Type 1 Diabetes Mellitus Gregory E. Peterson, DO, FACP The Diabetes Center Diagnostic & Critical Care Medicine, PC

Type 1 Diabetes Mellitus

Gregory E. Peterson, DO, FACP

The Diabetes Center

Diagnostic & Critical Care Medicine, PC

Objectives for Iowa School Nurses Type 1 Diabetes Mellitus

Ketonuria

Incretin therapy in diabetes management

Types of insulin: Analog insulin in basal and bolus therapy

Strategies to optimize blood glucose levels

Hypoglycemia and Hyperglycemia

Explore tools to management: insulin pens, insulin pump, blood glucose meters, blood glucose sensors


Autoimmune destruction of the insulin-producing ß-cells in the islets of Langerhans

In the new classification of diabetes, immune mediated type 1 diabetes is called type 1A

Some rarer cases in which an autoimmune etiology cannot be determined (type 1B); said to be idiopathic.

Diabetes Mellitus in children

The clinical diagnosis of diabetes in a previously healthy child requires a high index of suspicion. The earliest symptoms are related to hyperglycemia.

Older children and adolescents typically present with polyuria (due to the glucose osmotic diuresis), polydipsia (due to the increased urinary losses), and fatigue. Other findings include weight loss, nocturia (with or without secondary enuresis), daytime enuresis, and vaginal or cutaneous moniliasis

Diabetes Mellitus in children Children with weight loss, anorexia,

vomiting, and abdominal pain, which at times can mimic appendicitis or gastroenteritis should be considered

DKA


Type 1 diabetes occurs in genetically susceptible subjects.

Triggered by one or more environmental agents, and usually progresses over many months or years, during most of which the subject is asymptomatic and euglycemic.

A large percentage of the functioning ß-cells must be lost before hyperglycemia appears,


Research tools, not for clinical practice:

1. Genetic Markers

2. Immunologic Markers

Genetic Markers: Type 1 Diabetes

6 percent in offspring and 5 percent in siblings (versus 0.4 percent in subjects with no family history)

The risk in siblings is importantly influenced by the degree of genetic similarity, falling from 33 percent in identical twins

HLA halotypes: (12.9%) 2 (4.5%) 1 (1.8%) 0

Immunologic Markers

islet-cell antibodies (ICA)

insulin autoantibodies (IAA)

antibodies to glutamic acid decarboxylase (GAD)

Immunologic Marker for Type 1 DM

40% within five years versus 3% with single auto-antibodies).

Progression to multiple islet auto-antibodies was fastest in children who developed their first autoantibody by age two years.

Children with the earliest evidence of autoimmunity are at greatest risk for and progress more quickly to the development of type 1 diabetes.

Periodic testing for islet auto-antibodies appears to help assess the risk of diabetes in children of parents with type 1 diabetes.

Prevention Recommendations (Research)

Test individuals at risk for type 1 diabetes progression for GAD65 and IA-2 autoantibodies

If they are present and confirmed in a subsequent sample, tests for insulin and islet cell antibodies can be done.

The occurrence of multiple antibodies against islet autoantigens serves as a surrogate marker of disease in primary or secondary intervention strategies aimed at halting the disease process.

Genetic typing for susceptibility or protective HLA alleles can also be performed. This information can be used to ascertain if a high-risk subject is eligible to be entered into an ongoing prevention trial.

Ketonuria

Always check for ketones in urine with blood glucose over 250mg/dL

Presence reflects abnormal metabolism

Key feature of DKA: Hyperventilation

Life threatening event

Ketonuria1. Children with diabetes will develop ketosis if they omit

insulin injections. Untreated ketosis results in nausea, vomiting, abdominal pain, rapid deep breathing, dehydration, lethargy, and ultimately, ketoacidosis.

2. Ketones should be tested if the child has signs of a systemic illness, such as fever and, especially, vomiting, even if the blood glucose is normal.

3. The presence of moderate or large ketones will require extra dosing of insulin to reverse ketosis.

4. Contact parents/medical team.

5. If the child is not vomiting, liberal fluid intake will help prevent dehydration and increase urinary excretion of ketones.

