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Boone County Fire District EMS Education-EMT Course EMT 22 Lesson-Resources AMS . Blood Glucose

● Screencast

● Older Screencast (still valid and good)

● Glucose Paste / EMT Med Admin

● Things to Know:

○ Insulin’s function in the body.

○ The basics of diabetes mellitus including Type 1 and Type 2.

○ Field assessment and management of hypo- and hyperglycemia.

• Watch this short video on Insulin function • Watch this 9 minute video from Khan Academy on blood sugar levels • Watch this 5 minute video on diabetes

• Further (OPTIONAL) video resources on diabetes • Diabetes is a disorder of glucose metabolism or difficulty metabolizing carbohydrates, fats,

and proteins. • There are two types of diabetes. Type 1 diabetes typically develops in childhood and

requires daily insulin to control blood glucose. Type 2 diabetes typically develops in middle age and often can be controlled with diet, activity, and oral medications.

o Type 1 patients do not produce sufficient (or any) insulin. o Type 2 patients produce insulin but its function is ineffective.

▪ “Insulin Resistance”—-Type 2 diabetics may be taking oral medications to assist with their blood glucose control. Glyburide and Glipizide are common medications that act to increase insulin production. Metformin is very commonly encountered medication that increases the action of insulin. Avandia and Actos are newer agents in widespread use that address the insulin resistance directly.

• Diabetes mellitus is the formal name for the standard type of diabetes that we typically encounter. “Diabetes insipidus ” occurs uncommonly (3 in 100,000) and involves an issue with the kidneys and related hormones and therefore its not part of our discussion at the EMT level.

• Both types of diabetes are serious systemic diseases, especially affecting the kidneys, eyes, small arteries, and peripheral nerves.

• Patients with diabetes have chronic complications that place them at risk for other diseases, such as heart attack, stroke, and infections. Most often, however, you will be called on to

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http://www.youtube.com/playlist?list=PL59DB53F5C358E5DA


treat the acute complications of blood glucose imbalance. These include hyperglycemia (excess blood glucose) and hypoglycemia (insufficient blood glucose).

o Most EMS calls for “diabetics ” involve hypoglycemic patients who have taken their insulin but did not eat sufficiently.

o Diabetes is a disease of high blood sugar yet most EMS contacts with diabetics are low blood sugar incidents because the patients take their insulin but fail to eat sufficiently or on time.

• Hyperglycemia is typically characterized by excessive urination and resulting thirst, in conjunction with the deterioration of body tissues.

o Hyperglycemic patients may present with flu-like symptoms or other vague presentations.

o Usually these patients get sick slowly and the treatment is also not quick. Contrast that with the much more rapid onset of hypoglycemia —-and its much more rapid fix in most cases.

• Hyperglycemia is usually associated with dehydration and ketoacidosis and can result in marked rapid (often deep) respirations; warm, dry skin; a weak pulse; and a fruity breath odor. Hyperglycemia must be treated in the hospital with insulin and IV fluids.

• Symptoms of hypoglycemia classically include confusion; rapid respirations; pale, moist skin; diaphoresis; dizziness; fainting; and even coma and seizures. This condition is rapidly reversible with the administration of glucose or sugar. Without treatment, however, permanent brain damage and death can occur.

• Because a blood glucose level that is either too high or too low can result in altered mental status, you must perform a thorough history and patient assessment to determine the nature of the problem. When the problem cannot be determined, it is best to treat the patient for hypoglycemia.

• Be prepared to give oral glucose to a conscious patient who is confused or has a slightly decreased level of consciousness; however, do not give oral glucose to a patient who is unconscious or otherwise unable to swallow properly or protect his or her own airway. • Oral glucose takes time to absorb buccally (through the oral mucosa). Similarly, glucose is

absorbed through the gastrointestinal tract relatively slowly. In both cases, expect some improvement in 10 minutes or more.

• Remember, in all cases, providing emergency medical care and prompt transport is your primary responsibility. • ALS providers may administer IV glucose ( “Dextrose 50% ” or “D50”) to reverse

hypoglycemia. Improvement in these patients is rapid. • ALS providers and some patient ’s family / caregivers may administer Glucagon IM to

reverse hypoglycemia. Glucagon, in this case, releases “glucose” stored in the body. (assuming there is sufficient storage —-mainly in the liver). Improvement in these patients takes much longer than IV therapy (varies —-expect 10 minutes or more).

• Remember, diabetic patients are statistically more likely to present with some other symptoms besides chest pain when they are having an MI. Diabetes is a disease that may cause decreased peripheral pain sensation.

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▾ Glucose • Food is broken down in the intestines into glucose that enters the bloodstream.

• Insulin is the “key” that opens doors in the cell for glucose to enter. Produced in

the pancreas. • Glucose that is not used immediately is stored in the liver and muscles (75% of it). ▾ Glucagon puts stored glucose into the bloodstream. Produced in the pancreas.

• Glucagon also converts free fatty acids into ketones that are converted by the liver into energy.

▾ Epinephrine suppresses insulin and stimulates glucagon so that the net effect is an increase in blood glucose levels.

• Epinephrine also stimulates ketone production. • Hypoglycemia causes epinephrine release which causes cool / pale / moist

skin and may vasoconstrict capillaries so inaccurately low fingerstick glucose reading.

• Patient may be altered, excited, tachycardic and hypertensive and may have chest pain / ACS symptoms or cardiac rhythm issues.

• Chronic diabetics may not have the epinephrine release signs. • Glucose paste buccally should be used (not orally—slower absorption) when

patients cannot safely eat and drink to raise their glucose levels.

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▾ Blood glucose levels fluctuate between 70’s and 120-140 normally. Maybe a bit

higher after a meal (180’s or so). Finger stick glucose level may be even lower than venous blood measurement (as much as 15%)

• Hyperglycemia—thirst and urination increase (glucose acts as a diuretic) or potentially confusion / coma in severe cases. These patients are dehydrated and have electrolyte issues.

▾ Diabetes mellitus—old terms persist (juvenile or adult onset, insulin-dependent

and non-insulin dependent) but are replaced by Type 1 and Type 2

▾ Type 1—pancreas is not producing insulin ▾ Patients take a variety of insulin replacements including some

short-acting and some long-acting. Some by injections including an insulin pen but others by insulin pump (external and potentially implanted) or by inhalation.

• “Brittle diabetics” have short term wide fluctuations and are frequently seen by EMS

▾ Type 2—insuin is produced but is not effective to some degree

• cells develop a resistance to insulin (the “key” won’t open the door) • obesity—fat cells have fewer insulin receptors • diet, exercise and meds—some meds decrease glucose absorption

from the intestines while others work on the liver or pancreas or more directly on the cells

• issues—pancreas may over-produce insulin to compensate for insulin resistance but insulin can increase atherosclerosis / hypertension / fat storage / cause clots to not be broken down

• Gestational diabetes—placental hormones cause insulin resistance that

usually resolves after delivery but may cause hypoglycemia in newborn

• Risks for diabetics—in addition to noted above include peripheral neuropathy which may lead to poor peripheral circulation and thus more likelihood of injury with decreased healing; increased risk for kidney disease and blindness

• Signs—polydipsia (thirst), polyuria (excessive urination), polyphagia

(hunger—cells need sugar so patient is stimulated to eat even though excess sugar is already circulating but cannot get into the cells) (the terms themselves are Advanced Provider level but the signs and symptoms are for all levels)

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▾ DKA—diabetic ketoacidosis—presents in patients who don’t yet know they

are diabetic as well as poorly controlled diabetics; hyperglycemia detected in the field but ketones in blood and urine plus acetone / acidosis detected in ER. Frequently triggered by an infection.

