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Management of the Acute Diabetic

Management of the Acute Diabetic. Developed by: Institute for Emergency Medical Education. Purpose:. To enhance the EMT's understanding of the normal physiology as it applies to transportation and utilization of glucose, and how it fits into the Krebs' Cycle

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Management of the Acute Diabetic

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  1. Management of the Acute Diabetic Developed by: Institute for Emergency Medical Education

  2. Purpose: • To enhance the EMT's understanding of the normal physiology as it applies to transportation and utilization of glucose, and how it fits into the Krebs' Cycle • Improve the EMT's understanding of the pathophysiology of Diabetes and how to appropriately mange an acute Diabetic state • To enhance the EMT’s understanding of electronic glucose monitoring

  3. Learning Objectives: • Student will have a basic understanding of the normal functioning transport system for glucose and how it is utilized by the body and will have a working knowledge of the Pancreas and the Krebs' Cycle. • Students will understand the Pathophysiology of the Diabetic disease process

  4. Learning Objectives: • Students will be able to identify the Acute Hyperglycemic (DKA) patient and appropriately treat him/her to the EMT's level of training, utilizing both clinical judgment and blood glucose testing devices

  5. Learning Objectives: • Students will be able to identify the Acute Hypoglycemic patient and treat appropriately to the level of the EMT's training, utilizing both clinical judgment and blood glucose testing devices. • The Basic EMT will know how to operate an electronic glucose monitor

  6. Overview • A & P as it pertains to Diabetes and Glucose metabolism • Pathophysiology of Diabetes as it relates to Hyperglycemia and Hypoglycemia • Assessment and management of Diabetic Emergencies • Glucose measurement

  7. Anatomy and Physiology: Diabetes • Pancreas • Located in the abdomen attached to the intestines but behind the stomach • Responsible for the Production of the hormone Insulin

  8. Hormone: Insulin • Secretion by the Pancreas from the Beta Cells on the Islets of Langerhan • It is required by for the intracellular metabolism of glucose • Its release is primarily stimulated by glucose levels • Other stimulus for the its release include • Amino Acids • Fatty Acids • Ketones

  9. How is Insulin used in Liver cells? • Glucose enters Liver cells • Insulin is needed to activate the hormone Glucokinase • Glucokinase Promotes phosphorylation of glucose • First step in glucose metabolism • Activates the hormone Glycogen Synthetase • Necessary for glycogen formation

  10. What is Glycogen? • It is stored sugar • We use it as a reserve energy supply • We only store sugar when insulin is present • Insulin doesn’t do the work Glycogen Synthetase does • But insulin must start the process off

  11. How does Insulin used in Muscle cells? • Resting muscle • Insulin is needed to transport glucose across the cell membrane • Insulin increases glycogen synthetase • Insulin inactivates the enzyme Phosphurylase • Insulin's presence facilitates Amino acid uptake and protein synthesis while preventing protein catabolism

  12. How does Insulin used in Muscle cells? • Active muscle • Glucose can enter without insulin • Glucose is oxidized to CO2 and H2O for energy production

  13. How does Insulin used in Adipose tissue? • Insulin is necessary for transport of glucose across cellular membrane • Promotion of glucose metabolism, fatty acid synthesis • Insulin will combine with fatty acids produced in the liver and in fat cells to form Triglycerides • Insulin presence decreases Lipolysis

  14. Lets watch a Movie….. KREB Cycle Video

  15. General Pathophysiology of Diabetes Mellitus • This condition is caused by either • Absolute or relative lack of Insulin • Or ineffective utilization of Insulin • In Insulin Dependent • Absolute lack of Insulin • In Noninsulin Dependent • Normal or near normal levels of Insulin

  16. When Insulin levels are normal • It is usually ineffective utilization of Insulin • Caused by a decrease number of Insulin Receptor Cells • Or Impaired Binding of Insulin to body cell • Caused by a receptor defect

  17. Problems associated with alterations in metabolism • The are seen when there is a lack, deficiency or under utilization of Insulin • These problems are • Hyperglycemia • Hypoglycemia • Diabetic Ketoacidosis • Nonketonic Hyperosmolar Coma

  18. Hyperglycemia • Caused by several factors • Over production of glucose due to an increase in • Glucogenesis • The formation of glycogen from noncarbohydrate sources such as Amino Acids or Fatty Acid • Glycogenolysis • Hydrolysis of glycogen into glucose • And a decrease in peripheral utilization of glucose

  19. Hyperglycemia • Caused by Protein Catabolism and loss of Amino Acids from muscle. • Caused by impaired Triglycerides Synthesis • Which increases the release of Free Fatty Acids from Adipose Tissue which increases Beta Oxidation of Fats

  20. Diabetic Ketoacidosis (DKA) • Most frequently seen in IDDM (Insulin Dependent Diabetes Mellitus) • Caused by Acute Insulin Insufficiency and is usually precipitated in the known Diabetic by stressors that increase Insulin needs • When there is insufficient Insulin for appropriate metabolism of glucose, fats, proteins • This causes inappropriate utilization of glucose, resulting in Hyperglycemia

  21. What does this mean to us? • Hyperglycemia increases dehydration and Lactic Acid build up • Hyperglycemia causes Acidosis • Acidosis results in hypoxia and coma

  22. Who will we see like this? • New onset (undiagnosed) Diabetics • Particularly young kids between 7 and 13 years old • Noncomplient IDDM patients

  23. Infection (serious local or systemic) Urinary infections Respiratory infections Major Surgery Trauma Major illness Therapy with Steroids Emotional upset or excessive stress Frequent precipitating factors:

  24. Signs and Symptoms of DKA/Hyperglycemia • Are usually associated with acidosis and the bodies compensatory mechanisms • Of Gradual onset • Usually greater than 48 hours

  25. Respiratory system Body's trying to remove acid by elimination of Ketones which causes Acetone Breath (fruity) Kussmaul's Respiration’s Central Nervous System Change in mental status Caused by Dehydration Acidosis & lack of glucose GI & GU Systems Nausea and Vomiting Caused by acidosis Polyuria attempting to remove ketones Which causes dehydration Circulatory System Hypotension Signs and Symptoms of DKA/Hyperglycemia by Body Systems

  26. Other Signs and Symptoms of DKA/Hyperglycemia • Loss of skin turgor/dry mucosa • Dehydration • Polydipsia • Dehydration • Polyphasia • Warm/dry skin • Tachycardia to Normal pulse

  27. Hypoglycemia • Major complication for patients treated with Insulin and Oral Hypoglycemic agents • Usually caused by too little food or too much Insulin/Oral Hypoglycemic agents

  28. Hypoglycemia • Alterations in mental status and bizarre behavior are caused by Brain cells being starved for food • The longer the duration of decrease, or no glucose, reaching Brain cells, the greater the chance of/or increasing the amount of damage sustained

  29. Quick onset of symptoms Headache/blurred vision Diaphoresis/Pallor Tachycardia with weak pulse/Palpitations Numbness of lips and tongue Alteration in mental status or Coma Emotional changes Confusion Irritability/Nervous Bizarre behavior Weakness/Fatigue Seizures/Trembling Incoherent speech Hunger Signs and Symptoms of Hypoglycemia

  30. Assessment Scene Size Up Scene Safety Body Substance Isolation Interventions Scene Size Up Make scene safe Retreat from scene Take appropriate BSI precautions Diabetic Assessment & Management

  31. Assessment Initial Assessment Nature of Illness General Impression AVPU Airway Breathing Circulation Baseline Vital Signs Interventions Initial Assessment Open Airway Suction Insert Adjunct Intubation if necessary Apply High Flow Oxygen or Ventilate Transportation Diabetic Assessment & Management

  32. Assessment Rapid/Focused History & Physical Exam (BLS & ALS) History of Diabetes Hx of present illness Onset Duration Last Dextrose Stick by patient Interventions Rapid/Focused History & Physical Exam (BLS & ALS) Oral Glucose If able to protect own airway May use household items Close monitor of airway with suction available Diabetic Assessment & Management

  33. Assessment Rapid/Focused History & Physical Exam (ALS Only) Obtain current Dextrose level Obtain Pre I.V. Blood Tubes Cardiac Monitor Repeat Dextrose 3-5 minutes Post D50W administration Interventions Rapid/Focused History & Physical Exam (ALS Only) Initiate IV access 0.9% Sodium Chloride Administer Dextrose 50% in Water if D-Stick is below 100mg/dl Administer Thiamine 100mg IV or IM Administer Glucagon IM if no IV access Diabetic Assessment & Management

  34. Note for ALS Providers • Consult with Medical control for additional Amp(s) of D50W • The Need for additional dosages of D50W is rare but should be guided by repeated dextrose analysis • Post D50W administration • you can expect a Glycogen Stores release • This may occur approximately an hour after the D50W which will raise the blood glucose again, but only if there are any glycogen stores left

  35. Assessment Detailed Exam Take a full SAMPE history Look for secondary problems On Going Exam Reassess interventions Revisit Initial & Focused Assessment Reassess Vital Signs Interventions Detailed Exam Based upon specific Findings On Going Exam Additional or new Therapies may be employed Diabetic Assessment & Management

  36. Normal values 60 - 150 mg/dl Abnormally low Below 60 mg/dl Less than 20 is very dangerous Abnormally high Above 200 mg/dl Extremely High Above 700 mg/dl Electronic Glucose Monitors REMEMBER: IT is all Relative to the persons Normal Range Your patient can show signs of Hypoglycemia with a blood sugar Of 100mg/dl

  37. Long Term Complications of Diabetes • Vascular changes • Decreased peripheral circulation (Caused by atherosclerosis & arteriosclerosis) • Thickening of capillary walls • Increase infection potential and severity, particularly in lower extremities Secondary to decreased circulation

  38. Long Term Complications of Diabetes • Nervous System damage • Peripheral • Degeneration causing tremors • Decreased sensory functions • Spinal • Slowed conduction through spinal tracts • CNS • Degeneration of brain tissues causing memory disturbances • Loss of/decrease in fine motor control

  39. Long Term Complications of Diabetes • Cardiovascular • Coronary Artery Disease • CVA/TIA • MI • Angina

  40. Long Term Complications of Diabetes • Renal • Changes in structures and function • Lesions • Causing • Hypertension • Edema • Nephrotic Syndrome

  41. Long Term Complications of Diabetes • Vision changes • Blindness • Cataracts • Caused by prolonged periods Hyperglycemia • Retinopathy • Lesions/Aneurysms on retinal vessels

  42. Summary • Diabetes is a disease that effects the bodies ability to properly use glucose for metabolism • The conditions of Diabetes we see are caused by the body compensatory mechanism when the disease is unchecked • Management of a Diabetic in an acute setting is to stabilize the ABCs and provide sugar • Long term management is designed to prevent peaks and valleys in blood sugar which are the causes of long term diabetic problems

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