ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training DOT National Standard EMT-Intermediate/85 Refresher DOT National Standard EMT-Intermediate/85

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!


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are needed to see this picture.MEDICAL EMERGENCIES

• 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


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are needed to see this picture.MEDICAL EMERGENCIES

• 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



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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


• Initial onset– Hyperosmalar Hyperglycemic Nonketotic Coma

(HHNC)• Polyuria• Polydipsia• Polyphagia



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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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are needed to see this picture.s/s, physical exam & assessment, diagnotics, monitoring, management, pertinent positives

• 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


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


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


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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– 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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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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– 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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are needed to see this picture.Differential diagnosis• In the field:• Alcohol• Epilepsy• Insulin• Overdose• Uremia• Trauma• Infection• Psychosis• Stroke

• 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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are needed to see this picture.Questions?• 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.

• 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.

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ICEnAXES ICEnAXES EMS & Wilderness Emergency Care Training DOT National Standard EMT-Intermediate/85 Refresher DOT National Standard EMT-Intermediate/85