• Dehydrated (dry mouth, poor skin turgor), altered mental status / altered LOC, rapid and deep breathing (to compensate for metabolic acidosis), may be tachycardic or even hypotensive; watch for hypokalemia and low magnesium (long QTc?); may have acetone odor to breath but not all medics can smell it. May have seizures

• Needs insulin and fluids (lots)

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▾ Advanced Providers—

• HONKS or HHNS—hyperosmolar non-ketotic syndrome or hyperglycemic hyperosmolar non-ketotic syndrome is not DKA because no acidosis is present yet patients present dehydrated and altered. Probably due to renal failure or insufficiency. Water moves to vascular space in response to hyperglycemia. Watch for electrolyte problems including hypokalemia.

• Alcoholic ketoacidosis—listed as special and strange case involving

hypoglycemia yet signs of DKA normally seen with hyperglycemia (dehydration, altered mental status)—treat hypoglycemia

• questionable need for glucose check in cardiac arrest (hypoglycemia is

no longer one of the H’s and T’s)

▾ Tx of hypoglycemia • D50 is thick syrup and can badly damage skin if the IV infiltrates so

dilution makes sense

• 25 grams should increase patient’s blood glucose rapidly and within 10 minutes should be at least in the normal range

▾ Glucagon—only works if enough stored glucose in liver and muscles;

should increase the blood glucose level 100 points in 10 minutes • Has positive inotropic and chronotropic effects especially when

given IV but why give it IV for hypoglycemia? Has other uses.

• Thiamine—for malnourished patients who are receiving glucose but can be given at the ER so many services no longer carrying this.

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CHECKLIST-GLUCOMETER USE

Task

Identifies the need for obtaining a blood glucose

Identifies the normal parameters for blood glucose

Clearly explains procedure to patient

Locate Glucometer

Locate Test Strip

Locate Needle or spring-loaded puncture device

Locate Alcohol swabs

Takes or verbalizes appropriate PPE precautions

Turns on glucometer and inserts test strip

Preps finger tip with alcohol prep

Lances the prepped site with needle/lancet device, drawing capillary blood

Disposes/verbalizes disposal of needle/lancet in appropriate container

Expresses blood sample and transfers it to the test strip

Dresses fingertip wound with pressure and alcohol prep

Records reading from glucometer and documents appropriately

Boone County Fire Protection District EMS Education

Glucose Metabolism


Cells need glucose to make energy so that they can function.!

Some cells can break down fats and proteins as a partial backup source to glucose.!

Brain cells and red blood cells are particularly sensitive to low glucose levels---they have no other source for energy other than glucose.


Insulin is needed to help glucose to get access into most body cells (except brain cells). Insulin functions as a key to unlock pores in cell membranes to allow glucose to enter.!

Insulin is secreted by the pancreas “on-demand” based on blood glucose levels.


Hypoglycemia is a condition of low blood glucose levels. Anyone can have this.!

Hyperglycemia is a condition of high blood glucose levels.


Hypoglycemia is assessed using a glucometer and gathering history.!

Hyperglycemia is assessed using a glucometer and gathering history.


Hypoglycemia is a condition of low blood glucose levels that tends to have a rapid onset with symptoms that may mimic shock.!

Hyperglycemia is a condition of high blood glucose levels that tends to have a gradual onset with symptoms that may mimic the flu or a GI illness.


Hyperglycemic Crisis types:!

Diabetic Keto-acidosis (DKA) (no insulin produced---fats broken down). May have rapid / deep breathing and possibly a “fruity” or “acetone” breath odor.!

Hyperosmolar Hyperglycemic Non-ketotic Coma (HHNC) (some insulin produced--sugar excreted) (aka HONKS)


Hypoglycemia is treated with glucose and resolves in a few minutes.!

Hyperglycemia is treated with insulin and resolves over many hours or days.


When in doubt, glucose should be given to the patient as it will correct hypoglycemia but it won’t make hyperglycemia any worse.


Patients can eat or drink to add glucose to their blood. Use caution in decreased level of consciousness.!

EMTs can give oral glucose paste to be absorbed buccally (cheek and gum).


Some patient’s families may have Glucagon for IM injection. Most EMT protocols do not allow assisted medication administration of Glucagon.!

Glucagon is a hormone that stimulates release of stored “glucose” from the liver (when available) to treat hypoglycemia.


Paramedics and AEMTs can administer IV glucose (“D-50” or “50% Dextrose”) to treat hypoglycemia.


Blood glucose levels:!

“Normal” is around 80-120 mg/dl!

Hypoglycemia symptoms begin around 50-60 mg/dl!

Hyperglycemia symptoms begin around 500-600 mg/dl


EMTs in Missouri can use a glucometer to obtain a blood glucose reading provided that they have received training in the use of these simple devices.


Hypoglycemic patients may appear:!

intoxicated!

to be having a stroke!

to be having a behavioral crisis!

actively seizing or post-ictal


Airway & Breathing must be managed.!

Hypoglycemia can occur with other conditions or with injuries.!

ANYONE can be hypoglycemic---you DO NOT have to be a diabetic.


Diabetes is a disease involving a a problem with insulin and therefore a disruption in the mechanism for glucose movement from the blood into the cells.!

Diabetic patients may present to EMS with either hypo or hyperglycemia.


Type 1 Diabetes involves a complete lack of insulin production by the pancreas---may be called “IDDM”.!

Type 2 Diabetes involves a decrease in the effectiveness of the insulin that is produced.


Type 1 Diabetics typically take insulin daily by injection or they receive insulin throughout the day via an insulin pump.!

Type 2 Diabetics typically use diet, exercise and oral medications to address their insulin function problems.


metformin (Glucophage)!

chlorpropamide (Diabinase)!

tobutamide (Orinase)

Meds for type 2’s

glipizide (Glucotrol)!

rosiglitazone (Avandia)!

glyburide (Micronase)!

pioglitazone (Actos)


Take-Away Key Points

Blood glucose levels must be checked in any altered mental status patient regardless of whether or not they have a history of diabetes.!

Airway & Breathing must be managed while glucose levels are assessed and managed.!

Hypoglycemia can cause seizures and mimic strokes or intoxication.

When is it safe to leave these patients at home?

The number of persons with diabetes in the United States has been rising steadily over the past fi ve decades, and the far-reaching effects of chronic hyperglycemia are staggering.

In this month’s article we will discuss the process of normal glucose metabolism, then review the patho-physiology of hypoglycemia.

We will use a case-based approach to explore hypo-glycemia in patients with type 1 and type 2 diabetes mellitus. In doing so, we will use the process of working through a differential diagnosis to show how to evaluate and weigh the evidence supporting or opposing hypo-glycemia as the etiology of a diabetic emergency and arrive at a working diagnosis prior to obtaining a blood glucose level.

For each case we’ll use information that can be obtained with a thorough clinical exam and a detailed understanding of the history of present illness and past medical history to determine the type of diabetes present as well as precipitating factors for the emergency.

