Download Slide 1

Be The
Pancreas
Caring for the
Patient with Diabetes
Millions of People
USA’s Growing
Population with Diabetes
Data from the National Diabetes Statistics Report, 2014 (released June 10, 2014)
- See more at: http://www.diabetes.org/diabetes-basics/statistics/#sthash.dC2iwT48.dpuf
Why Nursing is Vital & Well-Positioned
to Help Provide Good Diabetes Care
• Nursing sees the whole picture & plays many
roles in patient care
e.g, travel off unit, physical therapy, X-ray
 Amount of food eaten (carbs) or NPO status
 Patient’s day to day concerns
 Order changes (by various providers)
 Observer of changes in symptoms
 Nursing does most (if not all) of the patient education

Diabetes in the
Acute Care Setting
Basics – Review of Pathophysiology
Prevention/Treatment
1.
2.
I.
II.
3.
4.
5.
6.
Lifestyle Modifications
Insulin & Oral Agents
Hypo/Hyperglycemia Review
The Complications
Inpatient Diabetes Care/Patient Education
Case Studies
The Basics Review of the
Pathophysiology
of Diabetes
Basics
Energy Balance – Insulin Production
It All Starts with the
Eyes & Nose
Anyone Hungry???
Basics
Energy Balance – Insulin Production
Bloom S et al. Hormonal regulation of food intake. Physiol Rev 2005;85(4):1131-58.
Basics
Blood Glucose Regulation
Basics
Insulin Production
Basics
Insulin Uptake into the Cells
Harvard Health Publications
Basics-The Body’s Response
to Efficient Circulating Insulin
Hyperglycemia
Liver
Muscle
Glucose storage
Glucose uptake for energy
Adipose
tissue
Glucose uptake
Stored as fat
Euglycemia
Basics-The Body’s Response
to Little or No Circulating Insulin
Hyperglycemia
Liver
Defective
Glucose storage
Muscle
Defective
Glucose uptake for energy
Defective
Glucose uptake
↑ ↑ ↑ Hyperglycemia
Basics
Definition of Diabetes Mellitus
Diabetes mellitus is a group of metabolic diseases
characterized by hyperglycemia resulting
from defects in insulin secretion, insulin action, or both.
The chronic hyperglycemia of diabetes is associated
with long-term damage, dysfunction, and
failure of various organs, especially the eyes,
kidneys, nerves, heart, and blood vessels.
Basics – The Numbers & Targets




Normal fasting glucose
FPG <100 mg/dl (5.6 mmol/l)
Impaired fasting glucose (IFG) or “Pre-Diabetes”
FPG 100–125 mg/dl (5.6–6.9 mmol/l) or A1c 5.7-6.4%
Diabetes (with A1c or OGTT)
FPG ≥126 mg/dl (7.0 mmol/l) or A1c >6.5%
Targets*:




Critical Care 140-180 mg/dL
Non-critical care pre-meal <140 mg/dL
Non-critical care random <180 mg/dL
Outpatient: A1c <7%; 80-130 mg/dL for most patients;
individualize to patient health state
*ADA Standards of Medical Care in Diabetes – 2015
Basics – Glycated Hemoglobin or HbA1c
An HbA1c or “A1c” test is the measure of the average blood glucose
over the past 2-3 months. When BG are high, glucose molecules attach
to the hemoglobin in RBCs. The longer hyperglycemia occurs,
the more glucose binds to the RBC & the higher the A1c.
“Average Glucose”
Explaining & Communicating an A1c*
A1C
(%)
Average
Blood Glucose
Without Diabetes
<5.7
70-99
At Risk for Developing Diabetes
(sometimes referred to as “pre-diabetes”)
5.7-6.4
100-125
For Those Diagnosed with Diabetes
Good Control
American Diabetes Association Target <7%
Sub-Optimal Control
Action Needed to Improve Control >8%*
*An A1C goal of 8% may be set for a pt with
poor prognosis or frequent occurrences of
hypoglycemia
Very Poor Control
Immediate Action Needed to Improve Control
>9%
6
126
7
154
8
183
9
212
10
240
11
269
12
298
13
326
Basics – Diabetes Types
Key characteristics of type 1, LADA (latent autoimmune DM in adults), & T2DM.
Type 1 DM
LADA (Type 1.5) Type 2 DM
Typical age of onset
Youth or Adult
Adult
Progression to insulin
dependence
Rapid
Latent
(days/weeks)
(mos/years)
Slow (years)
Presence of
autoantibodies*
Insulin dependence
Yes
Yes
No
At diagnosis
Within 6 years
Over time,
if at all
Insulin resistance
No
Some
Yes
Adult
*Proteins that indicate the body has launched an autoimmune attack on the
insulin-producing beta cells in the pancreas.
Basics – Type 1 Diabetes (T1DM)

