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DHEC EMS Division

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  1. DHEC EMS Division Treatment of the Hypoglycemic Patient by the EMT-Intermediate

  2. OBJECTIVES TO UNDERSTAND……….. • The incidence, morbidity and mortality of endocrinologic emergencies related to Diabetes Mellitus and Glucose metabolism. • Risk factors associated with Diabetes. • Anatomy and physiology of structures involved with Diabetes and the normal metabolism and use of Glucose.

  3. OBJECTIVES • Formation of ketone bodies and its relationship to ketoacidosis. • How the kidneys excrete potassium and ketone bodies. • How insulin in the body works. • Assessment findings in the patient with Diabetic emergency. • The need for rapid intervention of the patient with abnormal blood glucose levels.

  4. OBJECTIVES • Pathophysiology of Type I and Type II Diabetes. • The effects of increased and decreased insulin levels on the body. • Management of the Diabetic emergency.

  5. DIABETES MELLITUS • A condition when there is inadequate insulin activity in the body. • Insulin is important for maintaining a normal glucose level. • Glucose is the ONLY substance that brain cells can use readily and efficiently use as an energy source.

  6. DIABETES MELLITUS • Over 8 million Americans have been diagnosed with Diabetes. • Researchers believe that the same number may be living with undiagnosed diabetes.

  7. Anabolism –vs- Catabolism • When a person eats, glucose is stored as glycogen, protein, and fat. This is called anabolism. • Insulin is responsible for this “build-up” of stored glucose. • The process of “Anabolism” uses energy.

  8. Anabolism –vs- Catabolism • If there is too much insulin, or too little food (glucose), the blood glucose level will drop to a level not sufficient to maintain energy for cells, specifically the brain cells. • There may be sufficient glucose stored as glycogen, but it is not in the bloodstream.

  9. Anabolism –vs- Catabolism • Glucagon is the dominant hormone that allows for the breakdown of stored glycogen for use as glucose. • In severe hypoglycemic states, glucagon may not work fast enough to restore adequate glucose levels in the blood for immediate use. • RESULT Brain cells do not have adequate energy, the patient may have an altered mental status.

  10. TRANSPORT OF GLUCOSE • Insulin is the hormone responsible for the transport of glucose. • The “diffusion” process is considered a “mediated” or “facilitated” transport. • Insulin must bind with the glucose molecule and “taxi” it across the cell membrane out of the bloodstream.

  11. TRANSPORT OF GLUCOSE • The elevation of insulin in the bloodstream may increase the rate of glucose transport out of the vascular system by 10 times, causing a rapid decrease of blood glucose levels. • Not having enough intake of glucose will lead to the same result.

  12. TRANSPORT OF GLUCOSE • Excessive use of energy (heavy work or exercise), or vomiting soon after eating, will also lead to a decrease of blood glucose levels. • The result in ANY case will lead to hypoglycemic states.

  13. USE of GLUCOSE –vs- FAT • If enough insulin is not present to transport the glucose, then the body catabolizes (breaks down) fat instead of glucose. • When this happens, the body produces ketone bodies in abundant quantities. • This is called “ketosis”.

  14. GLUCOSE REGULATION • If a person had a BGL of 80 mg/dL. • A meal is ingested. • In the first hour, the BGL may increase to 120 – 140 mg/dL. • The alpha and beta tissues of the “islets of Langerhans” and the liver produce glucagon and insulin. • Liver disease, or Pancreas insufficiency may lead to poor regulation of glucose.

  15. ALTERED GLUCOSE LEVELS • Levels lower than 80 mg/dL represent hypoglycemia. • Levels greater than 140 mg/dL represent hyperglycemia.

  16. THE ROLE OF THE KIDNEY • When blood passes through the tubules of the kidney, many substances are “reabsorbed” into the blood, and the waste is excreted. • Reabsorption of glucose depends on the amount present in the blood. • Reabsorption is essentially complete for levels up to 180 mg/dL.

  17. THE ROLE OF THE KIDNEY • When baseline BGL levels are above 180 mg/dL, some of the glucose is lost in the urine. • The urine is “sweet” with sugar, hence the name “mellitus”. • Glucose in urine is called “glycosuria”. • When glucose is in the urine, the osmotic pressure causes water to be excreted in excessive quantities.