Normal Glucose MetabolismThe pancreas plays an important role in the regu-

lation of blood glucose via the release of regulatory hormones. The pancreas is unique in that it has both exocrine and endocrine functions. The cells of the endo-

crine pancreas are located in groups called pancre-atic islets, or the islets of Langerhans, and account for just 1% of all the pancreatic cells. Each islet contains alpha cells and beta cells. Alpha cells produce and

| By Scott R. Snyder, BS, NREMT-P, Sean M. Kivlehan, MD, MPH, NREMT-P, & Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT

This CE activity is approved by EMS World, an

organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1 CEU.OBJECTIVES• Discuss normal glucose

metabolism• Review altered mental

status in a Type 1 diabetic patient

• Review hypoglycemia in a Type 2 diabetic patient

• Discuss patient refusal of transport

E

TiE

TTiiE

CONTINUING EDUCATION

There are two ways to take the CE test that accompanies this article and receive 1 hour of CE credit accredited by CECBEMS: 1. Go online to EMSWorld.com/cetest to download a PDF of the test. The PDF has instructions for completing the test. 2. Or go online to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail [email protected].

When is it safe to leave

Case Studies in Hypoglycemia

The CDC, in its National Diabetes Fact Sheet, reports that:

• 25.8 million people, or 8.3% of the U.S. population, have diabetes.

• Among U.S. residents 65 and older, 10.9 million, or 26.9%, had diabetes in 2010.

• About 1.9 million people 20 or older were newly diagnosed with diabetes in 2010 in the U.S., and it is estimated that 7 million people are undiagnosed.

• In 2005–08, based on fasting glucose or A1C levels (see sidebar), 35% of U.S. adults 20 or older had prediabetes. Among those 65 or older, the rate rose to 50%. Applying this percentage to the entire 2010 U.S. population yields an estimated 79 million Americans aged 20 years or older with prediabetes.

• Diabetes is the seventh-leading cause of death in the United States.

• Diabetes is a major cause of heart disease and stroke and the leading cause of kidney failure, nontraumatic lower-limb amputations and new cases of blindness among adults in the United States.1

What the Stats Say

54 AUGUST 2013 | EMSWORLD.com

CE ARTICLE

secrete the hormone glucagon, and beta cells produce and secrete the hormone insulin. Normal blood glucose levels are considered to be in the range of 70–110 mg/dL.

Insulin is released from beta cells in response to increased levels of blood glucose, as happens after meals (see Figure 1). Insulin is required for and increases the rate of glucose transport into the cells. This results in a decrease of blood glucose levels. After being trans-ported into tissue cells, glucose is used to generate ATP, allowing that particular cell to perform its work and therefore its role in the body. Insulin also increases the rate of glucose transport into muscle and the liver, where it is stored as glycogen, ready to be used in the future when needed. In addition, insulin increases the synthesis of fat in adipose tissue, creating yet another energy store that can be tapped into when blood glucose levels fall.

As blood glucose levels start to fall, the body determines that a “fasting state” has been created and releases counter-regulatory hormones in an attempt to

maintain the blood glucose levels neces-sary for normal brain function. These counterregulatory hormones include glucagon, epinephrine, norepinephrine, cortisol and growth hormone. Glucagon has the exact opposite effect of insulin and is secreted by the pancreatic alpha cells when blood glucose levels are low. Glucagon has the effect of mobilizing glycogen stores in the liver and adipose tissues. In the liver, glucagon results in the breakdown of glycogen into glucose (a process termed glycogenolysis), which is then released into the bloodstream, increasing blood glucose levels. Glucagon also results in the synthesis of glucose from non-carbohydrate substrates such as pyruvate, lactate, amino acids and fatty acids in the liver, a process termed gluco-neogenesis. In the adipose tissue, stored fats are broken down into fatty acids and released into the bloodstream. These fatty acids can be utilized as an energy source by the body’s cells.

When blood glucose levels decrease, epinephrine is also secreted from the adrenal medulla in an attempt to stimulate numerous metabolic changes to increase blood glucose. Epinephrine binding to alpha-adrenergic receptors in the pancreas inhibits insulin secretion by the beta cells, preventing a further decrease in blood glucose levels. Beta-adrenergic binding in the pancreas increases glucagon secretion by alpha cells, resulting in an increase in blood glucose levels. In addi-tion, epinephrine stimulates the pituitary gland to release adrenocorticotropic hormone (ACTH), which increases lipolysis (the breakdown of lipids into fatty acids) by adipose tissue. As a result of these actions, blood glucose and fatty acid concentra-tions increase, providing the materials for For More Information Circle 34 on

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The A1C test is a blood test used to diagnose diabetes mellitus. After diagnosis, it can be used to determine how eff ectively a patient manages their diabetes. The A1C test refl ects a patient’s average blood glucose level over the preceding 2–3 months. It measures what percentage of hemoglobin is glycated (has glucose bound to it). The higher a patient’s A1C level, the poorer their blood sugar control, and the higher their risk of complications.

The A1C Test

Figure 1: Regulation of Blood Glucose LevelsInsulin released

Glucose enters cellsBlood glucose levels fall

Hypoglycemia develops

Normal blood glucose levels70–110 mg/dL

GluconeogenesisIncreased lipolysis

Glycogenolysis in liverDecreased insulin secretion

Glucagon releasedCounterregulatory hormones released

Glucose introduced into body

CE ARTICLE

energy production in cells. In addition to the specifi c counterregulatory effects, the release of epinephrine also results in the characteristic cool, pale, diaphoretic skin we associate with developing shock.

Diabetes MellitusDiabetes mellitus, often referred to

simply as diabetes, is the most common disease of the endocrine system. It is actually a group of metabolic diseases in which a state of hyperglycemia (high blood sugar) exists as a result of inadequate insulin secretion from the pancreas, inadequate cellular response to the body’s natural insulin, or both.

The National Diabetes Data Group (NDDG) defines four major classifica-tions of diabetes mellitus: type 1 diabetes mellitus, type 2 diabetes mellitus, gesta-tional diabetes, and other specific types.2 Worth noting is that the other specific types include no fewer than 45 specific disease, genetic or drug- or medication-induced processes that can result in hyperglycemia.

Type 1 diabetes accounts for about 10% of all cases in the U.S. and occurs secondary to loss of insulin-producing beta cells located in the islets of Langerhans in the pancreas. It is char-acterized by decreased insulin secretion but a normal cellular response to insulin. It can occur in children and adults, and most often (90% of all cases of type 1 diabetes) occurs secondary to an auto-immune response during which the body’s immune system produces anti-gens that mistakenly target pancreatic beta cells for destruction by immune system T-cells. Once destroyed, beta cells do not regenerate. The rate of beta cell destruction can be variable, resulting in a rapid onset of the disease in some patients (mainly children) and a more gradual onset in others (mainly adults). Cellular sensitivity and responsiveness to insulin remain normal in type 1 diabetes; the issue is that there is not enough circulating insulin to maintain homeo-stasis. Patients with type 1 diabetes may require the administration of insulin to maintain normal glucose blood levels. These facts have led to the elimination of use of the terms insulin-dependent

diabetes mellitus and juvenile-onset diabetes mellitus.2

Type 2 diabetes is characterized by insulin resistance at the target tissues and usually also by a relative decrease in insulin secretion. Insulin resistance is a term used to describe the situa-tion in which tissues require higher levels of insulin and therefore higher-than-normal plasma concentrations of insulin to maintain normal intracellular and blood glucose levels. Patients with type 2 diabetes typically do not require insulin treatment to survive, but do require medication to increase the secretion of insulin or decrease insulin resistance at the target tissues. As is the case with type 1 diabetes, the traditional terms non-insulin-dependent diabetes mellitus and adult-onset diabetes are no longer used to describe type 2 diabetes, as the type 2 diabetic may indeed require insulin, and it can occur in the juvenile patient. Obesity is a major risk factor for type 2 diabetes, and increasing numbers of young patients are developing the disease as obesity increases in this population.