Characterized by labile glycemic control; sensitivity to
both insulin & glucose

Associated with microvascular and macrovascular
complications

Generally arises from an autoimmune process that
destroys the pancreatic β-cells

Reduced or absent glucagon release
Basics – T1DM Treatment
Before/After Discovery of Insulin
Elizabeth Hughes, 1918 (left), age 11, during starvation therapy.
Elizabeth Hughes, 1921 (right) age 14 after start of insulin therapy.
She lived until 1981; outlived her T1DM life expectancy by 60 years.
Basics – What is Insulin Sensitivity?

Insulin sensitivity is a term used to describe people
who require relatively normal or low levels of insulin
to process glucose.

A person who is insulin-sensitive needs only a
relatively small amount of insulin to keep blood
glucose levels in the normal range and to keep the
body’s cells supplied with the glucose they need.

T1DM & s/p total pancreatectomy patients are
usually insulin sensitive
Basics – Type 2 Diabetes (T2DM)

Characterized by chronic hyperglycemia; insulin
resistance

Associated with microvascular and macrovascular
complications

Generally arises from a combination
of defective insulin uptake and -cell dysfunction
Basics – What is Insulin Resistance?

Opposite of insulin sensitive, an insulin
resistant patient needs much more insulin to
achieve the same BG lowering effects.

Major defect in individuals with T2DM

Reduced biological response to insulin (will
require larger doses of insulin than T1DM)

Strong predictor of T2DM
Closely associated with obesity,
especially visceral adiposity

IR
Basics – Insulin Resistance
Reduced Response to Circulating Insulin
Insulin
resistance
Liver
 Glucose output
IR
Adipose
tissue
Muscle
 Glucose uptake
 Glucose uptake
Hyperglycemia
Basics – What is -cell dysfunction?


Major defect in individuals with type 2 diabetes
(inherited)
Reduced ability of -cells to secrete insulin in
response to hyperglycemia over time
Prevention/Treatment
Lifestyle Modifications
Prevention/Treatment
Changing Behaviors



Healthy Eating
Activity
Healthy Coping/Stress Management
R
E
L
A
P
S
E
The Transtheoretical Model (Prochaska & DiClemente, 1983)
Prevention/Treatment –
Healthy Eating

Moderate intake of carbohydrates (26-45% of daily
calories come from carbohydrates)







Men 3-4 servings or 45-60 grams per meal
Women 2-3 servings or 30-45 grams per meal
*Very low carb diets not endorsed (20-50g/day)
Increase consumption of vegetables and fruits and
low dairy products (DASH diet)
Reduce saturated fat, cholesterol and trans fat intake
(but not fat free)
Reduce sodium intake
Moderate intake of alcohol
ADA, 2015
Prevention/Treatment –
Activity



Children with diabetes or prediabetes – 60 minutes of
physical activity daily
Adults with diabetes or prediabetes – 150 min/week of
moderate-intensity aerobic physical ativity (50-70 of
maximum heart rate) spread over at least 3 days/week
with no more than 2 consecutive days without exercise
Adults with T2DM – twice weekly resistance training
Prevention/Treatment –
Activity

Evidence supports that ALL individuals, diabetes or
not, should reduce sedentary time, break up extended
time (>90 min.) spent sitting
ADA, 2015
Prevention/Treatment –
Healthy Coping
Short term stress response
Impact of counter-regulatory
hormones: epinephrine &
noepinephrine





Glycogen broken down into
glucose, raising blood glucose
Increased blood pressure
Increased breathing rate
Increased metabolic rate
Chang in blood flow patterns,
leading to increased alertness,
decreased digestion & renal
activity
Long-term stress response
Effects of glucocorticoids/ cortisol:

Proteins and fats broken down into
glucose, leading to increase blood
glucose
Effects of mineralocorticoids:


Retention of sodium ions & water by
the kidney
Increased blood volume & pressure
Prevention/Treatment –
Healthy Coping


Recognize stress, know your triggers and
understand it can be managed.
Learning/Practicing healthy techniques that help
you cope. (quiet time, exercise, music, reading,
talking with supportive friend)
Prevention/Treatment –
Healthy Coping

Setting realistic expectations & promoting healthy
coping behaviors








Setting realistic goals (think what we sometimes as our
patients to do)
Reasonable schedules
Regular exercise
Appropriate assertiveness
Eating Healthy
Getting enough sleep
Avoiding unhealthy behaviors
Breathe….
Frydenberg, E.Thriving, Surviving, or Going Under: Coping with Everyday Lives, Information Age, 2004
How to combat insulin resistance?