1

3

5

7

9

11

13

15

6 7 8 9 10 11 12

Retinop

Neph

Neurop

Microalb

RE

LA

TIV

E R

ISK

HbA1cSkyler, Endo Met Cl N Am 1996

Relative Risk of Progression of Diabetic Complications by Mean HbA1CBased on DCCT Data

HbA1c and Plasma Glucose

26,056 data points (A1c and 7-point glucose profiles) from the DCCT

Mean plasma glucose = (A1c x 35.6) – 77.3

Post-lunch, pre-dinner, post-dinner, and bedtime correlated better with A1c than fasting, post-breakfast, or pre-lunch

Rohlfing et al, Diabetes Care 25 (2) Feb 2002

ADA / AACE Targets for Glycemic Control

HbA1c < 6.5 %

Fasting/preprandial glucose < 110 mg/dL

Postprandial glucose < 140 mg/dL

Incretins

Amylin: Pramlinitide

GLP-1

- Exenatide

- Liraglitide

Pramlintide Adjunctive Therapy Offers Long-Term Glycemic Control

EuglycemiaEuglycemia

Healthy Subjects (n = 14)

Beta-CellWorkload

Beta-CellWorkload

Beta-CellResponse

Beta-CellResponse

Beta-CellWorkload

Beta-CellWorkload

Mean (SE)

Insulin and GLP-1 Responses to MealsInsulin and GLP-1 Responses to Meals

Glucagon-Like Peptide-1Glucagon-Like Peptide-1

GLP-1 Infusion Improves -Cell Insulin SecretionGLP-1 Infusion Improves -Cell Insulin Secretion

GLP-1 and First-Phase Insulin SecretionGLP-1 and First-Phase Insulin Secretion

Exenatide: Proportion of Patients Achieving A1C ≤7%Exenatide: Proportion of Patients Achieving A1C ≤7%

Exenatide: Effect on the -CellExenatide: Effect on the -Cell

Exenatide: Clinical PharmacologyExenatide: Clinical Pharmacology

ADA/EASD: Glucose-Lowering Interventions as Monotherapy—Step 2 (cont)ADA/EASD: Glucose-Lowering Interventions as Monotherapy—Step 2 (cont)

ADA/EASD: Glucose-Lowering Interventions as Monotherapy—Step 2 (cont)ADA/EASD: Glucose-Lowering Interventions as Monotherapy—Step 2 (cont)

EuglycemiaEuglycemiaEuglycemiaEuglycemia

Healthy Subjects (n = 14)

Beta-CellWorkload

Beta-CellWorkload

Beta-CellResponse

Beta-CellResponse

Beta-CellWorkload

Beta-CellWorkload

HyperglycemiaHyperglycemia

Type 2 Diabetes (n = 12)

Beta-CellWorkload

Beta-CellWorkload

Beta-CellResponse

Beta-CellResponse

Beta-CellWorkload

Beta-CellWorkload

Mean (SE)

The Pathogenesis of DiabetesThe Pathogenesis of DiabetesBeta-Cell Workload Outpaces Beta-Cell ResponseBeta-Cell Workload Outpaces Beta-Cell ResponseThe Pathogenesis of DiabetesThe Pathogenesis of DiabetesBeta-Cell Workload Outpaces Beta-Cell ResponseBeta-Cell Workload Outpaces Beta-Cell Response

Incretin Effect*

*

*

*

**

*

GLP-1 secreted upon the ingestion of food

*

*

*

*

* * *

*** *

** *

*

** * *

GLP-1GLP-1 GLP-1GLP-1GLP-1GLP-1

GEPeterson,DO,FACP

Exanetide reduced post prandial glucose and glucagon

Exanetide

Exanetide and placebo Exanetide and placeboExanetide and placebo

ADA: Clinical Practice Recommendations. 2008.