Case 1: AMS in a Type 1 Diabetic

You and you partner, both EMTs, are dispatched to a local shopping mall for a patient with altered mental status. You arrive to find a 52-year-old male sitting in a wheelchair in the care of his wife. She reports the patient “was fine a half hour ago, but is not acting like himself now.” During your primary exam you note the patient is conscious and knows his name but is confused as to time, place and event. He is able to follow commands. He has a strong and rapid radial pulse, and his skin is cool, slightly pale and slightly diaphoretic. His respiratory rate is normal with a good tidal volume, and he is in no respiratory distress. When asked about a chief complaint, he repeatedly responds, “I don’t know what happened.” You imme-diately radio dispatch and request ALS support.

The patient’s wife informs you he is a type 1 diabetic and he ate his normal breakfast this morning and took his usual dose of insulin. She further states that

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he is routinely compliant with his diet and insulin treatments and has not had “any issues with his sugar for a couple of years.” Your physical exam does not reveal any signs of trauma. You note that his pupils are slightly dilated bilaterally, equal and reactive to light. His lung sounds are clear and equal bilaterally. He has no facial droop, his speech is not slurred, and he has no neurologic defi-cits. While examining his lower extremi-ties, you determine he has cellulitis on his left lower leg extending from his foot to midway up the calf. You also note an ulcer on the dorsal surface of his foot that appears to be infected, with a purulent discharge from the wound. The patient’s wife says the ulcer is chronic but that the infection and cellulitis “have gotten worse over the past couple of days.”

His vital signs are heart rate 102/min, strong and regular; blood pressure 132/84 mmHg; respiratory rate 12/min

with good tidal volume; and pulse oxim-etry 97% on room air.

Your local scope of practice as an EMT does not include the use of a glucometer to determine the patient’s blood glucose level, but local protocol allows administration of oral glucose. You determine the patient is able to both protect his airway and follow commands, then have him self-administer 15 g. Within five minutes you note he is now alert to person, place and time. You explain to the patient that he had an episode of hypoglycemia and suggest he go to the emergency department for evaluation. He thanks you for responding and correcting it, but says he does not wish to be transported at this time.

Questions:• Prior to the patient’s improvement

with the administration of glucose, what would have been your best guess as to which was more likely, hypoglycemia or

hyperglycemia?• What is the prehospital manage-

ment of the conscious patient with hypo-glycemia?

• What criteria should be met in order to support this patient’s wish to refuse transport?

DISCUSSIONHyperglycemia and hypoglycemia

are both complications associated with type 1 diabetes.3 Hyperglycemia often occurs when a diabetic does not take their insulin or takes a dose inadequate to properly control blood glucose levels. A number of particulars in this case strongly suggested that hypoglycemia, not hyperglycemia, was the cause of this diabetic’s altered mental status. Specifically, the patient was a type 1 diabetic who had been compliant with his insulin, had a recent onset of infec-tion, experienced an acute onset of

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AMS, and showed signs of sympathetic nervous system activation.

Hypoglycemia is a frequent problem in patients with type 1 diabetes and should immediately be considered in all patients with altered mental status and a history of type 1 diabetes. Hypoglycemia can occur secondary to a number of

factors, including missing a meal, an overdose of insulin or oral antihypergly-cemics, other drug overdoses (Table 1), increased energy demands or disease (Table 2).4

This patient’s foot infection and cellulitis would cause increased metabo-lism and subsequent increased energy

demand, resulting in increased glucose utilization and the risk of hypoglycemia. In such cases, maintaining a normal dietary intake and insulin regimen may prove insufficient to maintain adequate blood glucose levels. Infections are common for patients with Type 1 diabetes. Maintain a high index of suspicion and look

for infection sources. Prehospital providers should

attempt to identify a source of infection in the diabetic patient with hypoglycemia.

Foot ulcers and cellulitis are common complications of diabetes and occur secondary to both the peripheral vascular insuf-fi ciency and peripheral neuropathy common with it. The peripheral neuropathy results in decreased pain sensation in the feet, allowing minor trauma and ulcer formation to occur unidentifi ed. Peripheral vascular insuffi ciency then leads to a decreased ability to fi ght infection. Other infections that can precipitate hypoglycemia and should be identifi ed include pneumonia and sepsis.

The acute onset of this patient’s AMS, reported by his wife, is another indication that hypoglycemia, not hypergly-cemia, is the cause. Both hypo-glycemia and hyperglycemia can result in AMS. The onset of AMS associated with hypoglycemia tends to be rapid, taking place over minutes to hours. This is because the AMS associated with hypoglycemia is a result of the rapid depletion of glucose, and the brain is often the first organ affected. The onset of AMS associated with hyperglycemia tends to be more gradual, taking place over days or even weeks. In addition to AMS, other neuro-For More Information Circle 37 on Reader Service Card

• Antimalarials• Ethanol• Pentamidine• Phenylbutazone• Propranolol• Salicylates

Table 1:DRUGS THAT CAN PRECIPITATE HYPOGLYCEMIA

• Addison’s disease

• Alcoholism• Anorexia nervosa• Hyperthyroidism• Hypothyroidism

• Islet cell tumors• Liver disease• Malnutrition• Renal

insuffi ciency• Sepsis

Table 2:COMORBIDITIES THAT CAN PRECIPITATE HYPOGLYCEMIA


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logic symptoms characteristic of hypogly-cemia include bizarre, uncharacteristic or combative behavior, seizures and coma.

The signs of sympathetic nervous system activation, specifically the patient’s tachycardia, dilated pupils and cool, pale, diaphoretic skin, are also char-acteristic of hypoglycemia. Recall that epinephrine is released in response to decreased blood glucose concentra-tions. Epinephrine is not released in response to hyperglycemia, so the signs and symptoms of epinephrine release strongly suggest that hypoglycemia is present. Other signs of epinephrine release include tremors, nervousness and palpitations.

Treatment for this patient can be achieved at the BLS level with the administration of oral glucose, as he is conscious and able to follow commands, reducing the risk of aspiration. This can be accomplished by administering a commercially available oral glucose preparation, typically 15 g of glucose in gel preparations or 4 g in tablet form, or by having the patient consume a sugar-containing beverage or food. Note that in many areas the presence of AMS in a known diabetic is an indication for the administration of oral glucose; an exact blood glucose determination with a glucometer is not necessary.

Very often a patient who has their hypoglycemia treated in the field will refuse transport to the ED for evaluation. In fact, many of these patients are at relatively low risk for a recurrence as long as some criteria are met. First, determine that the patient is indeed conscious, alert and oriented to person, place, time and event. A patient with AMS cannot make an informed decision regarding transport to the ED and should be transported under the principles of implied consent.

