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DIABETIC EMERGENCIES IN IMCU. INTRODUCTION Management of Diabetes and Hyperglycemia in IMCU setting involves the diagnosis and management of two different.

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Presentation on theme: "DIABETIC EMERGENCIES IN IMCU. INTRODUCTION Management of Diabetes and Hyperglycemia in IMCU setting involves the diagnosis and management of two different."— Presentation transcript:

1 DIABETIC EMERGENCIES IN IMCU

2 INTRODUCTION Management of Diabetes and Hyperglycemia in IMCU setting involves the diagnosis and management of two different situations.  Non-DM – a non-diabetic patient admitted to the IMCU and detected to have hyperglycemia for the first time.  DM – a known diabetic patient admitted to the IMCU with complications which may or may not be related to diabetes.

3 1. Non-DM: A non-diabetic patient admitted to the IMCU and detected to have hyperglycemia for the first time may have one of the following:  Undiagnosed DM  Stress hyperglycemia

4 Undiagnosed DM Stress HG  FH positive  Symptoms +  Ketosis +  Not benign  Irreversible  GHb elevated FH negative Symptoms – Ketosis – Benign Reversible GHb normal Management – control of HG with insulin, preferably

5 2. DM: The differential diagnosis of a known diabetic patient admitted to the IMCU in a semicomatose or comatose state includes the following.  Hypoglycemia  DKA  HNAD (HNKC)  Lactic Acidosis  Alcoholic ketoacidosis  Other acute complications – AMI / CVA – Stroke / Head injury or Trauma / Drug overdosage or Poisoning

6 HYPOGLYCEMIA

7 HYPOGLYCEMIA  Diagnosis of hypoglycemia is essentially clinical.  Documentation of hypoglycemia requires the presence of Whipple’s triad namely, symptoms of hypoglycemia, biochemical documentation of low plasma glucose values and prompt resolution of symptoms with administration of glucose.  If prompt clinical recovery is not seen or if the patient has a prolonged coma for more than one hour think of irreversible cerebral damage or other alternative causes for coma thus revising the diagnosis.

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17 DIABETIC KETOACIDOSIS

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39 HNKC

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41 Formula for calculating osmolarity -2(Na+ K+) + PG in mmol + BU in mmol Normal value -290 to 310 mOsm / l Level of consciousness worsens with increasing osmolarity

42 TREATMENT Fluid management (Loss of TBW – 25%) Insulin therapy Management of Electrolyte disturbances Treatment of the precipitating cause

43 LACTIC ACIDOSIS

44  Definition - Arterial WB lactate more than 5mmol/L -Arterial pH < 7.3  May coexist with DKA  Classified into Type A & Type B  Can be caused by biguanides  Carries a high mortality rate

45  Persistence of increased AG in a case of DKA even after resolution of ketones indicates co- existent LA  Treatment – treat the underlying cause Vasodilators / Vasoconstrictors / Sodabicarb / Sodium dicloroacetate / Carbicarb Dialysis for MALA

46 ALCOHOLIC KETOACIDOSIS

47  May follow a heavy alcoholic binge  Can co-exist with DKA / LA  Treatment – treatment of acidosis

48 OTHERS - AMI  Prevalence and incidence more  Comp. younger age group affected  Males and Females equally affected  Severity and extent more  Morbidity and Mortality more

49  General principles of treatment of AMI in DM does not differ from Non-DM  Relief of pain / O2 / ABC / Thrombolytic therapy / Antiplatelet therapy / Anticoagulant therapy / ACEI / Beta blockers / Supportive measures  In complicated cases treatment of arrythmias / LVF / Shock / Emergency PTCA and CABG

50 GIK  GIK infusion – High Dose - Low Dose  HD – 25 % Dex. + 50 U PI + 80 mmol KCl at 1.5 ml/kg/hr – 24hrs  LD – 10 % Dex. + 20 U PI + 40 mmol KCl at 1 ml/kg/hr – 24 hrs

51 GIK - ADVANTAGES  Larger amount of viable myocardium  Earlier the infusion is started the better is the benefit  HD GIK superior to LD GIK  43 % reduction in mortality

52 GIK – MECH. OF ACTION  Decreases ischemic injury protecting against subsequent myocardial dysfunction  Beneficial secondary metabolic effects decrease long term mortality  Improvement in general patient care incident to institution of insulin treatment

53  Thrombolysis (SK) benefits DM with AMI more than Non-DM with AMI  SK is not contraindicated even if patient has PDR  SK is indicated even in diabetic patient with cardiogenic shock

54 SURGERY PTS. WITH POST-OP BS >12.2.MMOL/L HAVE PTS. WITH POST-OP BS >12.2.MMOL/L HAVE GREATER INFECTION RATES GREATER INFECTION RATES INCREASED HOSPITAL STAY IN PTS WITH NEW INCREASED HOSPITAL STAY IN PTS WITH NEW HYPERGLYCEMIA HYPERGLYCEMIA INCREASED MORBIDITY & MORTALITY IN SICU INCREASED MORBIDITY & MORTALITY IN SICU PTS WITH HYPERGLYCEMIA PTS WITH HYPERGLYCEMIA

55 CVD & CORONARY CARE UNITS ADMISSION BG POSITIVELY CORRELATES WITH IN- ADMISSION BG POSITIVELY CORRELATES WITH IN- HOSPITAL & 1 YR MORTALITY HOSPITAL & 1 YR MORTALITY RATES WERE SIGNIFICANTLY LOWER IN PTS WITH RATES WERE SIGNIFICANTLY LOWER IN PTS WITH BG 11 MMOL/L BG 11 MMOL/L DECREASED CHF & REINFARCTION RATES IN PTS DECREASED CHF & REINFARCTION RATES IN PTS TREATED WITH INTENSIVE INSULIN THERAPY FOR TREATED WITH INTENSIVE INSULIN THERAPY FOR FIRST 24 HRS. FIRST 24 HRS.

56 MEDICAL ICU PTS RECEIVING INTENSIVE INSULIN THERAPY HAD SIGNIFICANT REDUCTION IN MORBIDITY. META ANALYSIS SHOWED THAT INTENSIVE INSULIN THERAPY IN INTENSIVE CARE PTS REDUCES IN –HOSPITAL MORTALITY.

57 GLYCEMIC TARGETS IN HOSPITALISED PTS INTENSIVE CARE UNITS-BG CLOSE TO 6.1 MMOL/L GENERAL MEDICAL & SURGICAL WARDS- FBS < 7.1 MMOL & ALL TIME RBS 10.0 –11.0MMOL/L PERI OPERATIVE BS –8.3MMOL/L

58 INSULIN PREFERABLE GLUCOSE LOWERING AGENT IN HOSPITALS PROVIDES FLEXIBILITY TO TITRATE EFFECTIVE IN HYPERGLYCEMIC EMERGENCIES SAFE IN CHF, RENAL & LIVER FAILURE. CAN BE USED PERI-OPERATIVELY CAN BE USED IN PTS WITH ENTERAL & PARENTERAL FEEDING

59 INTRAVENOUS INSULIN USES REGULAR HUMAN INSULIN NO ADVANTAGE OF USING RAPID ACTING ANALOGUES INDICATIONS : 1.DKA 2.HHS 3.PERI –OPERATIVE STATE 4.POST CARDIAC SURGERY/ORGAN TRANSPLANTATION 5.CARDIOGENIC SHOCK 6.NPO PTS WITH HIGH BS.

60 Thank you


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