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ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training
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DOT National Standard
EMT-Intermediate/85 RefresherDOT National Standard
EMT-Intermediate/85 Refresher
Welcome!
ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training
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• Allergic reaction• Possible overdose• Near-drowning• ALOC• Diabetes• Seizures• Heat & cold emergencies• Behavioral emergencies• Suspected communicable disease
• Allergic reaction• Possible overdose• Near-drowning• ALOC• Diabetes• Seizures• Heat & cold emergencies• Behavioral emergencies• Suspected communicable disease
ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training
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• Diabetes• Diabetes
• Perspective• Pathophysiology• Epidemiology• Physical Exam
Findings• Diagnostic Findings• Signs and Symptoms• Differential
considerations• Treatment
• Perspective• Pathophysiology• Epidemiology• Physical Exam
Findings• Diagnostic Findings• Signs and Symptoms• Differential
considerations• Treatment
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definition• Diabetes mellitus (DM) is a group of
metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both
• Diabetes mellitus (DM) is a group of metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion, insulin action or both
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description• Hyperglycemia further results in acute
& chronic complications of the disease, leading to significant morbidity and mortality
• Hyperglycemia further results in acute & chronic complications of the disease, leading to significant morbidity and mortality
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description• American Diabetes Association (one of
the following must be met):– Symptoms of diabetes & a causal plasma
glucose >200mg/dL
– Fasting plasma glucose >126mg/dL
– Two-hour plasma glucose >200mg/dL during a 75g, 2-hr oral glucose tolerance test
• American Diabetes Association (one of the following must be met):– Symptoms of diabetes & a causal plasma
glucose >200mg/dL
– Fasting plasma glucose >126mg/dL
– Two-hour plasma glucose >200mg/dL during a 75g, 2-hr oral glucose tolerance test
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description• Prediabetes
– Impaired fasting glucose• 100-125mg/dL
– Impaired glucose tolerance• 140-199mg/dL
• Prediabetes– Impaired fasting glucose
• 100-125mg/dL
– Impaired glucose tolerance• 140-199mg/dL
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epidemiology• 7% of the US population has diabetes
– 5-10% Type 1– 90-95% Type 2
• 7% of the US population has diabetes– 5-10% Type 1– 90-95% Type 2
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epidemiology• T2DM prevalence among youth is rising
– Old figure = 1 to 2% of diabetic children had T2DM
– New figure = 8 to 45% of diabetic children have T2DM
• T2DM prevalence among youth is rising– Old figure = 1 to 2% of diabetic children
had T2DM– New figure = 8 to 45% of diabetic children
have T2DM
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types• The National Diabetes Data Group
defines 4 major types of diabetes mellitus (DM)– Type 1 DM– Type 2 DM– Gestational Diabetes– Impaired Glucose Tolerance (Impaired
fasting glucose)
• The National Diabetes Data Group defines 4 major types of diabetes mellitus (DM)– Type 1 DM– Type 2 DM– Gestational Diabetes– Impaired Glucose Tolerance (Impaired
fasting glucose)
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New versus Old Names• Type 1 DM (aka: juvenile onset, insulin
dependent diabetes mellitus)
• Type 2 DM (aka: adult onset, noninsulin dependent diabetes mellitus)
• Type 1 DM (aka: juvenile onset, insulin dependent diabetes mellitus)
• Type 2 DM (aka: adult onset, noninsulin dependent diabetes mellitus)
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pathophysiology• Type 1 Diabetes
Mellitus– Abrupt failure of
production of insulin– Parental insulin
required to sustain life
– Autoantibodies implicated in the cell-mediated autoimmune destruction of beta cells of the pancreas
• Type 1 Diabetes Mellitus– Abrupt failure of
production of insulin– Parental insulin
required to sustain life
– Autoantibodies implicated in the cell-mediated autoimmune destruction of beta cells of the pancreas