Goals of Intensive Diabetes Management

Near-normal glycemia– HbA1c less than 6.5 to 7.0%

Avoid short-term crisis– Hypoglycemia– Hyperglycemia– DKA

Minimize long-term complications

Improve QOL

Comparison of Human Insulins / Analogues

Insulin Onset of Duration ofpreparations action Peak action

Regular 30–60 min 2–4 h 6–10 h

Aspart-Glulisine-Lispro 5–15 min 1–2 h 4–6 h

NPH 1–2 h 4–8 h 10–20 h

Glargine 1–2 h Flat ~24 h

Detemir 30 min Flat 24h

Short-Acting Analogs Aspart-Glulisine-Lispro

Convenient administration immediately prior to meals

Faster onset of action

Limit postprandial hyperglycemic peaks

Shorter duration of activity– Reduce late postprandial hypoglycemia– Frequent late postprandial hyperglycemia

Need for basal insulin replacement revealed

400

350

300

250

200

150

100

MealSC injection

50

00 30 60

Time (min)90 120 180 210150 240

Regular Lispro

500450400350300250

150

50

200

100

00 50 100

Time (min)150 200 300250

Pla

sm

a i

ns

uli

n (

pm

ol/

L)

Pla

sm

a i

ns

uli

n (

pm

ol/

L)

MealSC injection

Heinemann, et al. Diabet Med. 1996;13:625–629; Mudaliar, et al. Diabetes Care. 1999;22:1501–1506.

Short-Acting Insulin Analogs

Regular Aspart

Pharmacokinetic Comparison Aspart and Lispro

300

350

250

200

150

100

50

0

7 8 9 10 11 12 13

Aspart

Lispro

Fre

e In

sulin

(p

mo

l/L)

Time (hours)Hedman, Diabetes Care 2001; 24(6):1120-21

1 5 10 15 20 25 30

1 5 10 15 20Asp

Gly

ArgExtension

Substitution

Arg

Insulin GlargineA New Long-Acting Insulin Analog

Modifications to human insulin chain

– Substitution of glycine at position A21

– Addition of 2 arginines at position B30

Gradual release from injection site

Peakless, long-lasting insulin profile

Lepore, et al. Diabetes. 1999;48(suppl 1):A97.

6

5

4

3

2

1

00 10

Time (h) after SC injection

End of observation period

20 30

GlargineNPH

Glu

cose

uti

lizat

ion

rat

e(m

g/k

g/h

)

Glargine vs NPH Insulin in Type 1 DiabetesAction Profiles by Glucose Clamp

Glucose Infusion Raten = 20 T1DMMean ± SEM

SC insulin

4.0

3.0

2.0

1.0

0

24

20

16

12

8

4

0

0 4 8 12 16 20 24Time (hours)

mg

/kg

/min

µm

ol/k

g/m

in

Lepore M, et al. Diabetes. 2000;49:2142–2148.

NPH

Ultralente

CSII

Glargine

Glargine

Plasma Glucose

Time (hours)

220

200

180

160

140

120

12

11

10

9

8

7

0 4 8 12 16 20 24

mg

/dL

mm

ol/L

Lepore M, et al. Diabetes. 2000;49:2142–2148.

n = 20 T1DMMean ± SEM

SC insulin

NPH

Ultralente

CSII

GE Peterson,DO,FACP

Detemir: Basal Analog

Detemir Clinical Pharmacology

DetemirDetemir

Detemir

Detemir

GE Peterson, DO, FACP

Detemir

Insulin Detemir

GEPeterson,DO,FACP

Detemir

Detemir

GEPeterson,DO,FACP

Insulin Detemir Insulin DetemirInsulin Detemir

Insulin Detemir

GEPeterson,DO,FACP

Insulin Detemir

GEPeterson,DO,FACP

Treatment with basal insulin detemir is associated

Detemir

Overall Summary: Basal Insulin Analogs

Both insulin detemir and glargine appear to be effective

once daily duration.

Insulin detemir has less variability

Both have comparable glycemic control (FBG)

Insulin detemir appears to have lower risk of nocturnal

hypoglycemic events

Insulin detemir may be associated with less weight gain.

