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Diabetes in Critical Care Rhonda Jensen, RN, MS, CDE
Diabetes• Diabetes affects more than 29.1 million people in
the United States• Another 86 million people have pre-diabetes• During the last decade, diabetes prevalence has
risen 76% among people in their 30s• Incidence: >800,000 new cases diagnosed yearly• >2,000 cases diagnosed each day• Increasing incidence of type 2 in children and
adolescents• By 2025, the number is projected to surpass 300
million, making the disease pandemic
Two main types of DiabetesType 1 Diabetes
Autoimmune reaction to pancreatic beta cells
Pancreas makes little or no insulin
Type 2 Diabetes
Cells do not use insulin well (insulin resistance)
Liver makes too much sugar
May make large amounts of insulin
Ability for pancreas to make insulin decreases over time
Diagnostic testing Ketones – presence in the urine will
generally indicate type 1 diabetes Islet cell antibodies (ICA)- indicate active
autoimmunity directed against pancreatic beta cells and their product (insulin) Anti – GAD antibodies (Glutamic acid
decarboxylase C-peptide levels – clinical measure of
endogenous insulin levels (fasting 0.78 to 1.89ng/mL)
Type 1 Diabetes
1 in 10 people with Diabetes have type 1
Most people are under age 20 when diagnosed
Body can no longer make insulin
Insulin is always needed for treatment
Type 2 Diabetes9 out of 10 people with Diabetes have type 2
Type 2 is becoming more common in all age groups
Type 2 is more likely in people who:
Are overweightBelong to certain ethnic groupsHave a family history of type 2 diabetesHave had gestational diabetesAre inactive
Diabetes Diagnosis
Less than 100 mg/dLNormal
100-125 mg/dLPre-Diabetes
A1C 6.0*
126 mg/dL or higherDiabetes
Random BS >200A1C 6.5 *
Blood Sugar
Pre - Diabetes FPG 100 -125 mg/dl OGTT 140 -199 mg/dl People with pre-diabetes have and
increased risk of Type 2 Diabetes, heart disease and stroke
Diabetes Prevention losing at least 7% of total body weight Exercising 150 minutes per week
Glycemic Targets (2009 ADA Recommendations)
Intensive Care 140 - 180 mg/dl Insulin infusion is the preferred
treatment Non-critical Care Units
Less than 140 mg/dl pre-prandial 180 mg/dl maximal glucose Avoidance of hypoglycemia
Patient specific goals are the target
Oral Medications Sulfonylureas (glyburide, glipizide, glimepiride)
increase insulin secretion Causes weight gain Cheap Hypoglycemia
Sodium glucose co-transporter 2 (SGLT2) inhibitor ( Canagliflozin (Invokana),Empagliflozin (Jardiance),Dapagliflozin (Farxiga)
Decrease reabsorption of glucose by the kidney UTI Weight loss
Oral Medications Biguanides (Metformin)
Decrease hepatic gluconeogenesis excreted in urine - contraindicated for GFR <
60 Thiazolidenediones (TZD’s) (Actos, Avandia)
Decreases insulin resistance Associated with heart failure and edema
Alph-glucosidase inhibitors (Acarbose)
Prevent digestion of CHO Cause GI side effects
Medication
Dipeptidyl peptidase 4 (DPP-4) inhibitor (Januvia, Onglyza, Tradjenta, Nesina)
Stimulates insulin release Inhibits glucagon release Decreases gastric emptying
Glucagon-like peptide-1 (GLP-1) agonists ( injections: Byetta, Victoza, Trulicity , Tanzeum)
Stimulate glucose –dependent insulin release Inhibits postprandial glucagon release Slows gastric emptying SE – nausea
In many patients, insulin is the only choice
Diabetes Management Insulin
Many devices now to help people use insulin
Blood Glucose monitoring is critical
Insulin
Insulin Onset of Action Peak ActionDuration of
Action
Rapid Acting (Lispro aspart, glulisine)
5- 15 min 1- 2 hours 4-6 hours
Short Acting (Regular) 30-60 min 2- 4 hour 6- 10 hours
Intermediate acting (NPH)
1-2 hours 4- 8 hours 10 – 20 hours
Long Acting (glargine, detemir)
1 hour None 24 hours.