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Type 1 DM• Diabetic ketoacidosis (DKA) - initial
onset– hyperglycemia
• Polyuria• Polydipsia• Polyphagia• Ketosis
– Osmotic diuresis– Eventual coma - hypovolemia
• Diabetic ketoacidosis (DKA) - initial onset– hyperglycemia
• Polyuria• Polydipsia• Polyphagia• Ketosis
– Osmotic diuresis– Eventual coma - hypovolemia
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treatment• Type 1 Diabetes Mellitus
– Insulin• SC injections• Pumps
– Oral hypoglycemics• Insulin sensitizers with primary action in the liver
– Metformin• Insulin sensitizers with primary action in peripheral
tissues– Pioglitazone, rosiglitarzone
• Insulin secretagogues– Repaglinide,, nateglinide
• Carbohydrate absorption slowing agents– Acarbose, miglitol
• Type 1 Diabetes Mellitus– Insulin
• SC injections• Pumps
– Oral hypoglycemics• Insulin sensitizers with primary action in the liver
– Metformin• Insulin sensitizers with primary action in peripheral
tissues– Pioglitazone, rosiglitarzone
• Insulin secretagogues– Repaglinide,, nateglinide
• Carbohydrate absorption slowing agents– Acarbose, miglitol
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complications• Type 1 Diabetes Mellitus
– Complications• Hypoglycemia• Hyperglycemia• Retinopathy, neuropathy, nephropathy, CAD, CVA, “silent MI”
• Type 1 Diabetes Mellitus
– Complications• Hypoglycemia• Hyperglycemia• Retinopathy, neuropathy, nephropathy, CAD, CVA, “silent MI”
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Type 2 DM• Pathophysiology
– Usually middle-aged or older, overweight
– Insulin deficiency (insulin secretory deficit)
– Impaired insulin function related to poor insulin production
– Failure of insulin to reach the site of action• or, failure of end-organ response to insulin
• Pathophysiology– Usually middle-aged or older, overweight
– Insulin deficiency (insulin secretory deficit)
– Impaired insulin function related to poor insulin production
– Failure of insulin to reach the site of action• or, failure of end-organ response to insulin
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Type 2 DM• Initial onset
– Hyperosmalar Hyperglycemic Nonketotic Coma (HHNC)
• Polyuria• Polydipsia• Polyphagia
– Osmotic diuresis– Eventual coma - hypovolemia
• Initial onset– Hyperosmalar Hyperglycemic Nonketotic Coma
(HHNC)• Polyuria• Polydipsia• Polyphagia
– Osmotic diuresis– Eventual coma - hypovolemia
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Type 2 DM Treatment• Lower glucose levels on a consistent
basis to normal or near normal
– Lifestyle changes & metformin• Other oral antidiabetic agents• Insulin
• Lower glucose levels on a consistent basis to normal or near normal
– Lifestyle changes & metformin• Other oral antidiabetic agents• Insulin
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Gestational Diabetes
• Glucose intolerance of variable degree with onset or 1st recognition during pregnancy
• Glucose intolerance of variable degree with onset or 1st recognition during pregnancy
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Gestational Diabetes• Complications
– Miscarriages– Birth defects– Growth acceleration & fetal obesity
• Complications
– Miscarriages– Birth defects– Growth acceleration & fetal obesity
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• Hypoglycemia– ALOC– Lethargy– Confusion– Combativeness– Agitation– Seizures– Focal neurologic deficits– Unresponsiveness
• Hypoglycemia– ALOC– Lethargy– Confusion– Combativeness– Agitation– Seizures– Focal neurologic deficits– Unresponsiveness
• Hypglycemia– Anxiety– Nervousness– Irritability– N/V– Palpitations– Tremor– Sweating– Bradycardia– Salivation
• Hypglycemia– Anxiety– Nervousness– Irritability– N/V– Palpitations– Tremor– Sweating– Bradycardia– Salivation
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DKA• Diabetic ketoacidosis occurs primarily in patients
with type 1 diabetes.
• The incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with diabetic ketoacidosis.
• It can occur in patients with type 2 diabetes as well; however, this is less common.
• Diabetic ketoacidosis occurs primarily in patients with type 1 diabetes.
• The incidence is roughly 2 episodes per 100 patient years of diabetes, with about 3% of patients with type 1 diabetes initially presenting with diabetic ketoacidosis.
• It can occur in patients with type 2 diabetes as well; however, this is less common.
