment response within 3 months
HgbA1C >8% in patient who has been educated
about DM should begin insulin therapy
Questions--Discussion
0 التعليقات:
إرسال تعليق