Safety profile similar to that of human insulin

The Basal/Bolus Insulin Concept

Basal insulin– Suppresses glucose production between

meals and overnight– 40% to 50% of daily needs

Bolus insulin (mealtime)– Limits hyperglycemia after meals– Immediate rise and sharp peak at 1 hour – 10% to 20% of total daily insulin requirement

at each meal

Basal vs Mealtime Hyperglycemia in Diabetes

Riddle. Diabetes Care. 1990;13:676-686.

Pla

sma

Glu

cose

(m

g/d

L)

200

100

00600 1200

Time of Day1800 2400

Type 2 Diabetes

0600

150

250

50

Basal hyperglycemia Mealtime hyperglycemia

6-18

Normal

AUC from normal basal >1875 mgm/dL.hr; Est HbA1c >8.7%

When Basal Corrected

Pla

sma

Glu

cose

(m

g/d

L)

200

100

00600 1200

Time of Day1800 2400 0600

150

250

50


6-18

Normal


AUC from normal basal 900 mgm/dL.hr; Est HbA1c 7.2%

When Mealtime Hyperglycemia Corrected

Pla

sma

Glu

cose

(m

g/d

L)

200

100

00600 1200

Time of Day1800 2400 0600

150

250

50


6-18

Normal


AUC from normal basal 1425 mgm/dL.hr; Est HbA1c 7.9

When Both Basal & Mealtime Hyperglycemia Corrected

Pla

sma

Glu

cose

(m

g/d

L)

200

100

00600 1200

Time of Day1800 2400 0600

150

250

50


6-18

Normal


AUC from normal basal 25 mg/dL.hr; Est HbA1c 6.4%

Glucose Correction Factor

1700 Rule says:

John Smith’s Total Insulin Dose

60 units insulin/day

1700/40= 42

So, 1 unit Short Acting Analog will

lower BG about 40 mg/dl

Correction Bolus Formula

Example:

– Current BG: 220 mg/dl

– Ideal BG: 100 mg/dl

– Glucose Correction Factor: 40 mg/dl

Current BG - Ideal BGGlucose Correction factor

220 - 100 40

=3.0u

Intensive Therapy for Type 1 Diabetes

Careful balance of food, activity, and insulin

Daily self-monitoring BG

Patient trained to vary insulin and food

Define target BG levels (individualized)

Frequent contact of patient and diabetes team

Monitoring HbA1c

Basal / Bolus insulin regimen

Carbohydrate Counting

Most individuals need 1 Unit of insulin for every 15 GM of carbohydrate eaten.

Insulin/Carb varies with food eaten

Problems with fat content and time of day

Individual variation for time of day

Options in Insulin Therapy

Current

– Multiple injections

– Insulin pump (CSII)

Future

– Implant (artificial pancreas)

– Transplant (pancreas; islet cells)

1.0

0.8

0.6

0

Insulin

Time

Multiple Injection TherapyIntermediate & Short-Acting Insulin Pre-Meal

Injections1.0

0.8

0.6

0

Insulin

Time

Multiple Injection TherapyIntermediate & Short-Acting Insulin Pre-Meal

Injections1.0

0.8

0.6

0

Insulin

Time

Multiple Injection Therapy Intermediate & Short-Acting Insulin Pre-Meal

Case #1: DM 1 on MDI46 year old white male power line supervisor

DM 1 age 40

On MDI: 10 u lispro pre-meal, 20 u NPH HS

HbA1c 7.4%

SMBG avg 124 mg/dL based on 1.9 tests/day (fasting 171 mg/dL, noon 105 mg/dL, pm 125 mg/dL, HS 75 mg/dL)

Case #2: DM 1 on MDILantus (glargine) 20 u HS added in place of NPH

No change in behavior (diet, SMBG frequency)

Seen three months later (8-16-01)

HbA1c 6.3%

SMBG average 104 mg/dL (fasting BG 91 mg/dL, noon 126 mg/dL, pm 116 mg/dL, HS 126 mg/dL

NO HYPOGLYCEMIA

HAPPY

Insulin Pens

Lauritzen. Diabetologia. 1983;24:326–329.