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DKA
• The most common scenarios for DKA are – underlying or concomitant infection (40%)
– missed insulin treatments (25%)
– newly diagnosed, previously unknown diabetes (15%)
– Other associated causes make up roughly 20% in the various series.
• The most common scenarios for DKA are – underlying or concomitant infection (40%)
– missed insulin treatments (25%)
– newly diagnosed, previously unknown diabetes (15%)
– Other associated causes make up roughly 20% in the various series.
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HHNC
– The incidence of hyperosmolar hyperglycemic state (HHS) is <1 case per 1000 person/year
– making it significantly less common than DKA. As the prevalence of type 2 diabetes mellitus increases, the incidence of HHS will likely increase as well.
– The incidence of hyperosmolar hyperglycemic state (HHS) is <1 case per 1000 person/year
– making it significantly less common than DKA. As the prevalence of type 2 diabetes mellitus increases, the incidence of HHS will likely increase as well.
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Physical Exam Findings, Diagnostic Findings, S/S, pertinent positives
DKAMild
DKAModerate
DKASevere
HHS
Glucosemg/dL
>250mg/dL
>250mg/dL
>250mg/dL
>600mg/dL
pH 7.25-7.30
7.00-<7.25
<7.00 >7.30
Mental status
Alert Alert/drowsy
Stupor/coma
Stupor/coma
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Treatment
• Hyperglycemia - DKA• Hyperosmalar Hyperglycemia Nonketotic
Coma– Adults - All IVs macrodrip set (10-15 drops/ml)
– Pediatrics All IVs measured-vol solution administration (Volutrol)
– 0-6 yrs All IOs bolus with 60ml syringe, not Volutrol
• Hyperglycemia - DKA• Hyperosmalar Hyperglycemia Nonketotic
Coma– Adults - All IVs macrodrip set (10-15 drops/ml)
– Pediatrics All IVs measured-vol solution administration (Volutrol)
– 0-6 yrs All IOs bolus with 60ml syringe, not Volutrol
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Treatment
• Hyperglycemia - DKA• Hyperosmalar Hyperglycemia Nonketotic
Coma– Saline Lock or TKO: may generally use
interchangeably if fluid or medication not currently required but may be in future (exceptions are noted in specific PROTOCOLS).
– Saline locks avoid IV line entanglement during complex extrications, however TKO allows for immediate administration of fluids as needed
• Hyperglycemia - DKA• Hyperosmalar Hyperglycemia Nonketotic
Coma– Saline Lock or TKO: may generally use
interchangeably if fluid or medication not currently required but may be in future (exceptions are noted in specific PROTOCOLS).
– Saline locks avoid IV line entanglement during complex extrications, however TKO allows for immediate administration of fluids as needed
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Treatment: DKA & HHNC
– Maintenance fluids: stable pts with no contraindications to fluid (pulmonary edema):
– Adults: 120ml/hr (macrodrip 1 drop q 2-3 sec)
– Pediatrics: 2 ml/kg/hr or reference Broselow tape
– Fluid challenge:– Adults (SBP80-100 or HR>100): 500ml bolus (recheck VS
after bolus)
– Pediatrics: bolus only - no challenge indicated
– Maintenance fluids: stable pts with no contraindications to fluid (pulmonary edema):
– Adults: 120ml/hr (macrodrip 1 drop q 2-3 sec)
– Pediatrics: 2 ml/kg/hr or reference Broselow tape
– Fluid challenge:– Adults (SBP80-100 or HR>100): 500ml bolus (recheck VS
after bolus)
– Pediatrics: bolus only - no challenge indicated
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DKA & HHNC: Treatment
• Fluid bolus: • Adults (SBP<80): 1-L bolus wide open under pressure
• Repeat SBP <80: repeat bolus once, then contact base
• Pediatrics: shock, indicated by protocol: 20ml/kg/bolus
• If improvement: repeat bolus once then contact base
• Fluid bolus: • Adults (SBP<80): 1-L bolus wide open under pressure
• Repeat SBP <80: repeat bolus once, then contact base
• Pediatrics: shock, indicated by protocol: 20ml/kg/bolus
• If improvement: repeat bolus once then contact base
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DKA & HHNC: Treatment