Then determine if a nonpathologic explanation exists for the episode of hypoglycemia. For example, did the patient take their normal dose of insulin or oral antihyperglycemic medi-cation and skip a meal or eat less than normal? Doing so will often result in hypoglycemia. Did the patient exert themselves more than normal, increasing metabolic demand and depleting their

blood glucose? These scenarios do not necessarily require transport to the ED. A precipitating factor for the patient in this case appears to be an infection on his foot and leg, which is a very good reason he should be evaluated in the ED. He will need treatment for his infection. Any patient who takes oral antihypogly-cemics should be transported to the ED for evaluation.

In addition, any patient who refuses transport should be encouraged (if not required), preferably in front of the EMS crew, to eat a meal or snack consisting of protein, carbohydrates and fats, such as a sandwich. This will help prevent rebound hypoglycemia that can develop after administration of glucose. Glucose is a simple sugar and is rapidly absorbed by the digestive system, enters the blood-stream and is delivered into the body’s cells. As a result, blood glucose levels can again fall rapidly after the administration of oral or IV glucose. Eating a snack or meal containing complex carbohydrates, protein and fat will ensure a steady digestion and supply of blood glucose. Examples of such foods are an energy bar, left-over meal or peanut-butter-and-jelly sandwich.

An analogy can be drawn between nutri-ents and blood glucose and fuel for a fire. Oral glucose and carbohy-drates, fats and proteins are to blood glucose levels what gasoline and logs are to a fire. Pour gasoline onto a fire, and it burns very hot and quick. Administer oral or IV glucose, and blood glucose levels rise quickly but then lower quickly as the simple sugar is used up. Place logs on a fire, and they burn more slowly and for a long time. Likewise, feed a patient complex

carbohydrates, fats and protein, and they are digested and enter the bloodstream more slowly, maintaining blood glucose levels for a longer time.

To summarize, always ensure the patient who refuses transport to the ED after the administration of glucose eats a nutrient-rich snack or meal. In addition, try to ensure that the patient who has expe-rienced an episode of hypoglycemia and refused transport has someone with them who can call for EMS should the problem recur. They should not be left alone.

Case 2: Hypoglycemia in a Type 2 Diabetic

You, a paramedic, and your partner, an EMT, are dispatched to an uncon-scious person at a residential address. A 42-year-old female presents lying supine on a couch with snoring respirations, unresponsive to verbal stimuli. She opens her eyes and looks at you when you apply



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painful stimuli, but promptly becomes unre-sponsive if not kept stimulated. Your partner opens her airway with a head-tilt chin-lift and jaw thrust, and you insert a nasopha-ryngeal airway (NPA) to help keep it open. You note that her respiratory rate and tidal volume are normal, and she has a strong, rapid, regular radial pulse. Her skin is cool, slightly pale and slightly diaphoretic. Your administer oxygen via nasal cannula at 2 lpm. Her husband says she’s “not been feeling well and has an appointment to see her physician tomorrow.”

The patient has a history of type 2 diabetes, and her husband says she’s been compliant with her glipizide. He noticed this morning that she was devel-oping an altered mental status, and he called EMS when he was unable to easily wake her from sleep. A secondary exam reveals that her mucous membranes are dry and she has poor skin turgor. Vital signs are heart rate 112/min, strong and regular; blood pressure 104/60 mmHg; respiratory rate 14/min with good tidal volume; and pulse oximetry 94% on room air. It increases to 100% on 2 lpm via nasal cannula.

You perform a finger stick and find her blood glucose to be 32 mg/dL. The cardiac monitor reveals a sinus tachy-cardia, and you initiate IV access with an 18-guage angiocath to her left ante-cubital region and hang a 500 mL bag of normal saline with a macrodrip set flowing KVO. You also give 25 g of D50W and remove the NPA as the patient starts to regain consciousness.

By the time you’ve finished admin-istering the D50W, the patient wakes up and is conscious, alert and oriented to person, place and time. A repeat BGL shows a value of 324 mg/dL. The patient informs you that she’s had a two-day history of pain with urination and suspects she has a urinary tract infection. She also says she’s not been drinking as much water as she should and is “probably a bit dehydrated.” You

note her mucous membranes are dry. She confirms she has an appointment with her physician at 0900 the next day. Repeat vital signs are heart rate 100/min, strong and regular; blood pressure 108/62 mmHg; respiratory rate 12/min with good tidal volume; pulse oximetry 97% on room air.

You offer to transport the patient to the ED for evaluation, but she refuses. She says she believes this was an isolated incident. She realizes her illness will increase her risk of hypoglycemia due to increased metabolic demand, so she will eat more than usual. She also points out that her husband will be with her until she sees her physician tomorrow, and he can call EMS should problems recur.

Questions• What is the prehospital manage-

ment of the unconscious patient with hypoglycemia?

• Can you think of a strong argument as to why this patient should be trans-ported to the ED for evaluation?

DISCUSSIONCreating and maintaining a patent

airway and ensuring adequate ventila-tion and oxygenation are priorities in patients who present with an altered level of consciousness.

This patient presented with hypo-glycemia that resulted in a decreased LOC that subsequently interfered with her ability to maintain an open airway. Her snoring indicated her tongue was acting as an airway obstruction. This was corrected with a combination of a manual airway maneuver and BLS airway adjunct.

The use of the NPA was a good idea, as patients who are arousable with painful stimuli often have an intact gag refl ex, which is a contraindication for use of an oropharyngeal airway (OPA). In addition, an NPA is particularly handy in a patient (such as a diabetic with hypoglycemia) in whom you expect the level of conscious-ness to improve. If an OPA had been used with this patient, her gag refl ex would have been stimulated at some point as her LOC improved, and she may have gagged or even vomited, potentially compromising the airway. This was avoided with the use of an NPA, which will not stimulate the gag refl ex.

Ventilation assistance with a bag-valve mask was not necessary, as her ventilation was adequate. Administer oxygen to all patients with a diminished LOC or AMS; here the administration of 2 lpm of oxygen via nasal cannula was enough to improve her oxygen saturation.

If a patient with hypoglycemia has a decreased level of consciousness, cannot follow commands or is a risk for aspira-tion for any other reason, give D50W IV at a dose appropriate for the age group (Table 3). Take care to ensure the IV line is patent and no extravasation is present. Glucose preparations, especially D25W and D50W, are hyperosmolar and can cause significant ischemia and necrosis if allowed to infiltrate surrounding tissue.

If a hypoglycemic patient cannot take oral glucose and IV access cannot be established, glucagon can be admin-istered via the intramuscular or subcu-taneous routes. The onset of action is fairly rapid, about 10–20 minutes, and peak blood glucose levels are reached in about 30–60 minutes.3 Glucagon can also be administered IV, and 1 mg has an effect on blood glucose levels equivalent to about one 25 g ampule of D50W.3 As discussed above, glucagon increases blood glucose levels by stimulating

Medication Age group Dose/concentration Route Glucose Adult 25–75 g D50W IV Child 0.5–1 g/kg D25W IV Neonate 0.5–1 g/kg D10W IVGlucagon Adult 1–2 mg IV, IM, SC Child 0.025–0.1 mg/kg IV, IM, SC

Table 3:TREATMENT FOR HYPOGLYCEMIA

• The patient is conscious, alert and oriented x 4.

• There is an identifi able nonpathologic cause of the hypoglycemic episode.

• The patient does not take oral

antihypoglycemics.• There is no concurrent illness or

infection.• The patient is able to eat a meal.• The patient will not be left alone.

