DIABETIC KETOACIDOSIS By, Dr. ASWIN ASOK CHERIYAN Chair Person – Dr. JAYAMOHAN A.S.

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Presentation transcript:

DIABETIC KETOACIDOSIS By, Dr. ASWIN ASOK CHERIYAN Chair Person – Dr. JAYAMOHAN A.S.

What is Diabetes? Diabetes is a clinical syndrome characterized by hyperglycemia due to absolute or relative deficiency of insulin which leads to multiple organ dysfunction. Diabetes is a clinical syndrome characterized by hyperglycemia due to absolute or relative deficiency of insulin which leads to multiple organ dysfunction.

Types of Diabetes Type 1 Diabetes (I.D.D.M.) Type 1 Diabetes (I.D.D.M.) Type 2 Diabetes (N.I.D.D.M.) Type 2 Diabetes (N.I.D.D.M.) Other types like- Other types like- Gestational Diabetes mellitus Gestational Diabetes mellitus DM due to genetic defects in insulin action DM due to genetic defects in insulin action DM due to diseases of exocrine pancreas DM due to diseases of exocrine pancreas

Complications of Diabetes ACUTE ACUTE 1. Diabetic Ketoacidosis 2. Hyperosmolar Non-ketotic Diabetic Coma 3. Hypoglycemia 4. Lactic acidosis CHRONIC CHRONIC 1. Microvasular- Diabetic Neuropathy Diabetic Retinopathy Diabetic Nephropathy 2. Macrovasular- Coronary Artery Disease Peripheral Vascular Disease Cerebrovascular disease

Diabetic Autonomic Neuropathies like Diabetic Autonomic Neuropathies like Gastro paresis Gastro paresis Sexual Dysfunction Sexual Dysfunction Some Dermatological Complications are also present Some Dermatological Complications are also present

DIABETIC KETOACIDOSIS or DKA A major medical emergency A major medical emergency Usually seen in Type 1 Diabetic patients Usually seen in Type 1 Diabetic patients The incidence is higher in elderly patients The incidence is higher in elderly patients Mortality in developed countries - about 5-10% Mortality in developed countries - about 5-10% Mortality in developing countries – Mortality in developing countries – about 30–40% about 30–40%

Precipitating Factors Rapid decrease or no insulin intake Rapid decrease or no insulin intake Infections Infections Severe stress (physical and emotional) Severe stress (physical and emotional)

Pathogenesis DKA results from DKA results from Insulin deficiency and Insulin deficiency and Glucagon excess Glucagon excess

The key features in DKA are : Hyperglycemia Hyperglycemia Volume Depletion and Dehydration Volume Depletion and Dehydration Hyperketonemia Hyperketonemia Metabolic Acidosis Metabolic Acidosis

Clinical Presentation in DKA Polyurea with signs of dehydration Polyurea with signs of dehydration Nausea, Vomiting Nausea, Vomiting Abdominal pain Abdominal pain Tachypnoea – Kussmauls Breathing Tachypnoea – Kussmauls Breathing Weakness, Confusion Weakness, Confusion Altered Consciousness or Frank coma Altered Consciousness or Frank coma

On Examination the patient may have: Hypothermia Hypothermia Hypotension Hypotension Fruity odour of breath- Due to Acetone Fruity odour of breath- Due to Acetone

Investigations: Urine analysis- Presence of glucose and Ketones Urine analysis- Presence of glucose and Ketones Blood sugar analysis- Increase in plasma glucose levels Blood sugar analysis- Increase in plasma glucose levels Plasma ketone levels are raised Plasma ketone levels are raised Electrolyte levels Electrolyte levels Plasma Potassium Plasma Potassium Plasma Bicarbonate Plasma Bicarbonate Hydrogen ion concentration is raised Hydrogen ion concentration is raised Arterial pH is low Arterial pH is low Blood count and culture Blood count and culture ECG ECG Chest X-ray Chest X-ray

Diagnostic Criteria for DKA : Blood Glucose > 250 mg/dl Blood Glucose > 250 mg/dl Arterial pH < 7.3 Arterial pH < 7.3 Moderate degree of ketonaemia and/or ketonuria Moderate degree of ketonaemia and/or ketonuria

