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    EMERGENCIES IN DIABETES

    R Bowo Pramono

    PERKENI CABANG YOGYAKARTA

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    CV: dr. R Bowo Pramono SpPD K-EMD

    Lahir TEGAL 27-jan 1959 Istri: dr. Astuti, SpS, 2 putriDokter Umum: FK UGM 17-01-1985SpPD : FK UGM 24-11-1997K-EMD : 14-05-2008Pekerjaan: 1987-2002 PKM Kedung Waringin Bekasi 1999-2004 RSU Selong Lombok Timur 2004-2011 RS DR Sardjito/FK UGM

    2

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    DISCUSSION

    HYPOGLYCEMIA

    HYPERGLYCEMIC HYPEROSMOLARSTATE

    DIABETIC KETOACIDOSIS

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    HYPOGLYCEMIA Hypoglycemia is a blood glucose value of less

    than 50 mg/dl

    Clinically, it is defined by Whipple triad: lowplasma glucose level, symptoms consistentwith hypoglycemia, and resolution ofsymptoms with correction of plasma glucose

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    Epidemiology 30% of type 1 or type 2 diabetic patients on

    insulin therapy

    10% of type 2 diabetic patients

    Mortality rate 3-4% especially elderly takinglong acting oral hypoglycemic agents

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    Symptoms

    Adrenergic symptoms (catecholamine mediated):diaphoresis, palpitations, pallor, tachycardiaapprehension, anxiety, sensation of hunger

    headache, weakness,restlessness

    Neuroglycopenic symptoms:reduced intellectual capacity, irritability,confusion, abnormal behavior,convulsion, coma

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    Glucoregulatory factors

    Blood-glucose-loweringfactor

    Blood-glucose-raisingfactors

    Insulin

    Glucose-counterregulatoryfactors

    Glucagon

    Epinephrine

    Growth hormoneCortisol

    in minutes

    In hours

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    Physiologic response in hypoglycemia

    Blood glucose 56-48 mg/dl* adrenalin secretion

    * diaphoresis, tremor

    * reduced function of central nervous system Blood glucose

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    Syndromes of compromised glucosecounterregulation in type 1 diabetes mellitus

    Defective glucose counterregulation

    Impaired awareness of hypoglycemia

    Elevated glycemic threshold during intensive therapy

    Elevated glycemic threshold following recenthypoglycemia

    Elevated glycemic threshold during-adrenergicblockade

    The syndromes may occur in advanced type 2 diabetes mellitus(insulin-deficient)

    Autonomic failure

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    Risk factors

    Tight glycemic control

    Age

    Duration of diabetes

    History of hypoglycemia Sleeping

    Alcoholism

    Fasting

    Increased insulin sensitivity: fitness, body weight

    Clearance/metabolism of drugs: renal or hepaticinsufficiency

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    Mechanisms by which drugs increase thehypoglycemic effect of sulfonilureas

    Increase in half-life due to inhibition of metabolism orexcretion rate:ethanol, phenylbutazone, coumarin anticoagulants,chloramphenicol, doxycycline, sulfonamides,

    allopurinol

    Competition for albumin-binding sites:phenylbutazone, salicylates, sulfonamides

    Inhibition of gluconeogenesis, increase in glucoseoxidation, or stimulation of insulin secretion:ethanol, -adrenergic drugs, monoamine oxidaseinhibitors, tranylcypromine,

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    Management of hypoglycemia

    Mild hypoglycemia when self treatment withoral carbohydrate suffices

    Sever hypoglycemia when external help is

    required to effect recovery

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    Management of hypoglycemia: Prevention

    1. Early familiarization with the symptoms ofhypoglycemia

    2. Do reviewing at intervals

    3. Explain the relationship between insulinadministration, timing of meals, and exercise

    4. Explain methods of self-treating hypoglycemia

    5. Choose appropriate insulin regimens, dose scheduleswith appropriate therapeutic goals

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    Management of hypoglycemia: Treatment

    Mild hypoglycemia: oral glucose 15-20 g, wait 10-15 minthen check blood glucose. If glucose level does notincrease 18 mg/dl, give oral glucose again

    Severe hypoglycemia: solution 50 ml of dextrose 50%given intravenously, check blood glucose in 20 min. Ifit is still hypoglycemia administrate once again

    Glucagon 1.0 mg s.c/i.m/i.v. adverse effects includenausea, vomiting, and headache. Contraindicated tosulfonylureas-induced hypoglycemia. Ineffective in

    patient who is anorectic, or with protractedhypoglycemia

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    DIABETIC KETOACIDOSIS

    AND

    HYPERGLYCEMIC HYPEROSMOLAR STATE

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    Pathophysiology of diabetic ketoacidosis (DKA) andhyperglycemic hyperosmolar state (HHS)

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    laktic acid

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    DKA(DIABETIC KETOACIDOSIS)

    Occurs when muscle cells become so starved forenergy that body takes emergency measures &breaks down fat toxic acids as ketones

    Most common type 1 DM insufficient insulin to

    adjust raise of blood sugar Cause by extreme stress or illness Infection body produce adrenalin works

    against insulin

    Forget to take insulin

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    Signs & symptoms of DKA

    Deep, rapid breathing

    Sweet, fruity smell on breath

    Loss of appetite

    Nausea

    Vomiting

    Fever

    Stomach painWeight loss

    Fatigue

    Weakness

    Confusion

    Drowsiness

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    Clinical presentation

    Lost more than 5% body weight

    More than 35 breaths a minute

    Cant control blood sugarBecome confused

    Nausea and vomiting

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    What should you do?

    Check ketones if feeling especiallystressed or blood sugar persistently above240mg/dL

    High ketones in blood ketones excretedin urine.

    High ketones in urine should be treated & nhospitalized

    DKA can lead into coma and possibly death.

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    Treatment

    Correcting lost fluids through i.v. line

    Glucose infusion with insulin may stopketones production

    Decrease blood sugar level gradually,decreasing glucose rapidly mayproduce brain swelling

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    Al ith I I li I f i Th

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    Algorithm I.v. Insulin Infusion Therapy

    BG (mg/dL) Insulin infusion dose (u/hr)Algr1 Algr2 Algr3 Algr4

    < 60 = Hypoglycemia (need dextrose Tx)60-70 0 0 0 070-109 0,2 0,5 1 1,5

    110-119 0,5 1 2 3

    120-149 1 1,5 3 5150-179 1,5 2 4 7180-209 2 3 5 9210-239 2 4 6 12240-269 3 5 8 16

    270-299 3 6 10 20300-329 4 7 12 24330-359 4 8 14 28>360 6 12 16 28

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    HHS (HYPERGLYCEMIC HYPEROSMOLAR STATE)

    A high level of blood glucose may interfere bloodcirculation (level >600 mg/dl)

    Glucose uptake by the cells decreases, the glucosepassed from blood to urine draws tremendousamounts of fluid from body and producesdehydration

    Common in type 2 DM, especially who does notmonitor blood sugar, and who does not know have

    DM Trigger factors: high-dose steroid, diuretics,

    infection, illness, stress or drinking excessive alcohol

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    HHS: signs & symptoms

    Excessive thirst

    Increased urination

    Weakness

    Leg cramps

    Confusion

    Rapid pulse

    Convulsions Coma

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    What should you do?

    Check blood glucose level (> 600mg/dL) Emergency treatment can correct the

    problem within hours

    Give intravenous fluids to restore water tothe tissue

    Short acting insulin to help cells can uptakeglucose

    Without prompt treatment can be fatal

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