Hyperglycemia emergency for dm educators

Hyperglycemia Emergencies
Patho-physiology
Diabetes educators basics to remember

1. DKA & HHS Pathogenesis Dr Mohammad Daoud Consultant Endocrinologist KAMC -Jeddah

2. Objectives Introduction Definitions Pathogenesis S & S Management

3. Acute Diabetic Complications 1 -Hyperglycemia : High -Diabetic Ketoacidosis ( DKA )..Type 1 DM -Hyperosmolar Hyperglycemia Syndrome ( HHS ) ..Old Type 2 DM 2 -Hypoglycemia : Low

4. What controls your blood sugar? When we eat …blood sugar (Glucose) increases This stimulates insulin secretion Insulin moves the glucose out of the Blood Cells

5. Glucose :Facts Carbohydrates (Glucose) are the main calorie source for our body Extra CHO are stored as: G lycogen (liver and muscles) OR Fat (Adipose tissue)

6. Glucose :Facts The brain relies almost exclusively on glucose as a fuel, but cannot synthesize or store it Adequate uptake of glucose from the plasma is essential for normal brain function and survival

7. Glucose Physiology Glycogen Breakdown -Liver Increased Glucagon Energy Fat Synthesis Glycogen Synthesis Glucose release to blood (+) Pancreas secretion of Glucagon Blood Glucose Pool (+) Pancreas secretion of Insulin (+) Circulating Insulin Uptake of glucose by cells Decrease blood glucose

8. Glucose :Facts In case of CHO shortage ( ex: Starvation) OR Unable to use CHO ( ex: No insulin as in DKA) Body shifts gear to other sources of energy

9. Glucose :Facts Other sources of energy … Protein breakdown to amino acids and glucose synthesis Fat breakdown into FFA and ketones formation (with acidosis).. Minimal amount of Insulin can prevent Ketogenesis

10. What controls your blood sugar? -Insulin …Lowers -Glucagon…Increases -Other hormones Amount of CHO load Physical activity Stress factors Counter Regulatory Hormones

11. Hyperglycemia Hyperglycemia basic processes are : 1 -Impaired/decreased glucose use 2 -Increased gluconeogenesis ( Make up of glucose from other sources) 3 -Increased glycogenolysis ( breakdown of Glycogen to Glucose )

12. Hyperglycemia Due to variable reasons… Insulin deficiency (Absolute / Relative) Insulin Resistance Excess counter regulatory hormones (Glucagon, Cortisol…) Defected secretion of GLP-1…

13. Electrolyte Losses Renal Failure Shock CV Collapse Insulin Deficiency 13 Hyperglycemia Hyper- osmolality Δ MS Lipolysis  FFAs Acidosis Ketones CV Collapse Glycosuria Dehydration

14. Type 1 Vs Type 2 Type 1DM Immune system stops insulin from being made All ages : More in younger age groups Type 2 DM -Not enough insulin -Insulin resistance) Combination of the two Alpha cell defect Others: GLP-1 , SGLT2 Affects older age group C an affect childre n

15. Type 1 Vs Type 2 Treatment ? Type 1 DM The insulin must be replaced By injection or continuous infusion Type 2 DM Lifestyle changes (TLC) Medications : tablets and/or Insulin

16. Diabetic Hyperglycemic Crises O verlapping Syndromes Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Younger, type 1 diabetes Older, type 2 diabetes No hyperosmolality Hyperosmolality Volume depletion Volume depletion Electrolyte disturbances Electrolyte disturbances Acidosis No acidosis

17. Diabetic Ketoacidosis ( DKA ) Pathophysiology Unchecked gluconeogenesis  Hyperglycemia Osmotic diuresis  Dehydration Unchecked ketogenesis  Ketosis Dissociation of ketone bodies into hydrogen ion and anions  Acidosis Anion-gap metabolic 17 Often a precipitating event is identified ( infection, lack of insulin administration)

18. Hyperosmolar Hyperglycemic State ( HHS ) Pathophysiology Unchecked gluconeogenesis  Hyperglycemia Osmotic diuresis  Dehydration Presents commonly with renal failure Insufficient insulin for prevention of hyperglycemia but sufficient insulin for suppression of lipolysis and ketogenesis Absence of significant acidosis Often identifiable precipitating event (infection, MI) Major body water loss DKA 5-7 L HHS 8- 10 L