Fast (n = 12)

Semilente (n = 9)

Intermediate (n = 36)

Fra

ctio

n a

t in

j. si

te

1.00

0.75

0.50

0.25

06 12 18 24 36 42 4830

Hours after single SC injectionsFemoral region

Variability of Insulin Absorption

CSII <2.8%

SubcutaneousInjectable10% to 52%

Pump TherapyBasal & Bolus Short-Acting Insulin



Combined with SMBG, physiologic insulin requirements can be achieved more closely

Flexibility in lifestyle

History of Pumps

Paradigm Pump: Advantages

29% smaller, water resistant

Menu driven:

bolus, suspend, basal, prime, utilities

Reservoir based (easier to fill)

Silent motor

AAA batteries

Paradigm Pump: Advantages

Various bolus options

normal, square, dual, and “easy bolus”

Enhanced memory

Enhanced safety features

(low reservoir alarm, auto off, etc.)

Pump Infusion Sets

Softset QR Silhouette

Lauritzen. Diabetologia. 1983;24:326–329.

Pharmacokinetic Advantages CSII vs MDI

Uses only regular or very rapid insulin– More predictable absorption than modified

insulins (variation 3% vs 52%)

Uses 1 injection site– Reduces variations in absorption due

to site rotation

Eliminates most of the subcutaneous insulin depot

Programmable delivery simulates normal pancreatic function

Metabolic Advantages with CSII

Improved glycemic control

Better pharmacokinetic delivery of insulin

– Less hypoglycemia

– Less insulin required

Improved quality of life

8.18

8.58.2

8.9

6.96.977

7.6

6

7

8

9

10

Baseline 1 yr 2 yr 3 yr 4 yr

Adolescent (37) Adult (166)

Glycemic ControlH

bA

1c

Atlanta Diabetes Associates

CSII Reduces HbA1c

5.05.56.06.57.07.58.08.5.099.5

10.0

n = 58 n = 107 n = 116 n = 50 n = 25 n = 56Mean dur. = 36

Adolescents Adults

Mean dur. = 36 Mean dur. = 54 Mean dur. = 42 Mean dur. = 12 Mean dur. = 12

Chantelau E, et al. Diabetologia. 1989;32:421–426; Bode BW, et al. Diabetes Care. 1996;19:324–327;Boland EA, et al. Diabetes Care. 1999;22:1779–1784; Bell DSH, et al. Endocrine Practice. 2000;6:357–360;Chase HP, et al. Pediatrics. 2001;107:351–356.

Bell Rudolph Chanteleau Bode Boland Chase

Pre-pump Post-pump

Hb

A1

c

Ep

iso

des

/mo

nth

/pat

ien

t

0

2

4

6

8

10

12

insulin aspart human insulin insulin lispro

pp < 0.05 < 0.05

pp < 0.05 < 0.05

Symptomatic or Confirmed Hypoglycaemia

30% relative reduction

Bode et al: Diabetes Care, March 2002

7.197.57

9.2

5.00

6.00

7.00

8.00

9.00

10.00

Baseline 6 months 18 months

P = 0.026 P = 0.040

N = 11

CSII Usage in Type 2 PatientsThe Diabetes Center

Mean HbA1c (%)

Glycemic Control in Type 2 DM: CSII vs MDI in 127 patients

A1C

7.0

7.2

7.4

7.6

7.8

8.0

8.2

8.4

CSII MDI

Baseline

End of Study (24 wks)

Raskin, Diabetes 2001; 50(S2):A106

DM 2 Study: CSII vs MDI

Overall treatment satisfaction improved in the CSII group: 59% pre to 79% at 24 weeks

93% in the CSII group preferred the pump to their prior regiment (insulin +/- OHA)

CSII group had less hyperglycemic episodes (3 subjects, 6 episodes vs. 11 subjects, 26 episodes in the MDI group)

CSII Reduces Hypoglycemia

0

20

40

60

80

100

120

140

160

n = 55Mean age 42

n = 107Mean age 36

n = 116Mean age 29

n = 25Mean age 14

n = 56Mean age 17

Eve

nts

per

hu

nd

red

p

atie

nt

y ea r

s

Chantelau E, et al. Diabetologia. 1989;32:421–426; Bode BW, et al. Diabetes Care. 1996;19:324–327;Boland EA, et al. Diabetes Care. 1999;22:1779–1784; Chase HP, et al. Pediatrics. 2001;107:351–356.

