Management of the Acute Diabetic Developed by: Institute for Emergency Medical Education 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 How does Insulin used in Muscle cells? Active muscle – Glucose can enter without insulin – Glucose is oxidized to CO2 and H2O for energy production 3/11/2016 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 3/11/2016 Lets watch a Movie….. KREB Cycle Video 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 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 3/11/2016 What does this mean to us? Hyperglycemia increases dehydration and Lactic Acid build up Hyperglycemia causes Acidosis Acidosis results in hypoxia and coma 3/11/2016 Who will we see like this? New onset (undiagnosed) Diabetics – Particularly young kids between 7 and 13 years old Noncomplient IDDM patients 3/11/2016 Frequent precipitating factors: Infection (serious local or systemic) Urinary infections Respiratory infections Major Surgery Trauma Major illness Therapy with Steroids Emotional upset or excessive stress 3/11/2016 Signs and Symptoms of DKA/Hyperglycemia Are usually associated with acidosis and the bodies compensatory mechanisms Of Gradual onset – Usually greater than 48 hours 3/11/2016 Signs and Symptoms of DKA/Hyperglycemia by Body Systems Respiratory system – Body's trying to remove acid by elimination of Ketones which causes – Acetone Breath (fruity) – Kussmaul's Respiration’s – Nausea and Vomiting Caused by acidosis – Polyuria Central Nervous System – Change in mental status – Caused by Dehydration Acidosis & lack of glucose GI & GU Systems attempting to remove ketones Which causes dehydration Circulatory System – Hypotension 3/11/2016 Other Signs and Symptoms of DKA/Hyperglycemia Loss of skin turgor/dry mucosa – Dehydration Polydipsia – Dehydration Polyphasia Warm/dry skin Tachycardia to Normal pulse 3/11/2016 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 3/11/2016 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 3/11/2016 Signs and Symptoms of Hypoglycemia 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 3/11/2016 Diabetic Assessment & Management Assessment – Scene Size Up Scene Safety Body Substance Isolation Interventions – Scene Size Up Make scene safe Retreat from scene Take appropriate BSI precautions 3/11/2016 Diabetic Assessment & Management 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 3/11/2016 Diabetic Assessment & Management 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 3/11/2016 Diabetic Assessment & Management 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 3/11/2016 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 3/11/2016 Diabetic Assessment & Management 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 3/11/2016 Electronic Glucose Monitors 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 REMEMBER: IT is all Relative to the persons Normal Range Your patient can show signs of Hypoglycemia with a blood sugar Of 100mg/dl 3/11/2016 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 3/11/2016 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 3/11/2016 Long Term Complications of Diabetes Cardiovascular – – – – Coronary Artery Disease CVA/TIA MI Angina 3/11/2016 Long Term Complications of Diabetes Renal – Changes in structures and function – Lesions – Causing Hypertension Edema Nephrotic Syndrome 3/11/2016 Long Term Complications of Diabetes Vision changes – – – – – Blindness Cataracts Caused by prolonged periods Hyperglycemia Retinopathy Lesions/Aneurysms on retinal vessels 3/11/2016 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 3/11/2016