19. Hyperglycemia Precipitating Factors Stress: through excess counter regulatory hormones: -Glucagon -Catecholamines (Adrenaline and Nor-Adrenaline) -Cortisol Medications : Steroids, Thiazides ,Beta blockers,… Stopping DM medications Acute illness: Infections (ex;UTI, Pneumonia) ,MI (ACS), Stroke , Acute Pancreatitis, Burn Others: Trauma ,Alcohol, Drug abuse (cocaine ) Feeding (NGT/ PEG/ TPN)

20. DKA -Precipitating Factors Inadequate insulin treatment N oncompliance Insulin error or insulin pump malfunction Poor “sick-day” management New onset diabetes (20 -25%) Acute illness Infection ,CVA, MI ,Acute pancreatitis Drugs: Steroids ,Clozapine or olanzapine Cocaine Lithium , Terbutaline

21. HHS -Precipitating Factors Acute illness : Infection : Pneumonia UTI, Sepsis CVA, MI, Pancreatitis , PE, Severe burns… Endocrine Acromegaly ,Thyrotoxicosis, Cushing's syndrome Drugs Ex ;Steroids Thiazides,TPN Previously undiagnosed DM

22. Hyperglycemia What is DKA? Severe hyperglycemia ; 250-300 mg/dl Ketonemia : ketone bodies in the blood ( β -OH-butyric acid, Acetoacetic acid and Acetone) Acidosis: PH <7.3 = Lack of insulin

23. Hyperglycemia Ketosis Acidosis Adapted from Kitabchi AE, Fisher JN. Diabetes Mellitus. In: Glew RA, Peters SP, ed. Clinical Studies in Medical Biochemistry . New York, NY: Oxford University Press; 1987:105. DKA : Definition

24. Hyperglycemia DKA Inadequate insulin & excess glucagon,catecholamines… Body cannot burn glucose properly Glucose builds up in the bloodstream

25. Hyperglycemia DKA Symptoms of DKA include : Nausea, vomiting Abdomen/Stomach pain Frequent urination Excessive thirst Weakness, fatigue Speech problems Confusion /Unconsciousness

26. Hyperglycemia DKA Signs of DKA include : Kussmaul respirations : Heavy, deep breathing Fruity breath – the smell of ketoacid Tachycardia Supine hypotension, Orthostatic drop of BP ( feel dizzy when standing ) Dry mucous membranes Poor skin turgor Confusion /Unconsciousness

27. Hyperglycemia DKA Inadequate insulin … Fat comes out of fat cells (Free Fatty Acids)…. Free Fatty Acids >> Liver (Mitochondria/ Glucagon) Used as an alternative energy source Makes ketoacids (   ketones ) out of the fat s

28. Hyperglycemia HHS 1- Severe hyperglycemia 2- S. Osmolality > 320 msom/kg 3- Severe dehydration 4- No ketonemia 5- No acidosis

29. HHS There is just enough insulin to keep fat in fat cells and prevent ketone /acids formation ketone levels are usually normal in HHS .

30. Hyperglycemia Hyperosmolarity Ketoacidosis HHS DKA

31. Take Home Messages

32. Hyperglycemic Crisis DKA & HHS Life threatening emergencies DKA …Mostly Type 1 –Young Insulin Deficiency -Acidosis HHS ….Type 2 DM –Older Worse degree of dehydration Both : Similar precipitating factors Electrolytes disturbances

33. DKA Vs HHS Diabetic Ketoacidosis (DKA) Hyperglycemic Hyperosmolar State (HHS) Absolute (or near-absolute) insulin deficiency, resulting in Severe hyperglycemia Ketone body production Systemic acidosis Severe relative insulin deficiency, resulting in Profound hyperglycemia and hyperosmolality (from urinary free water losses) No significant ketone production or acidosis Develops over hours to 1-2 days Develops over days to weeks Most common in type 1 diabetes, but increasingly seen in type 2 diabetes Typically presents in type 2 or previously unrecognized diabetes Higher mortality rate

34. DKA & HHS Early aggressive management Hydration Insulin Electrolytes disturbances Rx Look for precipitating factors : Treat and teach to avoid ..if possible 35

35. Predischarge Checklist Education Diet information Treatment goals “Survival Skills” training “Medic-Alert” bracelet Provide : Glucose monitor and strips Medications, insulin, needles Contact phone numbers

36. Thank You Any Questions ?