Bode Rudolph Chanteleau Boland Chase

Pre-pump Post-pump

48.1

34.539.3 40.1 39.8

0

10

20

30

40

50

60

Baseline(MDI)

15 days 6 mos 18 mos 36 mos

-28% -18% -16% -17%

* P <0.001

** * *

n = 389 n = 389 n = 298 n = 246 n = 187

Insulin Reduction Following CSII

Normalization of Lifestyle

Liberalization of diet — timing & amount

Increased control with exercise

Able to work shifts & through lunch

Less hassle with travel — time zones

Weight control

Less anxiety in trying to keep on schedule

N = 165Average Duration = 3.6 yearsAverage Discontinuation <1%/yr

Continued 97%

Discontinued 3%

Current Continuation RateContinuous Subcutaneous Insulin Infusion (CSII)

Bode BW, et al. Diabetes. 1998;47(suppl 1):392.

Pump Therapy Indications

HbA1c >7.0%

Frequent hypoglycemia

Dawn phenomenon

Exercise

Pediatrics

Pregnancy

Gastroparesis

Hectic lifestyle

Shift work

Type 2

Marcus. Postgrad Med. 1995.

Poor Candidates for CSII

Unwilling to comply with medical follow-up

Unwilling to perform self blood glucose monitoring 4 times daily

Unwilling to quantitate food intake

Current Candidate Selection

Patient Requirements

– Willing to monitor and record BG

– Motivated to take insulin

– Willing to quantify food intake

– Willing to follow-up

– Interested in extending life

What Type of Bolus Should You Give?

9 DM 1 patients on CSII ate pizza and coke on four consecutive Saturdays

Dual wave bolus (70% at meal, 30% as 2-h square):

9 mg/dl glucose rise

Single bolus: 33 mg/dl rise

Double bolus at -10 and 90 min: 66 mg/dl rise

Square wave bolus over 2 hours: 80 mg/dl rise

Chase et al, Diabetes June 2001 #365

Treatment of Hypoglycemia

Education

–Glucose tablets

–Glucagon

Call healthcare team

–Any hypoglycemic events requiring assistance

Treatment of Hyperglycemia

If blood glucose is above 250 mg/dl

– Take a correction bolus by pump– Check BG again in 1 hr

If still above 250 mg/dl

– Take correction bolus by syringe– Change infusion set and reservoir– Check BG again in 1 hr

If BG has not decreased

– Increase correction bolus by syringe– CALL PHYSICIAN

If HbA1c is Not to Goal

SMBG frequency and recording

Diet practiced

– Do they know what they are eating?

– Do they bolus for all food and snacks?

Infusion site areas– Are they in areas of

lipohypertrophy?

Other factors:– Fear of low BG– Overtreatment of low BG

Must look at:

Evolution of Diabetes Management Technologies

Insulin Injections

Urine Test Strips

Glucose Sensor

ArtificialPancreas

1999197819221900s 1977

Urine Tasting

1776

BG Meters

Insulin Pump Therapy

Continuous Glucose Monitoring System CGMS

Pilot Study: CGMS in Young Children with Type 1 Diabetes

• Evaluate the functionality of the MiniMed CGMS in children less than 7 years of age

• Evaluate hypoglycemic patterns in young children using the MiniMed CGMS

• Adjust insulin/dietary regimens based on sensor patterns to prevent hypoglycemia and hyperglycemia

