10_lecture_diabetes acute complication hypoglycemia and dka steno approved
TRANSCRIPT
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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%
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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
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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
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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
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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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