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

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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

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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

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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

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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