10_Lecture_Diabetes Acute Complication Hypoglycemia and DKA STENO Approved

8/13/2019 10_Lecture_Diabetes Acute Complication Hypoglycemia and DKA STENO Approved

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Slide 1

Diabetes Acute Complications Hypoglycemia and DKA

Lecture:

30 minutes


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Slide 2

Management of HypoglycemiaLecture

Main Learning Points

Understand the hypoglycemiamechanism and how hypoglycemiashould be treated

Understand how to adjust OAD - orinsulin dosage after hypoglycemicevents

Understand what causes a DKA event,how DKA is treated and what to do ifyou experience a patient with DKA


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Slide 3

What is hypoglycemia?

neurogenic symptoms due to low plasma glucoselevels

Low plasma glucose levels defined as:

70 mg/dL (ADA)1


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Slide 4

Why address hypoglycemia in diabetes training

Reducing HbA1clevels associated with prevention ordelay in complications and death

Hypoglycaemia is a limiting factor in achievingglycaemic targets

Hypoglycaemia is associated with morbidity and rarely

even be fatal

Optimizing glycaemic control is of obvious importance:

$465 billion USD spent to treat diabetes and itscomplications in 2011; hypoglycaemia is cost-intensive

6.8% of global all-cause mortality attributed to diabetes

in 2010 (4 million deaths)

Cryer et al 2003. Diabetes Care; 26,6: 1902-1912. IDF Diabetes Atlas tthed., 2009. Roglic and Unwin2010. Diabetes Research and Clinical Practice; 87: 15-19


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Slide 5

Most common symptoms of Hypoglycemia

Patients (%)

Circumoral paraesthesia

Difficulties in concentration

Slurred speech

Blurred vision

0 20 40 60 80 100

Hunger

Palpitations

Vertigo

Cold feeling

Anxiety

Euphoria

Weakness

Tremor

Sweating

Headache

Nausea

Pramming 1991


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Slide 6

Sequel of hypoglycaemia

Mild symptomatic hypoglycaemia

No direct serious clinical effects

May impair subsequent hypoglycaemia awareness

Severe hypoglycaemia associated with Stroke and transient ischaemic attacks

Memory loss/cognitive impairment

Myocardial infarction

Injury (direct/indirect) Death

Turner et al. (UKPDS 33), 1998. The Lancet; 352: 837-853


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Slide 7

Risk Factors of Hypoglycemia

General risk factors for hypoglycaemia:1,2

delayed or missed meal

consuming a smaller meal than planned

exercise

use of diabetes medications

drug/alcohol consumption

increased insulin sensitivity or decreased insulin clearance

Risk factors for major hypoglycaemia:3,4

age/duration of diabetes treatment

intensive glycaemic control

hypoglycaemia unawareness sleep

antecedent hypoglycaemia

history of major hypoglycaemia

1.Briscoe & Davis. Clin Diabetes 2006;24:11521; 2. ADA Workgroup on Hypoglycemia. DiabetesCare 2005;28:12459. 3. Frier. Diabetes Metab Res Rev 2008;24:8792; 4. Cryer. Diabetes2008;57:316976


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Slide 8

Hypoglycaemic events occur more often in Type 1diabetes patients and are less frequent and less severein Type 2 diabetes patients both on conventional andintensive therapy

Adapted from DCCT Research Group. Diabetes 1997. Adapted from Bonds D., data presented atADA 2009

Events

per

100

Patien

tYears

HbA1c(%)

Conventional Therapy

0

1020

30

40

50

60

70

80

90

100

6.0 6.5 7.0 7.5 8.0 8.5 9.0

ACCORD (T2 DM)

DCCT (T1 DM)

Events

per

100

Patien

tYears

HbA1c(%)

Intensive Therapy

0

1020

30

40

50

60

70

80

90

100

6.0 6.5 7.0 7.5 8.0 8.5 9.0

DCCT (T1 DM)

ACCORD (T2 DM)


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Slide 9

Prevention of Hypoglycemic Events

Education

Symptoms

Self management

Proper food intake in therapy

Repetitive education in patients with decreased cognitive

function

Self monitoring blood glucose (SMBG)