Loss of body fat

Exercise

Good blood glucose control

Stress management

Adequate sleep

Food choices-moderation, reduced
carbohydrate intake
IR
Treatment with
Diabetes
Medications
Treating with Insulin
Insulin
Onset of
Action
Peak
Duration of Action Comments
Rapid Acting Analogs:
lispro, Humalog®
aspart, Novolog®
glulisine, Apidra®
5-15 min.
30-90
min.
3 to 5 hours
For nutritional &
correction coverage
Short Acting:
Regular, Humulin R®
Regular, Novoloin R®
30 min.
2 to 4
hours
5 to 8 hours
For nutritional &
correction coverage
Long-Acting Analogs:
glargine, Lantus®
detemir, Levemir®
1-2 hours
Peakless
20-26 hours
Given daily or split
twice daily for basal
needs
Intermediate Acting:
NPH, Humulin N®
NPH, Novolin N®
1-3 hours
8 hours
12-16 hours
Given twice daily for
basal needs
Mixed Insulin:
Humulin/Novolin 70/30®
Humalog 50/50®
Humalog 75/25®
Novolog 70/30®
30 to 60 min. Varies
5 to 15 min.
10-16 hours
Given twice daily for
basal/nutritional
needs. Must eat with
mixed insulin intake.
Treating with Insulin
Insulin
Onset of
Action
Peak
Duration of
Action
Comments
Inhaled Insulin:
Afrezza® (insulin
human) Inhalation
Powder
5-15 min.
30-90
min.
3 to 5 hours
For nutritional &
correction coverage
Humulin R U-500®
30 min.
2 to 4
hours
Up to 24 hours
5x more concentrated
than U-100 regular
insulin. Used in
patients requiring >200
units/ day. Dosed twice
daily.
peakless
Up to 40 hours
U300-Just received
FDA approval. Next
generation Lantus.
Less hypoglycemia
than glargine.
Degludec – awaiting
CV studies, 2015-106
marketing to start
Ultra Long Acting Insulin: 1-2 hours
Sanofi Aventis’ U300®
degludec, Tresiba®
Insulin response to blood glucose levels
(no Diabetes)
Insulin Effect
180mg/dL
Blood Glucose Levels
99mg/dL
70mg/dL
Breakfast Lunch
Dinner
Body releases insulin in response
to actual glucose levels
Body releases a small amount of
insulin 24/7 to keep blood glucose
stabilized.
Basal-Nutritional Therapy
-mimicking the body’s natural insulin response-
Insulin Effect
180mg/dL
Blood Glucose Levels
99mg/dL
70mg/dL
Breakfast Lunch
Dinner
Rapid Acting Insulin
Long Acting Insulin
(i.e. lispro-Humalog)
(i.e. glargine-Lantus)
3 Reasons to Administer Insulin for BG Control
Always Ask Yourself
“Why Am I Giving this Dose of Insulin”?

Basal-long acting to suppress
gluconeogenesis between meals or at night

Nutritional/Bolus-rapid/fast acting to cover
intake of carbs (e.g. meals, Tube Feeds) &
prevent post-prandial/meal hyperglycemia

Correction (sliding scale)-rapid/fast acting
insulin to cover existing hyperglycemia
Insulin on Board



“Insulin on Board” simply refers to the
amount of insulin still circulating in the
bloodstream that may still be working.
Be mindful of what patient has already
received & how long it is acting
Prevent Over-Reaction-watch BG trends!
I
I
Insulin Stacking

Remember “Insulin on Board”

Stacking insulin refers to when a patient
receives more insulin before the previous
amount of insulin given has finished
working. This creates even more onboard
insulin.

