Download Free Medical Diabetic Ketoacidosis-DKA and Hyperglycemic Hyperosmolar State-HHS PowerPoint Presentation

Diabetic Ketoacidosis-DKA and Hyperglycemic Hyperosmolar State-HHS PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical PowerPoint presentation titled "Diabetic Ketoacidosis (DKA) & Hyperglycemic Hyperosmolar State (HHS)" by Ulrich K. Schubart, MD.

This medical PowerPoint presentation talks about Diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS). Both DKA and HHS are serious medical emergencies that can occur in people with diabetes. They are both caused by high blood sugar levels, but there are some key differences between the two conditions.

Tags : Diabetic Ketoacidosis, Hyperglycemic Hyperosmolar State, serious medical emergencies, diabetes, endocrinology, endocrinology PowerPoint presentation

Published on : Apr 18, 2023 | Views : 1614 | Downloads : 3

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Diabetic Ketoacidosis (DKA) &Hyperglycemic Hyperosmolar State (HHS) Ulrich K. Schubart, MD JMC/AECOM
Slide 2-

DKA/HHSPresenting Symptoms Nausea and Vomiting Polyuria and Polydipsia Weakness and/or Anorexia Abdominal Pain Visual Disturbances Somnolence
Slide 3-

DKA/HHSPresenting Signs Tachycardia Hypotension Dehydration Hypothermia Warm dry Skin Kussmaul Respiration Lethargy or Coma Fruity Odor
Slide 4-

Compensatory Hyperventilation in DKA From UpToDate Kety et al. JCI 1948
Slide 5-

DKA/HHS Precipitating Factors Infection Pneumonia Gastroenteritis UTI Sepsis Meningitis Influenza Mucormycosis Emotional Problems Trauma Acute Pancreatitis Myocardial Infarction Stroke Endocrine Acromegaly Thyrotoxicosis Cushing’s S. Omission of Antidiabetic Mx’s Drugs Any major Stress/Acute Illness
Slide 6-

DKA/HHS Drugs that can Precipitate Psychotropic Drugs Chlorpromazine Clozapine Risperidone Loxapine Steroids Immunosuppressants Beta Blockers Calcium Channel Blockers Diuretics Anticonvulsants Diazoxide
Slide 7-

DKA/HHSPathogenesis Precipitating Factors Glucagon Catecholamines Cortisol Growth Hormone Absolute Insulin Deficiency Relative Insulin Deficiency Lipolysis FFAs Proteolysis Gluconeogenesis Ketogenesis Glycogenolysis Minimal Lipolysis Gluconeogenic Substrates Ketoacidosis Hyperglycemia Hyperosmolality Glucosuria (Osmotic Diuresis) Loss of Water & Electrolytes Triglycerides Hyperlipidemia Dehydration Decreased GFR
Slide 8-

DKA/HHSEnhanced Glucose Production G-6-P cAMP Glycogen F-6-P F-1,6-P2 PYR PFK-2 Fat CO2 Glucose Alanine F-2,6P2 Glycerol Glucagon
Slide 9-

DKA/HHS Ketone Body Formation in Liver Fatty Acids Fatty Acyl-CoA Triglycerides Glucose Fatty Acyl-CoA Acetyl-CoA Acetoacetyl-CoA b-Hydroxy-b-methylglutaryl CoA Acetoacetate b -Hydroxybutyrate Acetone NADH NAD Glucagon
Slide 10-

DKA/HHS Glucagon-inducedCatabolic Cascade in Liver Glycogenolysis Glycogen Formation Gluconeogenesis Glycolysis Fatty acyl CoA Ketones Fatty Acids Malonyl-CoA CPT1 Acetyl-CoA Glucose Glucose ACC
Slide 11-

DKA/HHS Ketone Body Utilization in Muscle b -Hydroxybutyrate Acetoacetate Acetoacetyl-CoA Acetyl-CoA Citric Acid Cycle Succinyl-CoA Succinate CoA EXTACELLULAR MITOCHONDRION b -Hydroxybutyrate Acetoacetate Fatty Acids
Slide 12-

DKA/HHSGlucotoxicty & Lipotoxicity Relatively Short Term: Reversible Inhibition of: a) Glucose Uptake and Utilization in Insulin-Responsive Target Tissues b) Insulin Secretion Long-term: a) & b) + Apoptosis of Beta-Cells
Slide 13-