  18. THE ROLE OF THE KIDNEY • This leads to dehydration. It is called “osmotic diuresis”. • As the water (fluid or plasma) leaves the vascular system, potassium is excreted also, causing hypokalemia. • This result may lead to effects such as cardiac dysrhythmias.

  19. TYPE I DIABETES • Characterized by very low production of insulin by the pancreas. • Insulin may not be produced at all. • Commonly called: • Juvenile Diabetes • Insulin Dependent Diabetes Mellitus • IDDM • Less common than Type II Diabetes. • Accounts for most Diabetic related deaths.

  20. TYPE I DIABETES • This type is hereditary. • Before diagnosis and treatment, BGL levels of 300 to 500 mg/dL is not uncommon. • As the “osmotic diuresis” occurs, it accounts for the: • Polydipsia (constant thirst) • Polyuria (excessive urination) • Polyphagia (weakness and weight loss)

  21. TYPE II DIABETES • Associated with a moderate decline in insulin production. • A deficient response to insulin may be present. • Also called: • Adult onset Diabetes Mellitus. • Non insulin dependant Diabetes Mellitus. • NIDDM

  22. TYPE II DIABETES • Heredity may play a role. • Obesity is more likely to be the cause. • Much more common than Type I. • Accounts for about 90% of Diabetics. • Less serious than Type I Diabetes. • Ketoacidosis is not likely to occur. • Controlled diet is the usual treatment. • May require oral medications. • Only a few cases lead to insulin use.

  23. DIABETIC KETOACIDOSIS • Associated with Type I Diabetes. • Occurs with profound insulin deficiency coupled with increased glucagon activity. • Could be the result of: • Non-compliance with insulin injections. • Physiologic stress such as surgery or serious infection.

  24. DIABETIC KETOACIDOSIS • Glucose levels elevate in the vascular system, but are decreased in the cells due to the insulin deficiency. • Glucagon is released causing catabolism of fats, leading to ketone body production and accumulation. • Glucose is lost in the urine, and osmotic diuresis occurs. • Dehydration occurs because of fluid loss.

  25. DIABETIC KETOACIDOSIS • Blood pH decreases to dangerous levels because of the acidic nature of the ketone bodies. • The patient becomes comatosed and may die if the acidosis is not treated. • REMEMBER the patient may have a “fruity” odor on their breath. This odor resembles the odor of ETOH.

  26. DKA – SIGNS & SYMPTOMS • Onset is slow – (12 – 24 hours) • Increased urine production. • Excessive hunger and thirst. • Feeling weak, general malaise. • Tachycardia • Tachypnea & Hyperpnea • KUSSMAUL’s respirations. • Acetone “fruity” odor on breath.

  27. DKA – SIGNS & SYMPTOMS • May have cardiac dysrhythmias caused by low potassium levels. • Warm/dry skin. • Fever is not caused by DKA, and is usually a sign of infection. • ALS TREATMENT NEEDED IF FEASIBLE!!

  28. HYPOGLYCEMIA (INSULIN SHOCK) • This is a medical emergency! • It can occur when: • The patient takes too much insulin. • Eats too little for the insulin dose. • Overexerts or over-exercises. • Vomits soon after a meal. • Glucagon may take HOURS to work, so it is less effective in compensating.


  30. HYPOGLYCEMIA (INSULIN SHOCK)SIGNS & SYMPTOMS • Altered Mental Status (AMS) • Restlessness and Impatience • Inherent HUNGER • Anger or Rage • Bizarre behavior • Diaphoresis • Cool clammy skin • HYPOGLYCEMIA (INSULIN SHOCK)SIGNS & SYMPTOMS • Tachycardia • Seizure • Coma • Sudden onset • S/S may be similar to CVA!!!!! IF UNRESPONSIVE… CALL FOR ALS BACK-UP!

  31. HYPOGLYCEMIA (INSULIN SHOCK)ASSESSMENT • SAMPLE history. • Take and record vital signs. • Administer high concentration O2. • Look for medical alert indicators: • Bracelet • Necklace • Pocket card • Tattoo • Look in the refrigerator for insulin. • Look for insulin syringes.

  32. HYPOGLYCEMIA (INSULIN SHOCK)TREATMENT • Call for ALS back-up!! • Perform blood glucose check. • If patient has S/S of hypoglycemia, (and/or) if the BGL is < 70 mg/dL, start an IV with 0.9% NaCl (Normal Saline) and administer D50W 25 Grams, 50 ml. • NOTE: if patient is alert enough to swallow, you may administer 1 to 2 tubes Instant Glucose (12 – 25 Grams). • Re-check BGL after 2-3 minutes.

