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DIABETIC EMERGENCIES IN IMCU. DR.P.DHARMARAJAN M.D., Dip. Diab., Asst. Prof. of Diabetology, Dept. of Diabetology, Madras Medical College & Govt. General Hospital, Chennai – 600 003. INTRODUCTION.
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DIABETIC EMERGENCIES IN IMCU DR.P.DHARMARAJAN M.D., Dip. Diab., Asst. Prof. of Diabetology, Dept. of Diabetology, Madras Medical College & Govt. General Hospital, Chennai – 600 003.
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.
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
FH positive Symptoms + Ketosis + Not benign Irreversible GHb elevated FH negative Symptoms – Ketosis – Benign Reversible GHb normal Undiagnosed DMStress HG Management – control of HG with insulin, preferably
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
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.
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
TREATMENT • Fluid management (Loss of TBW – 25%) • Insulin therapy • Management of Electrolyte disturbances • Treatment of the precipitating cause
LACTIC ACIDOSIS • 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
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
ALCOHOLIC KETOACIDOSIS • May follow a heavy alcoholic binge • Can co-exist with DKA / LA • Treatment – treatment of acidosis
OTHERS - AMI • Prevalence and incidence more • Comp. younger age group affected • Males and Females equally affected • Severity and extent more • Morbidity and Mortality more
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
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