Profiles of Insulin
0 2 4 6 8 10 12 14 16 18 20 22 24
Plas
ma
insu
lin
leve
ls
Short acting (6–10 hours)
Intermediate acting (12–20 hours)
Hours
Long acting (20-26 hours)
Rapid acting (4–6 hours)
Physiologic Blood Insulin Secretion Profile
Plasma Insulin (µU/mL)
4:00
25
50
75
8:00 12:00 16:00 20:00 24:00 4:00
Breakfast Lunch Dinner
Time
8:00
Adapted from White JR, Campbell RK, Hirsch I. Postgraduate Medicine. June 2003;113(6):30-36.
Analog Insulin Time-Action Patterns
Time (hours) SC injection
Normal insulin secretionat mealtime
QD (basal) Analog Insulin
Baseline Level
Theoretical representation of profile associated with Basal Analog Insulin
Ch
an
ge
in s
eru
m in
su
lin
Analog Insulin Time-Action Patterns
Time (hours) SC injection
Normal insulin secretionat mealtime
Baseline Level
Theoretical representation of profile associated with rapid-acting Insulin Analog
Ch
an
ge
in s
eru
m in
su
lin
Rapid-Acting Insulin Analog
Regular Insulin Time-Action Patterns
Time (hours) SC injection
Normal insulin secretionat mealtimeRegular insulin (human)
Baseline Level
Theoretical representation of profile associated with Regular Insulin (human)
Ch
an
ge
in s
eru
m in
su
lin
NPH Insulin Time-Action Patterns
Time (hours) SC injection
Normal insulin secretionat mealtimeNPH insulin (human)
Baseline Level
Theoretical representation of profile associated with NPH Insulin
Ch
an
ge
in s
eru
m in
su
lin
Concentrated insulin formulation
U 500 Concentrated regular insulin (5x more
concentrate) Available in insulin vial
Troujeo Concentrated Lantus – 300units /ml
Humalog U – 200 – Pen
Multiple Daily Injections
Bolus Rapid Acting Insulin
Onset of action within15 minutes Peak action in 1 hour Duration of action 3-4 hours
Basal Long Acting Insulin
Duration of action is about 24 hours Typically about ½ of your total daily
insulin need
Insulin to Carb Ratios
Using rapid or short acting insulin to cover the blood sugar rise occurring with meals
Dosed immediately pre or post meal Based on the amount of carbohydrate
eaten Omitted if meal is omitted Given in addition to sliding scale or
correction insulin
Glycemic Targets
Intensive Care 110 mg/dl
Non-critical Care Units 110 mg/dl preprandial 180 mg/dl maximal glucose
Current Research Conclusions
Hyperglycemia in hospitalized patients is associated with adverse outcomes
Tight control results in a decrease in septicemia
Tight control can result in an increase in Hypoglycemic events (<40 mg/dl)
Factors to consider Patient population – CABG and surgical
patients seem to benefit from tighter control ? Glucose variability – has been found to be
a predictor of mortality in some studies Standardized insulin infusion protocols with
low hypoglycemic rates are necessary
Hypoglycemia
Clinical risk for hypoglycemia
Changes in caloric intake Changes in clinical status Changes in medications – vasopressors,
steriods Medication error – ordering and
administration Poor coordination of BG testing, insulin
delivery and meals Patient age, co morbidities, and oral
medications Poor communications with transfers
Hypoglycemia
Mild Adrenergic symptoms
Tachycardia, pale, diaphoresis, irritable, anxiety, hunger
Can treat themselves
Moderate Neuroglycopenic
Headache, weak, hypotension, agitation, confusion
May need help to treat
Severe Neuroglycopenic
Coma, seizures
Rule of 15
15 gm CHO3-4 glucose tablets8 oz glass of milk4 oz juice7 lifesavers4 oz pop
Wait 15 minutesBS increased 15 mg/dl
Severe Hypoglycemia 50 of D50 IV Administer Glucagon injection
Mix Give injection into a large muscle
Stay with person and keep them on their side
When awake feed them a protein snack – sandwich
Hypoglycemia Causes
Glucose uptake is too rapid Tumors Exercise
Excessive Insulin Tumors Insulin Administration Sulfonylurea
Glucose release inadequate Alcohol Liver dysfunction
Risk Factors for Hypoglycemia in the Elderly
Impaired autonomic nervous system function
Diminished glucagon secretion Poor or irregular nutrition Cognitive disorder Use of alcohol or other sedating agent Polypharmacy Renal or hepatic failure
Is Your Patient with Diabetes Pumped Up?