Study Design: Timeline

Clinic Visit 1 Clinic Visit 2 Clinic Visit 3 Clinic Visit 4

0 Months 2 Months 4 Months 6 Months

Sensor 1A

Sensor1B

Two weekslater

Sensor 2A

Sensor2B

Two weekslater

Sensor3A

Sensor 3B

Two weekslater

Third pair of runs is optional

Results

• 19 children enrolled between 12/02 and 7/03• 102 runs, (99 were successful,

>24 hours of data)• 422 days and 319 nights of data collected• Each sensor worn for on average 75.1 ± 25 hours

and provided on average 916 ± 306 glucose values per run

• Total of 88,865 glucose values collected, of which 45,310 were between 8 pm and 8 am

Results: Adverse Events

• Adverse events included mild irritation and rash at the insertion site, which did not require therapy.

• No infections occurred. • The sensor was removed before 48 hours on 11

of 102 runs. Reasons for removal included– fell out (5)

– serial alarms due to low signal (5)

– parents’ preference (1)Fructose. Micro.magnet.fsu.edu

Post-breakfastexcursion

Nocturnal lows

Glucose Trends: CT

Glucose Trends: NB(1)

NPH “run-out”

NPH “run-out” NPH

NPH

NPH

Glucose Trends: NB(2)

NPHNPH

CGMS data on Jackson Pollack

Hypoglycemia Duration and Frequency

• Duration of hypoglycemia did not differ based on age (<5, ≥5yr), pump v. MDI, or HbA1c (<8, ≥8.0%)

• Frequency of mild hypoglycemia was higher in children on the pump (1.1 v. 1.8 episodes per day of monitoring, p<0.05)

• Frequency of severe hypoglycemia did not differ based on insulin regimen

• Frequency of mild or severe hypoglycemia did not differ based on age or HbA1c

Results: Timing of Hypoglycemia

0

10

20

30

40

50

60

70

80

90

100

12a-4a 4a-8a 8a-12p 12p-4p 4p-8p 8p-12a

Severe

Mild

Time of Day

No. ofEpisodes

Conclusions

• CGMS can be used successfully in young children:– Well tolerated without significant adverse effects– Accuracy is acceptable– Defines consistent patterns

• Nocturnal hypoglycemia in young children with diabetes is common– Severe hypoglycemia most frequently occurs between 4a-8a– Duration of hypoglycemia is longer at night

Conclusions

• Post-prandial hyperglycemia is common, especially after breakfast

• HbA1c is positively correlated with severity of glucose rise after breakfast and lunch; a similar association is not seen at dinner

• CGMS can be used to define and assess algorithms which address typical glycemic excursions

Glucose. Micro.magnet.fsu.edu

NEED FOR A CONTINUOUS GLUCOSE SENSOR

• Prevent nocturnal hypoglycemia• Improved diabetes management

– Post prandial highs– Dawn phenomenon

• “Close the loop” and allow for an “artificial pancreas”

• With 4 blood tests/day– 14,600 finger pokes in 10 years– Yet only 0.2% of minutes each day are measured

GLUCOSE MONITORING SYSTEMS - EXTERNAL

Physician downloads data for retrospective analysis

Com-Station and software packages combine data from:

– Sensor

– Models 508 and 507C insulin pumps

– Traditional glucose meters

Physician Product

Role of the School Nurse

Developmental, cognitive, and physical status of the student within his/her family structure to determine the ability of the student to independently manage diabetes care at school.

Identifying and coordinating the medical interventions the student requires at school, based on orders from the health care provider and the nursing assessment of the student;

Determining the nursing interventions and school accommodations needed for all school activities based on the developmental cognitive, and physical status of the student;Identifying and coordinating the interventions for school activities, which may include blood glucose monitoring, insulin administration, dietary intake, and instruction in identifying signs of and response to hypoglycemia/hyperglycemia;

Assisting the student in determining realistic and achievable personal goals for attaining self-care and independence in the management of her/his health.

Documents

Type 1 Diabetes Mellitus Gregory E. Peterson, DO, FACP The Diabetes Center Diagnostic & Critical Care Medicine, PC