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Management of the Acute DiabeticManagement of the Acute Diabetic

Developed by:

Institute for Emergency Medical Education

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Purpose: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

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Learning Objectives: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

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Learning Objectives: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

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Learning Objectives: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

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Overview 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

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Anatomy and Physiology: Anatomy and Physiology: DiabetesDiabetes Pancreas

– Located in the abdomen attached to the intestines but behind the stomach

– Responsible for the Production of the hormone Insulin

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Hormone: InsulinHormone: 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

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How is Insulin used in Liver How is Insulin used in Liver cells?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

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What is Glycogen?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

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How does Insulin used in Muscle How does Insulin used in Muscle cells?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

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How does Insulin used in Muscle How does Insulin used in Muscle cells?cells? Active muscle

– Glucose can enter without insulin– Glucose is oxidized to CO2 and H2O for

energy production

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How does Insulin used in How does Insulin used in Adipose tissue?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

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Lets watch a Movie…..Lets watch a Movie…..

KREB Cycle Video

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General Pathophysiology of General Pathophysiology of Diabetes MellitusDiabetes 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

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When Insulin levels are normal 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

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Problems associated with Problems associated with alterations in metabolismalterations 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

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HyperglycemiaHyperglycemia 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

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HyperglycemiaHyperglycemia 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

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Diabetic Ketoacidosis (DKA)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

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What does this mean to us?What does this mean to us? Hyperglycemia increases dehydration and

Lactic Acid build up Hyperglycemia causes Acidosis Acidosis results in hypoxia and coma

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Who will we see like this?Who will we see like this? New onset (undiagnosed) Diabetics

– Particularly young kids between 7 and 13 years old

Noncomplient IDDM patients

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Frequent precipitating factors: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

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Signs and Symptoms of Signs and Symptoms of DKA/HyperglycemiaDKA/Hyperglycemia Are usually associated with acidosis and

the bodies compensatory mechanisms Of Gradual onset

– Usually greater than 48 hours

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Signs and Symptoms of Signs and Symptoms of DKA/Hyperglycemia by Body SystemsDKA/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

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

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Other Signs and Symptoms of Other Signs and Symptoms of DKA/HyperglycemiaDKA/Hyperglycemia Loss of skin turgor/dry mucosa

– Dehydration Polydipsia

– Dehydration Polyphasia Warm/dry skin Tachycardia to Normal pulse

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HypoglycemiaHypoglycemia Major complication for patients treated

with Insulin and Oral Hypoglycemic agents

Usually caused by too little food or too much Insulin/Oral Hypoglycemic agents

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HypoglycemiaHypoglycemia 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

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Signs and Symptoms of Signs and Symptoms of HypoglycemiaHypoglycemia 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

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Diabetic Assessment & Diabetic Assessment & ManagementManagement Assessment

– Scene Size Up Scene Safety Body Substance

Isolation

Interventions– Scene Size Up

Make scene safe Retreat from scene Take appropriate BSI

precautions

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Diabetic Assessment & Diabetic Assessment & ManagementManagement 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

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Diabetic Assessment & Diabetic Assessment & ManagementManagement 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

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Diabetic Assessment & Diabetic Assessment & ManagementManagement

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

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Note for ALS ProvidersNote 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

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Diabetic Assessment & Diabetic Assessment & ManagementManagement 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

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Electronic Glucose MonitorsElectronic 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 RangeYour patient can show signs of Hypoglycemia with a blood sugarOf 100mg/dl

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Long Term Complications of Long Term Complications of DiabetesDiabetes 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

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Long Term Complications of Long Term Complications of DiabetesDiabetes 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

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Long Term Complications of Long Term Complications of DiabetesDiabetes Cardiovascular

– Coronary Artery Disease– CVA/TIA– MI– Angina

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Long Term Complications of Long Term Complications of DiabetesDiabetes Renal

– Changes in structures and function– Lesions– Causing

Hypertension Edema Nephrotic Syndrome

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Long Term Complications of Long Term Complications of DiabetesDiabetes Vision changes

– Blindness– Cataracts– Caused by prolonged periods Hyperglycemia– Retinopathy– Lesions/Aneurysms on retinal vessels

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SummarySummary 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