Management of DKA : Insulin Therapy Insulin Therapy Fluid replacement Fluid replacement Replacement of Electrolytes Replacement of Electrolytes Correction of Acidosis Correction of Acidosis Antibiotics Antibiotics

Insulin Therapy Rapid acting insulin is used Rapid acting insulin is used Bolus- 10 units of insulin iv + 10 units s/c Bolus- 10 units of insulin iv + 10 units s/c Followed by iv infusion of 50 units of plain insulin in 500ml normal saline at the rate of 30 drops/min (10 units/hr) Followed by iv infusion of 50 units of plain insulin in 500ml normal saline at the rate of 30 drops/min (10 units/hr) till RBS < 250 mgm% till RBS < 250 mgm% Once RBS < 250 mgm%, Stop iv insulin infusion Once RBS < 250 mgm%, Stop iv insulin infusion Start s/c insulin 8 th hrly with iv DNS, ie. 2/3 rd the dose of total insulin given so far. Start s/c insulin 8 th hrly with iv DNS, ie. 2/3 rd the dose of total insulin given so far.

Points to be noted during insulin therapy : If blood glucose does not fall within two hours of treatment- the dose of insulin should be doubled If blood glucose does not fall within two hours of treatment- the dose of insulin should be doubled A more rapid fall in glucose should be avoided as hypoglycemia can be precipitated and a serious complication of Cerebral Edema may develop A more rapid fall in glucose should be avoided as hypoglycemia can be precipitated and a serious complication of Cerebral Edema may develop

Fluid Replacement : Early and rapid rehydration is essential Early and rapid rehydration is essential Usual regimen- Usual regimen- 2 pints of NS in the first half hour 2 pints of NS in the first half hour + 2 pints of NS in the next hour 2 pints of NS in the next hour + 2 pints of NS in the next 2 hours 2 pints of NS in the next 2 hours An accurate record of fluid input and output must be maintained. An accurate record of fluid input and output must be maintained.

Replacement of Electrolytes : Potassium Replacement Potassium Replacement Bicarbonate Replacement Bicarbonate Replacement

Additional Procedures : Catheterization if no urine is passed after 3 hours Catheterization if no urine is passed after 3 hours Nasogastric tube to keep Stomach empty in unconscious patients Nasogastric tube to keep Stomach empty in unconscious patients Antibiotics should be given to treat the infections Antibiotics should be given to treat the infections

Monitoring : Blood glucose and electrolytes hourly for 3 hrs and every 2-4 hrs thereafter Blood glucose and electrolytes hourly for 3 hrs and every 2-4 hrs thereafter Temperature, Pulse, Respiration and BP hourly Temperature, Pulse, Respiration and BP hourly Urinary output and ketone levels Urinary output and ketone levels ECG ECG

Complications of DKA : Cerebral Edema Cerebral Edema Hypoglycemia Hypoglycemia Acute Respiratory Distress Syndrome Acute Respiratory Distress Syndrome Thromboembolism Thromboembolism DIC DIC Acute Circulatory Failure Acute Circulatory Failure Myocardial Infarction Myocardial Infarction

Prognosis : Poor prognostic signs at admission are Hypotension, Azotemia, Deep Coma and Associated illness. Poor prognostic signs at admission are Hypotension, Azotemia, Deep Coma and Associated illness.

Prevention : Prevention of DKA can be attained to a certain level – Prevention of DKA can be attained to a certain level – By making the patients aware of the importance of insulin during an illness and the reasons never to discontinue insulin without consulting with the doctor first. By making the patients aware of the importance of insulin during an illness and the reasons never to discontinue insulin without consulting with the doctor first. By making the patients aware of the importance of routine blood glucose evaluation and the use of supplemental short or rapid acting insulin's. By making the patients aware of the importance of routine blood glucose evaluation and the use of supplemental short or rapid acting insulin's. The importance of treating an infection at the earliest. The importance of treating an infection at the earliest.

Last but not the Least…..

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