When insulin stacking can lead to serious
episodes of hypoglycemia.
Insulin Pump Therapy
Insertion Set – holds delivery
canula in place in the
subcutaneous tissue
Insulin Pump – preprogrammed
technology that holds all basal,
nutritional and correction
coverage settings. Basal insulin
delivered around the clock.
Nutritional and correction boluses
manually entered dependent on
carbohydrate intake and blood
glucose levels.
Continuous Glucose Monitoring
aka “Sensor”
Sensor – held in place in the
subcutaneous tissue
Receiver – blood glucose levels
wirelessly transmitted to receiver
to give user blood glucose trends.
CGM & insulin pump
technology combined.
Oral Antidiabetic
Agents
Oral Agents – Target Organs
Oral Agents
Drug Class
Name
How it Works
Biguanides
metformin – Glucophage®,
glucophage XR®, Fortamet®,
glumetza®, Metromin ER®
Decreases liver glucose
production and increases
insulin sensitivity.
Sulfonylureas*
glimepiride/Amaryl®
Longer-acting agents that
glipizide/Glucotrol® & Glucotrol XL® increase insulin release
glyburide/DiaBeta®/Micronase®
from the pancreas.
Thiazolidinediones
(TZD)
pioglitazone/Actos®
Increases insulin
sensitivity and decreases
liver glucose production.
Meglitinides*
nateglinide/Starlix®
repaglinide/Prandin®
Short-acting agents that
increase insulin release
from the pancreas.
*Watch for hypoglycemia especially if patient not eating/NPO
Sutter Health. Diabetes Handbook, 2014
Oral Agents
Drug Class
Name
How it Works
Alpha-Glucosidase acarbose/Precose®
Inhibitors
miglitol/Glyset®
Blocks carbohydrate
digestion and absoprtion
to help keep blood
glucose levels normal
after meals.
DPP-4 Inhibitors
sitagliptin/Januvia®
saxagliptin/Onglyza®
linagliptin/Tradjenta®
alogliptin/Nesina®
Stimulates the pancreas
to respond better to
glucose and decreases
liver glucose production.
SGLT-2 Inhibitors
canagliflozin/Invokana®
dapagliflozin/Farxiga®
empagliflozin/Jardience®
Decreases re-absorption
of glucose in the kidneys.
Sutter Health. Diabetes Handbook, 2014
Oral Antidiabetic Meds in
Hospitalized Patients






Most oral agents are optimized in outpatient settings.
If a patient is NPO or eating very little in the wake of
illness, oral agents may cause hypoglycemia.
However, the stress of most illnesses can cause
insulin resistance & worsen control with agents alone.
Contrast dye: 48 hour post test hold of metformin
Renal Failure: Contraindicated for metformin & SFU
(e.g. glyburide)
Where do we go from outpatient oral agents to
inpatient insulin... Start with a Correction Scale!
Other Injectables
Drug Class
Name
How it Works
GLP-1 Receptor
Agonists
exenatide/Byetta®/Bydureon®
liraglutide/Victoza®
Helps the pancreas make
more insulin when blood
glucose is high. Reduces
glucose production in the
liver and slows absorption
of food.
Amylin Analog
pramlintide/Symlin®
Reduces the amount of
glucose made by the
liver. Lowers blood
glucose levels after meals
and decreases appetite.
Sutter Health. Diabetes Handbook, 2014
Diabetes Treatment Pitfalls
in the Hospital

Home medication plan dc’d & pt put on insulin scale only

Pt not on CHO controlled diet

RNs/NAs not accurately watching pt nutrition intake for
pts on insulin or oral meds therapy

MDs not changing insulin plans when hyper/hypoglycemic

Large doses of long acting insulin given then pt made
NPO (“overbasalization”) or TF stopped with large dose
on board

Pt hypoglycemia over treated resulting in rebound
hyperglycemia
Hypoglycemia
&
Hyperglycemia
S/Sx Hypo- Hyperglycemia
Hypoglycemia
 Shakiness, trembling
 Sweating (diaphoresis)
 Blurred vision
 Dizziness (feeling lightheaded)
 Cognitive impairment
 Feeling nervous or anxious
 Weakness
 Numbness, tingling of
mouth and lips
 Tired
 Headache
 Sudden hunger
 Nauseous
 Rapid heart beat (tachycardia)
Hyperglycemia
 Increased thirst (polydipsia)
 Increase in urination (polyuria)
 Urine may contain ketones
 Labored breathing
 Fatigue
 Increase in appetite
(polyphagia), or decrease in
appetite
 Headache, stomachache
 General aches and pain
 Changes in behavior or
temperament
Hypoglycemia Treatment

“15/15 Rule” for mild hypoglycemia
15 grams of simple carbohydrate (CHO)
 ½ cup juice (PO)
 glucose tablets/gel (PO)
 ½ vial IV dextrose (NPO)
 glucagon (NPO)
 For BG <50mg/dL, give 30 grams simple CHO
 If next scheduled meal >1hour, give a snack