– Pediatric Shock: SBP<(70+2x age in years) per PROTOCOL: Pediatric Parameters
– In the case of fluid challenge or bolus: Contact base as soon as possible. If communication failure, continue per guidelines to a maximum of 3-L in adults and 60ml/kg in pediatrics
– Pediatric Shock: SBP<(70+2x age in years) per PROTOCOL: Pediatric Parameters
– In the case of fluid challenge or bolus: Contact base as soon as possible. If communication failure, continue per guidelines to a maximum of 3-L in adults and 60ml/kg in pediatrics
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DKA & HHNC: Treatment
Fluid Challenge or Bolus Procedure
• Check vitals & lung exam after each fluid challenge/bolus
• As vitals change refer back to the table above for fluid guidelines (I.e., initial SPB=80, give 1-L bolus; recheck SBP=90, give 500ml bolus; recheck)
• If signs of pulmonary edema (crackles, respiratory distress, increased respiratory rate) develop during IV fluid administration, decrease to TKO & contact base for fluid orders
Fluid Challenge or Bolus Procedure
• Check vitals & lung exam after each fluid challenge/bolus
• As vitals change refer back to the table above for fluid guidelines (I.e., initial SPB=80, give 1-L bolus; recheck SBP=90, give 500ml bolus; recheck)
• If signs of pulmonary edema (crackles, respiratory distress, increased respiratory rate) develop during IV fluid administration, decrease to TKO & contact base for fluid orders
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DKA & HHNC: Treatment
– Notes
– If PROTOCOL orders IV fluid, refer to this PROCEDURE for gauge, IV number, & fluid rate. If IV fluid orders differ from this it will be indicated in the specific protocol.
– If it is likely that pt will not be transported, contact base prior to IV attempts
– Notes
– If PROTOCOL orders IV fluid, refer to this PROCEDURE for gauge, IV number, & fluid rate. If IV fluid orders differ from this it will be indicated in the specific protocol.
– If it is likely that pt will not be transported, contact base prior to IV attempts
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Treatment• Hypoglycemia
– See ALOC protocol- Adult & Peds
• Hyperglycemia– Support ABCs– Airway mtg | vomiting/aspiration
prevention– Large bore IV– Fluids
• Hypoglycemia– See ALOC protocol- Adult & Peds
• Hyperglycemia– Support ABCs– Airway mtg | vomiting/aspiration
prevention– Large bore IV– Fluids
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• In the field:• Alcohol• Epilepsy• Insulin• Overdose• Uremia• Trauma• Infection• Psychosis• Stroke
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• Perspective• Pathophysiology• Epidemiology• Physical Exam Findings• Diagnostic Findings• Signs and Symptoms• Differential considerations• Treatment
• Perspective• Pathophysiology• Epidemiology• Physical Exam Findings• Diagnostic Findings• Signs and Symptoms• Differential considerations• Treatment
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– Marx, John A. ed, Hockberger & Walls, eds et al. Rosen’s Emergency Medicine Concepts and Clinical Practice, 7th edition. Mosby & Elsevier, Philadelphia: PA 2010.
– Tintinalli, Judith E., ed, Stapczynski & Cline, et al. Tintinalli’s Emergency Medicine A Comprehensive Study Guide, 7th edition. The McGraw-Hill Companies, Inc. New York 2011.
– Wolfson, Allan B. ed. , Hendey, George W.; Ling, Louis J., et al. Clinical Practice of Emergency Medicine, 5th edition. Wolters Kluwer & Lippincott Williams & Wilkings, Philadelphia: PA 2010.
• References– Marx, John A. ed, Hockberger & Walls, eds et al.
Rosen’s Emergency Medicine Concepts and Clinical Practice, 7th edition. Mosby & Elsevier, Philadelphia: PA 2010.
– Tintinalli, Judith E., ed, Stapczynski & Cline, et al. Tintinalli’s Emergency Medicine A Comprehensive Study Guide, 7th edition. The McGraw-Hill Companies, Inc. New York 2011.
– Wolfson, Allan B. ed. , Hendey, George W.; Ling, Louis J., et al. Clinical Practice of Emergency Medicine, 5th edition. Wolters Kluwer & Lippincott Williams & Wilkings, Philadelphia: PA 2010.