Available Insulin Pumps
Omnipod Reservoir filled with insulin No tubing Self inserts with direction from PDA
Pump Components Pump
Syringe
Insertion Sets
Set Inserters
Insulin
Variety of Pump Tubing and Needle Sets
Basic Pump Functions Bolus Insulin
An infusion of insulin that is programmed by the patient as needed
Dose is based on previous programming of insulin/CHO ratio, sensitivity and target
Basal Rate A continuous infusion of insulin Pre-programmed to change at set times
Suspend Stops the pump
Temporary Basal Rate A short-term change in the rate of continuous infusion
Pump Use Insulin to CHO Ratio
Sensitivity Factor
Target
Insulin on Board time
Pump Troubleshooting Pump operating (battery working) Infusion site
intact not infected Age of site – over 3 days question insulin
absorption Insulin
Age of insulin Syringe full
Sensors Measures amount of sugar in the
interstitial fluid
Measure “blood sugar” for patient every 5 min
Reflect trends in BS movement not necessarily accurate
Some affected by Tylenol
Glucose Sensors
Minimed Real-Time
Freestyle Navigator
Dex-Com
Glucose Sensor Management
Should not be used for blood glucose readings
Do NOT throw away…the Transmitter is VERY expensive and NOT disposable. Please return to the patient!
MUST be completely removed (sensor and transmitter) before CT SCANS, MRI or any other type of exposure to radiation!
Hyperglycemia: DKA and HHS
Hyperglycemic illnesses in Diabetes
Diabetic Ketoacidosis (DKA) – occurs when there is little or no insulin to carry glucose into the cells. Blood glucose over 250 Usually in Type 1 diabetes Evolves quickly
Hyperglycemic Hyperosmolar State (HHS) – occurs when Hyperglycemia and dehydration become severe Blood glucose over 600 Usually in Type 2 diabetes Evolves slowly over days to weeks Progressive decline in level of consciousness Infection is the major initiating factor
DKA and HHS Mortality rate
DKA 2- 5% HHS 15%
Prognosis is worsened by Age – extremes of Coma and Hypotension
More common in adults Leading cause of death in children and
adolescents with type 1
Causes of Diabetic Ketoacidosis (DKA) and HHS
Insulin Deficiency Absolute (no insulin) (DKA)
New diagnosed Type 1 Insulin Pump failure
Relative (too little insulin) (HHS and DKA) Infection Other illness: CVA, MI, trauma, and drugs Inadequate insulin dosages
Elevation of Counterregulatory hormones Increase in lipolysis (ketone production) Increase in hepatic glucose production (gluconeogenesis) Decrease glomerular filtration rate
Hyperglycemia leads to osmotic diuresis Dehydration Electrolyte loss
DKA Pathophysiology
Insulin deficiency Decreasing glucose uptake Increased liver glucose production
(gluconeogenesis) Protein degradation Lipolysis – leading to Ketone bodies Metabolic Acidosis
Hyperglycemia leads to osmotic diuresis Dehydration Electrolyte loss – K+ and Na
DKA Symptoms Polydipsia and polyuria Weight loss Fatigue Dyspnea Vomiting Febrile illness Abdominal pain Polyphagia Dehydration
Severe DKA Symptoms
DKA symptoms: Hyperpnea – Kussmaul respirations Hypothermia Acetone breath Dehydration
Orthostatic hypotension Acute abdomen Mentation changes
Diagnostic Criteria
Initial Labs Glucose >300 Ketones – positive Arterial pH - 7.2 Creatinine, BUN – elevated HCT – elevated Bicarbonate (HCO3) Low NA – Varies K+ - level varies although total body
depletion always occurs WBC increased