Avoid Rebound HyperglycemiaDo not panic and over-treat mild hypoglycemia!
Home Hypoglycemia Treatment

“15/15 Rule” for mild hypoglycemia
 15 grams of simple carbohydrate
½ cup juice or sweetened soda
 glucose tablets
 glucose gel
 1 tablespoon sugar, honey or jam/jelly
 8 ounces of nonfat or 1% milk
 6 large jelly beans, 5 Life Savers, 15 Skittles or 4
Starburst


glucagon – family member instruction for
emergencies
The Complications
Diabetes Complications

Short Term






hypoglycemia
DKA/HHS (Hyperglycemic Hyperosmolar State, aka HONK
slow wound healing
dehydration
patients feel awful
Chronic Complications


Microvascular Disease
Macrovascular Disease
Complications of
Hyperglycemia
 Leading cause of blindness
 Leading cause of renal failure
 2/3 of DM have nerve damage
 >60% of amputations occur in diabetes patients
 Significant risk factor in birth defects and miscarriage
 Risk for heart disease and stroke 2-4x higher
Microvascular Complications



Nephropathy
Retinopathy
Autonomic & Peripheral Neuropathies
15
Retinopathy
Nephropathy
Neuropathies
Microalbuminuria
Relative Risk
13
11
9
7
5
3
1
6
7
8
9
10
HbA1c (%)
Courtesy of Sanofi-Aventis
11
12
Macrovascular Complications
Cardiovascular disease
 Cerebral vascular disease
 Peripheral vascular disease

Inpatient
Diabetes Care
Patient Education
The Patient on
Glucocorticoids Therapy
Impact On Glycemic Management:




Increased insulin resistance
Long-Acting insulin not a physiologic match
for glucocorticoids
Hyperglycemia worse in the postprandial
phase (or post-CHO intake)
Very important to start nutritional insulin when
pt eating or on TF!
Older Adults with Diabetes






Reduced life expectancy
High CVD burden
Reduced GFR
At Risk for Adverse Effects due to polypharmacy
More likely to be compromised with hypoglycemia
Individualize targets:



Less ambitious blood glucose targets
A1c 7.5-8%
Focus on drug safety
ADA/EASD Position Statement: Inzucchi, SE, et al. Diabetes Care. 2012; 35: 1364-1379
Inpatient Diabetes Care
Keeping the Patients Safe

Clarify, Clarify, Clarify-when in doubt, call
for help!

Notify Prescriber when hypoglycemia or
hyperglycemia occurs

Remember RN scope of practice with
decision to give or hold insulin

Don’t forget to involve the patient in
diabetes treatment plan!
Nursing Roles in
Good Diabetes Care
• Appropriate timing of point of care test (POCT),
•
•
•
•
•
•
insulin administration & meal delivery
Recognition of hyper/hypoglycemia &
appropriate management/documentation
Know when to hold insulin
What to do when tube feeding is interrupted & pt
has long acting insulin on board
Appropriate patient hand off
Patient self-management education
Are they safe for discharge?
Safe for Discharge
• Does patient have a glucose monitor for home
•
•
•
•
use? If not, know where to obtain one (e.g. hospital
supplies, diabetes educator, pharmacy)
Does patient know how to inject insulin and how
to prevent and to treat hypoglycemia?
Is patient clear about the diabetes plan after D/C?
(e.g. medication plan)
Does patient need more diabetes education?
Does patient have appropriate outpatient F/U
appointment with primary care or specialist?
Diabetes Survival Skills
Hospital setting is not ideal for learning but it may
be the only chance we get!
Survival skills








Diabetes disease process
Healthy eating basics
Hypo/hyperglycemia prevention and treatment
Medication use, frequency
Drawing and injecting insulin
Blood glucose monitoring
Target blood glucose when to call MD
Provide resources including OP education
Tips for Diabetes Education for
the Busy RN