  33. HYPOGLYCEMIA (INSULIN SHOCK)TREATMENT • If the patient awakes to a fully alert status, the EMT-I may cancel the Paramedic and transport the patient if none of the following are present. • Symptomatic bradycardia. • Symptomatic tachycardia. • Irregular pulse that is not normal. • Chest pain, or any other complaint that should be evaluated by a Paramedic.

  34. WHICH PATIENTS CAN YOU TREAT? The S.C. EMT-Intermediate MAY ONLY administer D50W to a patient who is at least 12 years of age!!


  36. THE PATIENT’s “R’s” • The “RIGHT” patient… • The “RIGHT” medication… • The “RIGHT” dose… • The “RIGHT” route… • The “RIGHT” expiration date…

  37. DEXTROSE 50 %D50W, 50% Dextrose-------------------------------------------------------------------------------INDICATIONS: Suspected or documented hypoglycemia. Altered LOC, or Coma/Seizure of unknown etiology.ADMINISTRATION: IO, IV through a free flowing line.DOSAGE:ADULT: 25.0 grams slow administration initial dose. May repeat doses based upon Medical Control Order or Protocols/Standing Orders for persistent hypoglycemia.PEDIATRIC: May be used for patients at least 12 years old, or weighing at least 55 kg. (120 pounds)

  38. CONTRAINDICATIONS • The ONLY “actual” contraindication to administering D50W is “known” hyperglycemia and infiltration or a “noticed” hematoma at the IV site. • Suspected CVA or TIA is a “relative” contraindication. Consider if the patient will suffer or die from the additional brain necrosis or from the hypoglycemia. Consult with Medical Control if CVA/TIA is suspected.

  39. COMPLICATIONS • The most dangerous complication is infiltration. It causes local tissue necrosis and could lead to cellular death. • Seek advise from MCP before D50W administration if CVA suspected. • Thick fluid, you should use at least an 18 ga. catheter if possible.

  40. Open here!!! Works MUCH better!!!

  41. ADMINISTRATION • Determine the need for the medication. • Select suitable site, start IV (medium bore or large bore). • Make sure the IV is PATENT!! • Verify the medication and expiration date. • Open and assemble the medication syringe. Expel the air from the syringe. • Attach the syringe to the injection port closest to the patient.

  42. ADMINISTRATION • Pinch the line, or cut the flow regulator off. • Begin the injection. • Periodically pull the syringe back (every 10ml) to ensure that the catheter is still inside the vein (you should aspirate blood each time). • Continue until the desired dose is given. • Document the dose and time. • Monitor for patient improvement. • Reassess Blood Glucose Level. • Cancel Paramedic response if patient improves.

  43. DRUG CALULATION FORMULA Desired dose divided by the dose on hand, multiplied by the volume supplied in, will give you the amount of volume you should administer. Desired Dose Dose on Hand X Volume = Amount

  44. D50W is supplied 25G in 50 mL. Give 14G to a patient. 14 Grams 25 Grams X 50 mL = 28 mL

  45. DRUG CALULATION FORMULA 14 divided by 25 = 0.56 0.56 multiplied by 50 = 28 (mL) Give 28 mL of the solution

  46. REPORTING • You are administering medication that is allowed by prescription ONLY. • This could be a “standing order” by your Medical Control Physician, or by on-line orders from the ED Physician. • The receiving physician MUST sign the report!!

  47. DHEC, Division of EMS D50W Administration by the EMT-I Skills Assessment Score Sheet Name: _______________________ Date: __________ Evaluator: ______________________ Determines AMS, applies high flow oxygen _____ Performs patient assessment to include BGL test _____ Calls for Paramedic back-up _____ Determines need for the medication _____ Prepares IV equipment _____ Selects suitable site _____ Attaches tourniquet _____ Start IV using aseptic technique _____ Secures IV, runs W/O to check for infiltration _____ Prepare D50W for injection (check exp date, etc) _____ Pinch or clamp line, or run wide open _____ Administer desired dose using “push-pull” method _____ Runs IV W/O to flush line _____ Reassesses mental status _____ Reassesses BGL _____ Evaluator signature ____________________________________ Date _____________