1. Acute Diabetic Emergencies Chapter 20

2. Objectives Understanding Diabetes Mellitus Acute Diabetic Emergencies Assessment Emergency Care

3. Understanding Diabetes Mellitus Glucose (Sugar) Major source of fuel for the cells Significantly affects brain cells Tendency to attract water when glucose molecule moves Excess spills off into urine

4. Hormones that control Glucose levels Insulin Increases the movement of glucose out of the blood into the cells Causes the liver to take up glucose out of the blood and convert it to glycogen Decreases the blood glucose level and facilitates the movement of glucose into the cells and liver Not needed to get glucose into the brain

5. Hormones that control Glucose levels Glucagon Converts glycogen stored in the liver back into glucose and released it back into the blood (opposite of insulin) Converts non-carbohydrate substances into glucose Increases and maintains the blood glucose level, converting glucogen and other substances into glucose

6. Hormones that control Glucose levels Other hormones (epinephrine) Released by the adrenal glands when blood glucose level is decreasing to a dangerous low level Stops the secretion of insulin and promotes the release of stored glucose from the liver and converts other substances to glucose

7. Normal metabolism and Glucose regulation Blood glucose level (BGL) increases within an hour of eating Insulin, released by the pancreas, increases movement of glucose into cells As body cells, liver and brain take up glucose, BGL lowers Pancreas secretes glucagon as BGL lowers Liver converts glycogen back to glucose, into bloodstream Glucose enters bloodstream and maintains normal range until next meal

8. Checking the BGL Glucose meters can determine blood glucose level Normal level 80 – 120 mg/dL Normal level after a meal 120 – 140 mg/dL Determine when patient last ate or drank Average BGL in a diabetic patient is 200 mg/dL Hypoglycemia - BGL of 60 mg/dL or less with signs/symptoms of 50 mg/dL with/without signs/symptoms Hyperglycemia – persistent BGL above 120 mg/dL Use glucometer in conjunction with information Confirm protocols allow you to check BGL (Whatcom county does) Test BGL prior to administration of oral glucose or sugar containing solution Ensure that you have all of the needed test equipment

10. Understanding Diabetes Mellitus Disturbance in metabolism of carbohydrates, fats, and proteins Lack of insulin being secreted by pancreas Inability of the cell receptors to recognize the insulin and allow glucose to enter at a normal rate Brain has more glucose than it needs, it does not require insulin, while the body cells are starving for glucose

11. Understanding Diabetes Mellitus Signs and symptoms Elevated BGL (hyperglycemia) Polydipsia – frequent thirst Polyuria – frequent urination Polyphagia – frequent hunger Prone to a wide variety of diseases and disorders involving blood vessels

12. Understanding Diabetes Mellitus - Types Type 1 Also called insulin-dependent diabetes mellitus (IDDM) Pancreas does not secrete insulin Peak age is 10 – 14 years Patient may suffer from diabetic ketoacidosis (DKA) or hypoglycemia

13. Understanding Diabetes Mellitus - Types Type 2 Also called non-insulin dependent mellitus Typically overweight and middle-age or older May suffer from hyperglyemic hypersmolar nonketotic syndrome (HHNS) More common than Type 1

14. Acute Diabetic Emergencies - Hypoglycemia Patient suffers from low BGL More common in Type IDDM patients Most dangerous acute complication – can result in brain cell death

15. Pathophysiology of hypoglycemia Insulin Shock BGL less than 60 mg/dL with signs/symptoms of hypoglycemia or less than 50 mg/dL regardless of signs/symptoms Patient takes insulin but with excessive results for one of these reasons; Patient takes insulin and does not eat a meal Patient takes insulin, eats a meal, but drastically increases activity beyond normal Patient takes too much insulin (either at once or forgets and takes another dose)

16. Signs/symptoms caused by epinephrine release Diaphoresis Tremors Weakness Hunger Tachycardia Dizziness Pale, cool, clammy skin Warm sensation

17. Signs/symptoms caused by brain cell dysfunction Confusion Drowsiness Disorientation Unresponsiveness (coma) Seizures Stroke-like symptoms Misinterpretation of signs can be deadly! Hypoglycemia unawareness

18. Emergency care for Hypoglycemia Important patient is given sugar to increase BGL as soon as possible Unresponsive patient, unable to swallow, or unable to obey commands; Establish airway Provide oxygen via NRB @ 15 lpm if breathing is adequate Provide positive pressure ventilation if needed Confirm ALS enroute or ask for upgrade Assess BGL

19. Emergency care for Hypoglycemia Responsive patient, patient able to swallow, or obey commands; Ensure airway is patent Assess BGL Administer one tube of oral glucose Continuously assess patient

20. Oral Glucose Heavy sugar gel raises glucose circulating in the blood and increases the amount of glucose available to the brain Criteria for administration; Not altered mental status History of diabetes controlled by medication or BGL below 60 mg/dL Ability to swallow Patient does not meet all of the three, treat as altered mental status with unknown history