Criteria for Allowing Hypoglycemic Patients to Refuse Transport/Follow-up

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glycogenolysis in the liver. As such, glucagon would be ineffective at correcting hypoglycemia in any patient who has diminished glycogen stores, as in patients with alcohol-induced hypoglycemia.

IV access was obtainable in this patient, 25 g of D50W was admin-istered, and the patient regained consciousness. When the question of transport to the ED arose, she offered a valid argument for not going. However, the patient should be advised that diabetics who use sulfonylurea antihyperglycemic agents are at particular risk for prolonged, severe and recurring episodes of hypoglycemia.3

Sulfonylureas are a class of medication widely used in the treat-ment of type 2 diabetes and promote the increased secretion of insulin from the pancreas. Medications in this class include chlorpropamide, glipizide and glibenclamide (glyburide). Any impairment of liver or kidney function will decrease clearance of the drug, increasing plasma concentrations and the risk of hypoglycemia. The patient in this case had a UTI and reports drinking less water than she should. In addi-tion, her elevated heart rate, low blood pressure and dry mucous membranes are characteristic of dehydration. Both a UTI and dehydra-tion could by themselves affect kidney function sufficiently to result in decreased clearance of her glipizide. Consequently, her blood levels of glipizide could increase and result in episodes of hypoglycemia.

In addition to impaired liver or kidney function, an overdose of a sulfonylurea will result in an oversecretion of insulin, elevated blood insulin levels and hypoglycemia. In addition to glucose administration, these patients require treatment with a medication to inhibit further insulin secretion (such as octreotide, a somatostatin analog) and subsequent lowering of blood glucose levels. Metformin (Glucophage) and oral agents in the thiazolidinedione class, common medications used in the treatment of type 2 diabetes, have a different mecha-nism of action than the sulfonylureas and rarely cause significant or prolonged hypoglycemia.

While in many cases it is relatively safe to support a patient’s desire to refuse medical care, in this case providers should strongly advocate for evaluation in the ED. The risk of recurring, severe and prolonged episodes of hypoglycemia must be made perfectly clear. If a patient does not meet the criteria for declining transport (see sidebar) and you feel they should be evaluated by a physician, contact medical control, give a report and produce documentation that clearly demonstrates the patient refused transport against medical advice.

REFERENCES1. Centers for Disease Control and Prevention. 2011 National Diabetes Fact Sheet, www.cdc.gov/diabetes/pubs/factsheet11.htm.2. Expert Committee on the Diagnosis and Classifi cation of Diabetes Mellitus. Report of the expert committee on the diagnosis and classifi cation of diabetes mellitus. Diabetes Care, 2003 Jan; 26 Suppl 1: S5–20.3. Cydulka RK, Maloney GE Jr. Chapter 124: Diabetes Mellitus and Disorders of Glucose Homeostasis. In: Marx J, Hockberger R, Walls R, Rosen’s Emergency Medicine, 7th ed. Mosby, 2010.4. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide, 7th ed. New York: McGraw-Hill, 2011.

Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. E-mail [email protected].

Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the Univer-sity of California, San Francisco. E-mail [email protected].

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is performance improvement coordi-nator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. E-mail [email protected].

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This dangerous metabolic derangement can be fatal without proper care

oth hypoglycemia and hyperglycemia are true medical emergencies. As we discussed last month, hypoglycemia often has a rapid onset and can impact any patient whose body is not provided an adequate glucose

supply. While anyone can experience hypoglycemia, it is most common in patients who have been diag-nosed with diabetes and whose natural insulin does not function normally.

Patients with diabetes also risk developing hypergly-cemia, a complex and dangerous metabolic derange-ment that can be fatal without proper care. The American Diabetes Association says that in 2011 there were a stag-gering 25 million patients with diabetes and 79 million with pre-diabetes across the United States.

This month’s CE article explores the consequences

of hyperglycemia on the body and the life-threatening emergencies it can cause.

Diabetic Disease ProgressionRecall that insulin secretion is stimulated by eating.

Insulin secretion is not stimulated between meals, and a decline in the body’s blood glucose levels inhibits the pancreatic islets’ insulin secretion and stimulates the secretion of glucagon, which allows glucose levels to remain in a normal range. Figure 1 demonstrates the rela-tionship between blood glucose levels and the pancreas.

With the exception of very few organs, such as the brain and the kidneys, the body’s tissues require insulin for glucose to pass through the cell walls. For patients with diabetes mellitus (DM), either their pancreas doesn’t produce enough insulin or their insulin is not functioning

| By Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, Sean M. Kivlehan, MD, MPH, NREMT-P, & Scott R. Snyder, BS, NREMT-P

This CE activity is approved by EMS World, an

organization accredited by the Continuing Education Coordinating Board for Emergency Medical Services (CECBEMS), for 1 CEU.OBJECTIVES• Discuss diabetic disease

progression• Understand the scope of

hyperglycemic emergencies• Review physiology of

diabetic ketoacidosis • Discuss assessment

and management of hyperglycemic patients

TTiiE

TTiE

CONTINUING EDUCATION

There are two ways to take the CE test that accompanies this article and receive 1 hour of CE credit accredited by CECBEMS: 1. Go online to EMSWorld.com/cetest to download a PDF of the test. The PDF has instructions for completing the test. 2. Or go online to www.rapidce.com to take the test and immediately receive your CE credit. Questions? E-mail [email protected].

68 SEPTEMBER 2013 | EMSWORLD.com

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properly; without oral medications or injected insulin, the body’s tissues are unable to move glucose from the blood-stream into the cells, and dysfunction can ensue.

Glucagon is also released as the cells release chemical signals indi-cating they are not getting enough glucose. The patient may experience hunger because the cell’s signals indi-cate a lack of glucose despite the fact that there really is an adequate supply; it just cannot be moved into the cells. For patients with DM, this perceived lack of glucose can lead to blood glucose levels rising dangerously high without

the body being able to use or benefit from its presence.

Regularly experiencing rising glucose levels is harmful to the body. Diabetic retinopathy is the leading cause of blindness for individuals aged 25–74, with an annual incidence of 65,000.1

When patients regularly experience abnormal glucose metabolism and elevated blood glucose levels, chronic increased blood viscosity and a shunting of excess glucose into intracellular path-ways result in the production of harmful alcohol-based byproducts. In the retinal capillaries these byproducts degrade the capillary walls, leading to “outpouching”

or micro-aneurysms, as well as a break-down of the capillaries’ cell walls. Weakening the cell walls causes fluid shifts within the retina and a thickening of the cell walls. Over time blood flow can become inadequate, and the retina and nerves within the eye can experience hypoxia and eventually necrosis. This can manifest anywhere on the spectrum from blurred vision to vision loss.1

Nearly 50% of patients with diabetes mellitus experience some form of diabetic neuropathy, which is progressive nerve fi ber function loss and peripheral nerve dysfunction in the presence of diabetes.2

Nerve dysfunction impairs a patient’s

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Figure 1: Relationship between blood glucose levels and the pancreas.