DKA/HHSEssential to R/o Infection Look for meningeal signs - Head CT/MR followed by LP may be indicated Look for necrotic lesions in nasal turbinates to r/o mucormycosis For abdominal pain consider appendicitis cholecystitis pancreatitis diverticulitis PID Obtain CXR Check urine sediment
Slide 14-

DKA/HHS Hyperosmolality Measure and Calculate Serum Osmolality = 2 x measured Na+ (mEq/l) + glucose (mg/dl) /18 + BUN (mg/dl)/2.8 Osmolar Gap = Measured – Calculated Serum Osmolality Effective Serum Osmolality OsmEff (>320 =HHS) = 2 x measured Na+ (mEq/l) + glucose (mg/dl) /18
Slide 15-

DKA/HHS Sodium Correction Corrected Sodium = Measured Sodium + 1.6 x plasma glucose (mg/dl) – 100 100
Slide 16-

DKA/HHS Metabolic Acidosis Plasma Anion Gap = Na+ - [Cl- + HCO3-] (mEq/l)
Slide 17-

DKA/HHSDiagnosis (Average Values)
Slide 18-

DKA/HHSTypical Water and Electrolyte Deficits
Slide 19-

DKA/HHSPoor Prognostic Indicators Advanced Age Low pH Hypotension Marked Hyperosmolality High BUN Associated Diseases
Slide 20-

DKA/HHSTreatment Considerations Precipitating Cause evident in 80% ECG indicated in all adult patients Isotonic NaCl preferred for initial rehydration IV Insulin preferred mode of administration Potassium depletion in all patients Prevention is long-term goal of management Bicarbonate administration rarely indicated
Slide 21-

DKA/HHSOther Considerations in Tx Type & Cross-match as indicated Blood (and other) Cultures as indicated Aspirate Gastric Contents if Comatose Catherize if needed for Output Measurement Give Oxygen if indicated Keep patient NPO
Slide 22-

DKA/HHSEssential Components in Tx IV Fluids Insulin Potassium
Slide 23-

DKA/HHSEssential Components in Tx IV Fluids 2-3 L 0.9% saline during first 3 h Subsequently, 0.45% saline at 150-300 ml/h Add 5% dextrose when plasma glucose reaches 250 mg/dl
Slide 24-

DKA/HHSEssential Components in Tx Insulin 10 U/h iv infusion of short-acting insulin Increase rate 2-10 fold if no response by 4 h Decrease to 1-2 U/h when acidosis is corrected Administer sc insulin before stopping iv infusion
Slide 25-

DKA/HHSEssential Components in Tx Potassium 10-20 mEq/h when plasma K<6.0, ECG normal, urine flow documented 40-80 mEq/h when plasma K <3.5 or if bicarb is given
Slide 26-

DKA/HHS Clinical Monitoring
Slide 27-

DKA/HHSMonitoring Lab Values
Slide 28-

DKA/HHSMonitoring Therapy
Slide 29-

DKA/HHSStimulation of Glucose Utilization and Glycogen Formation by G-6-P Glycogen F-6-P F-1,6-P2 PYR PFK-2 Fat CO2 Glucose F-2,6P2 Insulin
Slide 30-

DKA/HHS -inducedAnabolic Cascade in Liver Glycogenolysis Glycogen Formation Gluconeogenesis Glycolysis Fatty acyl CoA Ketones Fatty Acids Malonyl-CoA Acetyl-CoA Glucose Glucose CPT1 ACC TG Insulin
Slide 31-

DKA/HHS Adverse Effects of Severe Acidosis Impaired Cardiac Contractility Decreased Response to Vasoconstrictors Inhibition of Respiration
Slide 32-

DKA/HHS Potential Adverse Effect of Bicarbonate Administration Significantly Increased Risk of Hypokalemia Decreased Tissue Oxygen Delivery
Slide 33-

DKA/HHSIndications for ConsideringBicarbonate Administration pH < 7.0 or HCO3- < 5.0 K+ > 6.5 Hypotension refractory to fluid replacement Severely impaired LV function Respiratory depression Marked late hyperchloremic acidosis Significant lactic acidosis
Slide 34-

Compensatory Hyperventilation in DKA From UpToDate Kety et al. JCI 1948
Slide 35-

DKA/HHSComplications of Therapy Hypoglycemia Hypokalemia or Hyperkalemia Fluid Overload Hyperchloremic Acidosis Cerebral Edema ARDS Thromboembolic Episodes
Slide 36-

DKA/HHSPrevention Education of Patient and Health Care Providers