Exercise planning

Measuring blood glucose before exercise

Consuming carbohydrate Adjust insulin dose based on the blood glucose level

Right type and dose for therapy


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Slide 10

Treatment of mild Hypoglycemia

First: 1020 g fast-acting carbohydrate, e.g.:

36 glucose tablets

90180 ml fizzy drink or squash (not diet)

Two teaspoons of sugar added to a cup of cold drink

50100 ml energy drink (e.g. Lucozade)

Then:

If next meal is due, add extra carbohydrate

If next meal is not due, eat longer-actingcarbohydrate, such as biscuits or a sandwich

Treating early signs

RCN 2004


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Slide 11

Treatment of moderate-to-major Hypoglycemia

Patient requires assistance with treatment

If conscious: Carer should help the patient to consume

1020 g fast-acting carbohydrate

Dextrose gel may be useful

If unconscious: Dont put anything in patients mouth

IM or SC glucagon or IV glucose should beadministered

Emergency services should be called

Treating late signs

RCN 2004; Cryer 2010

IM: intramuscular, SC: subcutaneous, IV: intravenous


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Slide 12

Adjusting Dosage after a Hypoglycemic Event

If hypoglycemic events are

repeated, OAD and / or Insulin

dosages should be reduced

OAD: Depending on drug

Insulin: Initially decrease

with 2 units / day


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Slide 13

Diabetes Ketoacidosis


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What is Diabetes Ketoacidosis

Watkins et al. In: Diabetes and its Management 2003

Acute decompensated metabolic state due to

severe insulin deficiency

over-activity of glucagon & other counter-regulatoryhormone

Common in Type 1; Rare in Type 2

Potentially life-threatening

High mortality

Incidence : 5-8 /1000 diabetic persons/yr

Mortality rates 9-14 % - Has improved with insulin use 2%

Slide 14


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Why are patients developing ketoacidosis

The most common events that cause a person withdiabetes to develop diabetic ketoacidosis are:

infection such as diarrhea, vomiting, and/or highfever (40%)

missed or inadequate insulin (25%)

newly diagnosed or previously unknown diabetes(15%)

Various other causes may include a heart attack,stroke, trauma, stress, alcohol abuse, drug abuse, andsurgery.

Approximately 5% to 10% of cases have noidentifiable cause

Slide 15


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FAKTOR PENCETUS KAD

INSULIN

HIPERGLIKEMIAPEMECAHAN

JARINGAN LEMAK

HYPEROSMOLARITY ASAM LEMAK BEBAS

DIUREUSIS OSMOTIK OKSIDASI

EKSKRESI GLUKOSA URINE PEMBENTUKAN

KETON

PENURUNAN VOLUME

ASIDOSIS KETOSIS

KAD

KEASAMAN

DARAH

PENINGKATAN URINE

K+

Acetoacetate

Beta-Hydroxybutyrate

acetone

glucagon


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How to Diagnose Diabetes Ketoacidosis

Anorexia

Nausea

Vomiting

Thirst

Polyuria

Weakness

Abdominal pain

Weight loss

Tachycardia

Hypotension

Hypothermia

Impaired consciousness

Warm dry skin

Kussmaul respiration

Acetone odour on breath

Symptoms Signs

Slide 17


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Diabetes Ketoacidosis Definitions

Diabetes Care, Vol. 29, Number 12, December 2006

DKA is defined as:

Increase serum concentration of ketonesgreater than 5 mEq/L (betahydroxybutirate acid > 0,6)

Blood glucose level greater than 250mg/dL (although it is usually muchhigher),

Blood pH less than 7.3

Ketonemia and ketonuria arecharacteristic, as is a serum bicarbonatelevel of 18 mEq/L or less (< 5 mEq/L isindicative of severe DKA)

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KRITERIA Dx KAD


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Diagnosis of DKA

Gambaran Klinis: Paling penting nafas

Kussmaul+ Laboratorium

LABORAT:

Hyperglycemia > 250 mg/dl

Ketonuria and ketonemia

Acidosis (PH< 7.3 or bica < 15 mmol/l)