Fran Milner, w

ww.franim

ation.com

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sensory and motor functions and can also impair autonomic nervous system functions. Neuropathy is exacerbated by peripheral vascular disease. The irregular fl uctuations in blood glucose levels harm distal capillaries and break down the cell walls over time, resulting in poor perfusion of the distal tissues. Diabetic-induced periph-

eral vascular disease (PVD) is a particular problem in the hands and feet. Larger vessels are also affected by PVD, becoming stiff as the vessel walls thicken from years of transporting blood viscous from increased glucose levels. Combined, neuropathy and PVD lead to an overall decreased quality of life and put patients at risk for falls, ulcers,

dysrhythmias and ileuses.The exact mechanism for diabetic

neuropathy is unclear but appears to be exacerbated by hyperlipidemia, hypertension, smoking and obesity. Prehospital providers are unlikely to diagnose diabetic neuropathy but are likely to see its manifestations as patients present with impaired fine motor func-tion, extremity tremors, tripping and toe dragging, and complaints of progressive limb weakness over extended periods of time.2

Asymmetrical diabetic neuropathy is not uncommon and presents with one extremity weaker than its pair. Do not confuse this with stroke-like symptoms that have a sudden onset and are likely to affect an entire side of the body rather than just one extremity.

In reality, diabetes impacts every one of the body’s organ systems. Diabetic neuropathy impairs nerve function and the patient’s ability to sense injury. One consequence is that wounds can go unnoticed, unmanaged and risk infection as PVD results in decreased blood flow to the extremity and thereby delays healing. Foot infections are the single most common problem diabetic patients experience.3 These can impact the bones, skin and soft tissues of the foot, and when combined with peripheral vascular disease and kidney dysfunction can lead to complications ranging from amputation to severe sepsis.3 Infections stress the body’s metabolism and in both diabetic and nondiabetic patients can lead to hyperglycemic emergencies. In one study of patients with sepsis, hyper-glycemia developed in 20% of nondia-betic patients and 70% of those with diabetes.4

Hyperglycemic Emergencies

Patients with diabetes mellitus must manage their blood sugar levels daily. When they fail or suffer another illness, they risk developing one of two serious metabolic derangements: hyperosmolar hyperglycemic state (HHS) or diabetic ketoacidosis (DKA). They are similar in presentation, with their biggest differences For More Information Circle 48 on Reader Service Card


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being the severity of their dehydration and the patient’s level of acidosis.Patients without diabetes can still develop hyperglycemic emergen-

cies. As many as 40% of patients diagnosed with HHS will have no prior diabetic history.5 Diabetic ketoacidosis presents in newly diagnosed and previously unknown diabetic patients in 15% of cases.6 A recent study also demonstrated the benefit of routinely determining blood sugars in patients with suspected infections, particularly pneumonia. In this 2,124-patient study, 67% developed stress/illness-associated hyperglycemia requiring treatment.7 Additional studies have demon-strated that severe body stresses, including severe sepsis, surgery and trauma, can all trigger hyperglycemia, and this hyperglycemia predicts an increased mortality.8

Both HHS and DKA are fairly common, with HHS affecting roughly 1 in 500 patients with DM,5 and DKA accounting for 50% of diabetic-related hospital admissions for patients under 19.6 The latter demonstrates that DKA is more common in younger patients; it most commonly presents in patients younger than 20, while the median age of a patient with HHS is 60. More attention is given to DKA in most prehospital and emergency medicine settings, though its 2% mortality is significantly lower than the 20% with HHS.5,6

When a patient with diabetes becomes ill, such as with an infection, their body is stressed worse than other patients’ because the illness-induced increased metabolic demand alters their insulin and glucose needs. Specifi cally their body needs additional glucose and insulin, and the amount by which the need changes is diffi cult to anticipate. This increased metabolic demand is also complicated by increased fl uid loss, placing the diabetic patient at risk for blood glucose elevation.

For diabetic patients, challenges eliminating glucose via the kidneys complicate their illness. When blood glucose levels are normal, the kidney filters and reabsorbs glucose as a normal part of renal func-tion. As glucose levels exceed 180 mg/dL, the renal tubules become saturated with glucose, and additional reabsorption is not possible. Glucose remains in the renal tubules, which causes additional water and electrolytes to diffuse into the renal system and be excreted as urine. This process is known as osmotic diuresis. Osmotic diuresis leads to excessive urine production and a profound decrease of the total body water level; patients can be dehydrated by up to 9 liters. With the excessive urine production patients also experience electrolyte loss, and their dehydration exacerbates the hyperglycemia.5

Hyperosmolar Hyperglycemic StateThis complex cascade of events leads to a hyperosmolar hypergly-

cemic state where patients have dangerous hyperglycemia and their blood serum is dangerously hyperosmolar. Hyperglycemia is present whenever blood glucose levels rise above 250 mg/dL. Hyperosmolarity describes a state of increased osmotic pressure. Osmotic pressure refers to the amount of “pull” fluids experience between the two sides of a semipermeable membrane. There is always some osmotic pres-sure between these sides, and fluids shift from areas of lower osmotic pressure to areas of higher osmotic pressure. As osmotic pressure increases, fluids shift in greater volumes and with greater force.

Osmotic diuresis is an example of what happens in a hyperos-molar state. Because of excess glucose in the renal tubules, there is a greater force pulling fluids out of the bloodstream and into the renal system than the body would normally experience. Excessive For More Information Circle 49 on Reader Service Card

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glucose in the bloodstream also creates an increased osmotic pressure compared to the intracellular and extracellular spaces and causes fluids to shift from the cells into the bloodstream, dehydrating the cells. When the osmotic pressure is normal, fluids can shift freely back and forth between the bloodstream and these

other spaces. In hyperosmolar conditions fluids only shift into the bloodstream, leaving the extracellular and intracel-lular spaces fluid-deprived.

HHS was previously known as hyper-osmolar hyperglycemic non-ketonic coma (HHNC). This phrasing was dropped, as fewer than 20% of patients with HHS experience a decreased level of consciousness. The most impor-tant feature distinguishing HHS from diabetic ketoacidosis is that acidosis does not develop; the reasons for this are unknown.

Typically HHS develops slowly over several days and may take many weeks before symptoms become apparent. This slow onset promotes the slow and profound dehydration patients can experience. During this time both hyperglycemia and hyperosmo-larity drive a fluid shift that leads to intracellular dehydration and loss of electrolytes. The two most significant electrolytes depleted are sodium and potassium. Their elimination is acceler-ated by increased osmotic diuresis, or excessive urination.

Patients with HHS experience blood glucose levels in excess of 600 mg/dL and can exceed 1,000 mg/dL. The relative slow onset of HHS permits the slow devel-opment of profound dehydration. This can lead to focal and global neurologic deficits, including loss of fine motor skills, tremors and in severe cases seizures and mental status changes. Table 1 highlights the neurological changes common in HHS. The body’s serum osmolarity shifts during HHS from the normal baseline of 280–290 mOsm/kg (a narrow range) to more than 320 mOsm/kg. This is a significant change that causes a strong pull of fluids from the extra- and intracel-lular spaces into the bloodstream, thus enhancing fluid availability for elimina-tion via the kidneys.