22. Acute Diabetic Emergency - Hyperglycemia Diabetic patient is suffering from a lack of insulin and a high BGL Patients may suffer diabetic ketoacidosis (DKA) or hyperglycemic hyperosmolar nonketotic syndrome (HHNS) from being hyperglycemic

23. Diabetic Ketoacidosis Pathophysiology Most common in Type 1 Brain has an excess amount of glucose, other body cells are starving due to insufficient amount of insulin Effects include dehydration, acidosis, and cardiac disturbances

24. Diabetic Ketoacidosis Causes Infection that has upset the insulin and glucose balance Inadequate dose of insulin Medications such as Thiazide, Dilantin, or steroids Types of stress such as surgery, trauma, pregnancy, or heart attack Change in diet

25. Diabetic Ketoacidosis Assessment findings; Polyuria Polyphagia Polydipsia Nausea and vomiting Poor skin turgor Tachycardia Rapid, deep respirations (Kussmaul respirations) Fruity or acetone breath (ketone buildup) Positive orthostatic tilt test

26. Diabetic Ketoacidosis Other Assessment findings; BGL greater than 350 mg/dL Muscle cramps Abdominal pain Warm, dry, flushed skin Altered mental status Coma

27. Diabetic Ketoacidosis Emergency Care Establish and maintain patent airway Provide oxygen via NRB @ 15 lpm Provide positive pressure ventilation with supplemental oxygen, if needed Determine BGL If unsure, administer glucose if patient is able to swallow Contact med control

29. Hyperglycemic Hperosmolar Nonketotic Syndrome (HHNS) Pathophysiology Most common in Type 2 Causes the BGL to increase dramatically 600 – 1200 mg/dL Glucose draws large amounts of water into urine Less fat burned for energy than in DKA (lesser production of ketones) May be first indication that patient is diabetic

30. Hyperglycemic Hperosmolar Nonketotic Syndrome (HHNS) Causes; Diabetic condition Trauma Burns Dialysis Drugs Heart attack Stroke Infection Head injuries

31. Hyperglycemic Hperosmolar Nonketotic Syndrome (HHNS) Assessment findings; Tachycardia Fever Positive orthostatic tilt test Dehydration Polydipsia Dizziness Poor skin turgor Altered mental status Confusion Weakness Dry oral mucosa Dry, warm skin Polyuria Nausea and vomiting

32. Hyperglycemic Hperosmolar Nonketotic Syndrome (HHNS) Emergency Care Same as DKA When in doubt, or protocol does not allow to distinguish between the diabetic emergencies, treat the patient as if they are hypoglycemic to prevent brain death or patient’s death

33. Size-up and Primary Assessment Assess in same manner as Altered Mental Status with no know history of diabetes Err on caution, administer oral glucose if you do not have a glucometer Look for clues that may lead you to diabetes – medications Look for medical aler tags or other medical identification

34. History and Secondary Assessment Ask SAMPLE history questions Medications to look for; Insulin (Humulin, Novolin, Iletin, Semilente Actos Diabanese, Glucamide Orinase Micronase, Diabeta Tolinase Glucotrol Humalog Glucohage Glynase Exantide (Byetta) Exubra

35. History and Secondary Assessment Important Questions Did the patient take his medication the day of episode? Did the patient eat or skip regular meals on that day? Did the patient vomit after eating? Did the patient do any unusual exercise or physical activity? Was the onset of altered mental status gradual or fast? Are there any other signs/symptoms associtated with the altered mental status? Is there any evidence of injury? Was there a period in which the patient regained normal mental status and deteriorated? Did the patient have a seizure? Does the patient appear to have a fever or other signs of an infection?

36. History and Secondary Assessment Signs and symptoms; Rapid onset of altered mental status after missing or vomiting a meal, unusual exercise, or physical work Intoxicated appearance Tachycardia Cool, moist skin Hunger Seizure activity Uncharacteristic or bizarre behavior, combativeness Anxiousness or restlessness Bruising at insulin injection site on the abdomen Stroke symptoms (in elderly patient) BGL < 60 mg/dL

37. History and Secondary Assessment

38. Emergency Medical Care Establish and maintain an open airway Determine if patient is alert enough to swallow Administer oral glucose Whatcom County EMS Protocol page 17: Use of oral glucose or any other substance of similar consistency, is not recommended unless ALS is more than 15 minutes away If patient is able to swallow, administer oral glucose (15 min. threshold met) or substance high is simple sugar Be prepared for patient to vomit Provide supplemental oxygen Maintain body temperature Transport Reassess to determine oral glucose is working Retest BGL If BGL improving and mental status, patient is likely suffering from hypoglycemia If not, patient may be suffering from another condition Communicate and record any changes in the patient’s condition

40. Testing the Blood Glucose Level

41. Questions ????