Comparing Laboratory Values for DKA and HHS
Lab Test DKA HHNKSGlucose 250-800 600-2000
Ketones Large Absent or small
pH < 7.30 Normal
HCO3 < 15 Normal
Sodium Varies Varies
Potassium Varies Varies
Osmolality Normal Increased
Acid Base Metabolic Acidosis
Mild Lactic Acidosis
Goals of Therapy Correct fluid loss with IV fluids Correct hyperglycemia with insulin Correct electrolyte disturbances: potassium Correct acid-base balance Treat concurrent infection if present Prevent complications Support Vital Functions
Breathing Provide patient and family education
Correction of Fluid Loss
Oral Fluids if tolerated 0.9% NS or LR
1-3 L during first 2 hour depending on B/P and volume correction
250 ml/h of 0.45 % NS – goal is to replace ½ of the water deficit in first 12-24 hours
When glucose <300 change to D5W ½ NS Risk with resuscitation: Cerebral edema
More common in pediatrics
Correction of Hyperglycemia
Insulin increases glucose utilization, decreases hepatic glucose production and inhibits the release of FFAs
Short acting insulin provided IV Initial dose for infusing is 0.1 U/kg/h
Provide insulin to restore glucose Insulin drip or Sub Q (SQ absorption is reduced
with dehydration) Insulin drip of Regular insulin
Tubing should be preflushed Drip rates should be validated with another RN Once started the insulin drip should not be
interrupted or “bolused” Goal is to decrease blood glucose no more than 75
to 100 mg/dl per hour Risk is Hypoglycemia – results in rebound ketosis
Correction of Electrolyte and Acid Base
Replace potassium Very critical to successful resuscitation Low potassium means a general body depletion, insulin infusion
and acid base correction with decrease the potassium levels Insulin drives potassium into the cells and will lower the serum
potassium K+ > 6 – no replacement needed K+ 4.5 -6 - 10 mEq/h of KCL K+ 3- 4.5 mEq/L – 20 mEq/h of KCL
Monitor for EKG changes with potassium levels Hypokalemia – prolonged QT and depressed T waves Hyperkalemia – Peaked T waves
Monitor hourly and infusion stopped if K+ level >5 In severe hypokalemia, hold insulin gtt
Acid – base balance Sodium bicarb only if acidosis is life threatening Rapid correction of acidosis with sodium bicarbonate may
worsen hypokalemia Sodium bicarb has been correlated with cerebral edema in
children
Complications of Treatment
Cerebral edema Leading cause of DKA mortality in children
occurs in 1% of episodes and is associated with a mortality rate of 40-90%
Decreases in LOC should be carefully monitored and MRI used to confirm
Risk is related to severity and duration of DKA Fatal complication – can result from the rate of fluid
rehydration Hypoglycemia Cardiac arrhythmias – resulting from hypokalemia Hyperglycemia
Resulting from interruption in insulin treatment
Current Levels of Diabetes Control
What proportion of people with diabetes have….. Controlled BP (, 130/80mmHg) 40% LDL at goal (<100) 36% A1C at the goal level (<7) 49.8%
What proportion have met all three? 7.3%
A Constellation of Complications
Gastropathy
Autonomic Neuropathy
Renal Disease
Peripheral Neuropathy
Retinopathy/ Macular
Edema
HypertensionCardiovascular
Disease
Dyslipidemia
Peripheral
Vascular Disease
Erectile Dysfunction
Diabetes
Hypertension
73% of adults with diabetes have pressures greater to or equal to 130/80 mm Hg or use prescription drugs for hypertension
Hyperlipidemia