Provide instruction about insulin or oral diabetes agents and
side effects when administrating doses
Encourage patient to self – administer insulin
Discuss impact of carbohydrates on blood glucose when
meal tray present
Use active listening skills and ask open questions to involve
patient in self-care
Write insulin doses on whiteboard or paper at bedside so
patient understands insulin plan
“Chunk & Check”
Include education in end of shift hand off
Case Studies:
Practice
Actual Events
Case Study-Practice
Basal-Nutritional-Correction Dosing
 Check
BG qac, qhs & 0200
 Basal: 20 units Lantus QHS
 Nutritional: 6 units of lispro (Humalog) QAC
 Correction Scale lispro QAC
70-100
101-150
151-200
201-250
251-300
301-350
>351
 Correction
70-200
201-300
301-400
>400
-2 units (negative correction)
No insulin
+2 units
+4 units
+6 units
+8 units
+10 units call MD
Scale lispro QHS
No Insulin
2 units
4 units
Call MD
Case Study-Practice
Basal-Nutritional-Correction Dosing
1.
It is 0745, pt BG 209 mg/dL, pt will eat at 0800, How much
insulin do you give at what time?
2.
It is 1200, pt BG 185 mg/dL, pt is NPO for a 2pm test, How
much insulin do you give at what time?
3.
It is 1715, pt BG 85 mg/dL, pt will eat at 1730. How much
insulin do you give at what time?
4.
It is 2130, pt BG 143 mg/dL. Pt is ready for bed. How much
insulin you give at what time?
Case Study-Actual Events
Insulin Stacking

38 yo M admitted from OSH for ascites

Hx ESLD 2° to Hep C, ESRD, TIDM, blind, substance abuse
& psych issues

0400 BG: 422 mg/dL –10 units lispro SC

0600 BG: 404 mg/dL –14 units lispro SC

0700 BG: 91 mg/dL

0800 BG: 18 mg/dL –D50 1 ½ ampules & ate 100%
breakfast

0900 BG: 260 mg/dL, daily glargine (Lantus) 5 units given

1000 BG: 170 mg/dL
Case Study-Actual Events
Insulin Stacking

What caused the BG to drop so quickly?

What clues could the MD have looked for before
prescribing STAT insulin doses?

What clues could the RN have reviewed for before
giving STAT insulin doses?

Was an 1 ½ amp of D50 too much correction?

Was it safe to give daily glargine (Lantus) dose?
Case Study-Actual Events
Hypoglycemia with Nutritional Insulin

67 yo M s/p heart transplant

Hx Cardiomyopathy, T2DM, HTN, Hyperlipidemia

1155 BG: 145 mg/dL – pt nutritional dose is 17 units
lispro with Lunch; trays were on unit, RN gave 17
units lispro SC

1205: PT took patient for a walk

1245– pt c/o dizziness to PT, PT reported Sx to RN,
BG: 60 mg/dL
Case Study-Actual Events
Hypoglycemia with Nutritional Insulin


What likely caused BG to drop so quickly?
What could have been done by the RN to prevent
the hypoglycemic event?
Case Study-Actual Events
Hypoglycemia with TF Hold

74 yo M s/p abd surgery 2° to SBO

Hx T2DM on Metformin at home, HTN,
Hyperlipidemia, GERD

Pt on TF, with 60 units glargine (Lantus) qdaily at
0800

1145 BG: 145 mg/dL, 60 units glargine given SC

2130 TF stopped as pt had loose stool

0030 BG 85 mg/dL

0245 Pt had LE Sz, BG checked at 38 mg/dL
Case Study-Actual Events
Hypoglycemia with TF Hold

What likely caused hypoglycemia?

What could have been done by the MD/RN
to prevent the hypoglycemic event?
Case Study-Actual Events
Hypoglycemia with TF Hold, part 2

0245 Pt had LE Sz, BG checked at 38
mg/dL, RN gave D50 IVP

0310 BG: 77 mg/dL, D50 IVP repeated

0400 BG: 125 mg/dL

0730 AM shift RN noticed pt diaphoretic, BG
52 mg/dL
Case Study-Actual Events
Hypoglycemia with TF Hold, part 2

What likely caused second episode of
hypoglycemia?

What should be the next steps to prevent
another hypoglycemic event?
Case Study-Actual Events
Hospital Induced Diabetic Ketoacidosis








Pt 47 yo M, s/p R-shoulder replacement, Hx T1DM
on insulin pump at home (pump off for surgery)
PACU BG 489 20 units Regular given
Pt admitted to medical floor
1700 BG 267, pt given 6 units lispro
2130 BG 336, pt given 3 units lispro
(Next day) 0800 no BG, “RN missed BG check”,
no labs ordered
1130 BG “critical high”, Chem 7 sent
BG 670, anion gap 27.4…DKA
Case Study-Actual Events
Hospital Induced Diabetic Ketoacidosis



What happened?
Who else played a role in the hyperglycemic
event?
Lessons learned?
Questions?
Thank you for
great care in
patients with
diabetes!