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Objectives and Management of DKA Treatment

1. Search & treatprecipitating cause

2. Insulin iv (rapid / short-acting)

3. Replacing fluids

4. Replacing electrolytes -potassium & magnesium-if required

5. For GPs: If you observe aDKA case, immediatelysend the patient to thehospital

1. To normalize bloodglucose as soon aspossible with Insulin

2. To replace fluids andreverse ketoacidosis

3. Monitoring:

Vital signs

Fluid and electrolytebalance

Glycaemia

Objectives Management

Slide 21


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Terapi pada DKA

Fluid replacement

Electrolyte correction

Acidosis correction

Insulin therapy for hyperglycemia

Treatment of ppt cause


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TERAPI KAD REVISI1998

(ASKANDAR TJOKROPRAWIRO, 1987-1998)

FASE-I

1. Rehidrasi :NaCI 0.9% atau RL, 2L/2jam pertama, lalu 80 tt/m selama 4jam, lalu

30tt/m selama 18 jam (4-6 L/24 jam), diteruskan sampai 24 jam

berikutnya (20tt/m) : Rumus 2, 4, 18-24

2. IDRIV : 4-8 unit/jam i.v (Rumus Minus Satu)

3. Infus K :75 mEq (bila K + < 2.5 mEq/L), 50 mEq (K 2.5-3.0 mEq) dan 25 mEq

Per 24 jam (K + = 3.0-3.5 mEq/I)

4. Infus BIK :Bila pH 7.2-7.3 atau BIK < 12 mEq/I : 50-100 mEq langsung drip dalam2 jam (jangan bolus apabila pH > 7.0)

5. Antibiotika

Glukosa Darah 250 mg/dl atau reduksi

FASE-II

1. Maintenance :NaCI 0.9% atau Pot R (IR 4-8 u) & Maltosa 10% (IR 6-12 u)

bergantian : 20 tt/m2. Kalium :p.e (bila K + < 4 mEq/I) atau per os (air tomat/kaldu)

3. IR :3 X 8-12 U sc (Rumus Kali Dua)

4. Makanan Lunak :Kbh kompleks per oral

Rumus :2, 4, 18-24; Rumus 2, 80, 30, 20; Minus Satu; Kali Dua; Rumus 5-1;

Rumus 2, 5-1; Rumus 654321

GAMBAR 4 Protokol Terapi KAD-Revisi 1998


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Kelainan EKG Hipokalemia

prolongation of QT intervalST segment depression

Flat or diphasic T wavesProminent U waves

Prolongation of PR intervalSinoatrial block

Konsekuensi Hipokalemia:

AritmiaCardiac arrest

Otot pernafasan lemah


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Initial DKA Treatment in Primary Care

Slide 25

1. Evaluate vital signs and urinevolume2. IV line, start the rehydration3. Check the blood glucose

periodically (per hour if possible)

Prepare the patientfor Hospital

12: 12:3 1: 2:30 min. 30 min. 60 min.

Start insulin with bolus IV 180 mU/kgBW, and continue with insulin drip 90mU/hour/kgBW

Check blood glucose per hour with glucometer on the way to hospital

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Diabetes Acute Complication Hypoglycemia and DKALecture

Main Learning Points

Understand the hypoglycemiamechanism and how hypoglycemiashould be treated

Understand how to adjust OAD - or

insulin dosage after hypoglycemicevents

Understand what causes a DKA event,how DKA is treated and what to do ifyou experience a patient with DKA

Summary

The risk of hypoglycemia is one of thekey limiting factors in reaching optimalglucose targets

For Insulin, hypoglycemia is mainly a

phenomenon occurring in Type 1diabetes patients

Prevention of hypoglycemia requirespatient education, frequent bloodglucose monitoring and exerciseplanning

If hypoglycemia occur repeatedly,reduce the dosage of OAD and/orInsulin

DKA should be regarded as anemergency situation and prompttreatment with insulin is vital

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10_Lecture_Diabetes Acute Complication Hypoglycemia and DKA STENO Approved