Laboratory data is not typically available to prehospital providers but is available for most teams completing interfacility transports. A review of the lab data for patients with HHS should demon-strate that their pH is greater than 7.30 (normal is 7.35–7.45), which is only slightly more acidotic than normal. This For More Information Circle 50 on Reader Service Card

• Coma (uncommon)• Delirium• Drowsiness• Hemiparesis

• Lethargy• Seizures• Sensory defi cits• Visual disturbances

Table 1: Neurological Changes Common in HHS5


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is because patients tend to compensate well in HHS, and profound acidosis does not develop. Bicarbonate, a key part of the body’s buffer system, is normally 22–26 mEq/L and in HHS can be low (because it is being used to maintain the patient’s pH) but will be greater than 15 mEq/L. Hold on to these values for now, and compare them to the values found in patients with DKA. Finally, patients with HHS present with hyponatremia and hypokalemia.5

It is extremely important to identify the underlying illness that triggered HHS. While prehospital providers may not always be able to accomplish this, it is still important to be a detective and look. Infections such as pneumonia, upper respiratory system infections and sepsis, GI distress, and drug abuse can all cause HHC, as can the illnesses listed in Table 2. Stroke and myocardial infarction are both on the list; always consider these as contributing factors

to hyperglycemic states until they can be ruled out. Always perform a 12-lead EKG and stroke assessment on patients with hyperglycemia.

Diabetic KetoacidosisDiabetic ketoacidosis is an acute life-

threatening emergency most common in patients with diabetes mellitus. It is diag-nosed with uncontrolled hyperglycemia and the presence of ketoacidosis and defined by a serum ketone level greater than 5 mEq/L and a blood sugar over 300 mg/dL. One of the significant differences between DKA and HHS is the onset: DKA’s is rapid and develops within just a few days. DKA is most commonly caused by poor compliance with prescribed insulin administration. The causes of DKA are highlighted in Table 3.

Physiologically DKA is a complex metabolic state that begins when a patient has a relative or absolute insulin defi ciency as well as an increased pres-

ence of the counterregulatory hormones glucagon, cortisol and epinephrine. In this respect, and in the hyperosmotic state created by elevated blood sugar, DKA is quite similar to HHS. However, while the body’s pH in HHS is relatively normal, acidosis rapidly sets in during DKA as liver metabolism transitions to using free fatty acids as an alternative energy source. When free fatty acids are

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• Alcohol and drug abuse

• Anesthesia• Burns• GI hemorrhage• Hypothermia• Infections (UTIs,

pneumonia, etc.)• Intracranial

hemorrhage• Myocardial

infarction

• Pancreatitis• Pulmonary

embolism• Stroke• Medications,

including: Antiepileptics Antihypertensives Antipsychotics Beta blockers Corticosteroids Diuretics

Table 2: Common Hyperosmolar Hyperglycemic State Triggers5


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metabolized, ketogenesis leads to an accumulation of ketones and keto acids. The body can regulate and break down ketones and keto acids for a fi nite period, but if there is still an insulin shortage as this period passes and ketones are still being produced, they then rapidly accu-mulate in the bloodstream. The accumu-lation triggers nausea and vomiting and produces the fruity-odor breath charac-teristic of patients with DKA.6 Osmotic diuresis develops similar to in HHS and is exacerbated by the vomiting. Because the onset of this state is more rapid in DKA, dehydration is not as profound as in HHS

but can still exceed 6 liters of fl uid loss.Some of the differences between

HHS and DKA become evident when comparing the patient’s anticipated lab value findings. Diabetic ketoacidosis presents with a pH of less than 7.30 and a bicarbonate less than 15 mEq/L. These values signify that the body is becoming depleted of bicarbonate, a valuable acid buffer, and is unable to maintain a normal pH. Moderate DKA develops when the pH drops below 7.2 and the bicarbonate below 10 mEq/L. Severe life-threatening DKA is present when the pH is less than 7.1 and the bicarbonate is less than 5 mEq/L. These last patients are on the precipice of death.

In many respects DKA and HHS present similarly. It is reasonable to antic-ipate weakness, fatigue and malaise. Mental status changes are common, including confusion and disorientation. However, a decreased level of conscious-ness is rare. In addition, patients with

DKA are likely to experience nausea and vomiting as well as diffuse abdominal pain. Because profound dehydration is common, anticipate poor skin turgor. Finally, look for the hallmark symptoms of DKA: polyuria (excessive urination), poly-dipsia (excessive thirst), a fruity odor on the breath (from ketones) and tachypnea.

Anticipate profound tachypnea in patients with DKA, it is a compensatory mechanism to regulate acidosis. If the patient’s respirations are slowed and retuned to a normal rate, their acidosis could rapidly worsen.

Examining the Hyperglycemic Patient

The assessment of any patient with an acute illness requires a holistic approach. Avoid being sucked into only focusing on one complaint or body region.

Begin with a thorough history. Valuable information can be obtained here, including the presence of a diabetic


• Bacterial infection• Idiopathic• Medications

(corticosteroids)• Myocardial

infarction

• Pneumonia• Poor insulin

compliance (25% of cases)

• Surgery

Table 3: Triggers for Diabetic Ketoacidosis6


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history. Remember, though, that a history of diabetes is not required for a patient to develop hyperglycemia. If the patient has diabetes, determine what form and if they are compliant with their medications.

A typical OPQRST assessment can help you understand the progression of your patient’s current complaints. An increased length of illness may lead toward HHS if blood glucose is later found to be elevated. While interviewing the patient, be sure to determine the frequency of their urine output, not just when they went last; also determine how their fl uid intake has compared to urine loss. Good detective work can help predict the amount of loss. Inquire about recent weight loss; every 1 kg or 2.2 lbs of body mass loss equals roughly 1 liter of total body fl uid loss. Pay particular attention to signs of underlying illness or infection. With any cardiac-associated complaint, be sure to also perform a 12-lead EKG when allowed. Also, never hesitate to complete a neurological examination.

Early and regular vital sign moni-toring is essential. Expect tachycardia and tachypnea, as they are compensa-tory mechanisms of hyperglycemia and dehydration. When a patient experiences hyperglycemia, additional metabolic acids are produced, and the body wants to eliminate these as quickly as possible. Increased respirations are the fastest method, as carbon dioxide is exhaled and eliminated with each breath. Tachycardia develops as the dehydrated cardiovas-cular system works harder to continue transporting oxygen and nutrients to the body’s tissues with a decreased volume. Both develop early in illness progression.

While tempting, orthostatic vital signs are not predictive of volume status and will not help you in your differential diag-nosis.5 An important yet often forgotten vital sign is core temperature. Be sure to obtain one if possible whenever evalu-ating a patient with a diabetic-related complaint. Elevated temperatures suggest an infectious etiology of under-lying illness. Decreased core tempera-tures also suggest an underlying illness but carry a grave prognosis.

While orthostatic vital signs do not help predict fluid volume status, there are

symptoms to look for. Evaluate skin turgor by pinching the patient’s skin lightly. If it has a healthy fluid level, it should return to its normal position within about a second. When dehydrated, elasticity is lost, and the skin will experience a delayed return to its resting position. If the pinched skin stays elevated for longer

than 2 seconds following release, it is said that skin turgor is poor.

Blood glucose determination is essen-tial in hyperglycemic emergencies. The glucometers used at patient bedsides are regulated by the FDA and CLIA as waived point-of-care testing devices. Waived devices do not require the same preci-



sion as laboratory devices. An awareness of this is important because these “waived” glucometers are typically calibrated to be within 20 mg/dL.9 This means that a BGL of 72 could really be between 52 and 92 mg/dL. Additionally most waived glucometers can only provide results for blood sugars up to 600–700 mg/dL. Patients with HHS often have blood sugars over 800 mg/dL, and it is not uncommon to see values exceeding 1,000 mg/dL in severe cases. DKA tends to present with lower, though elevated, blood sugars from 300 mg/dL up.

ManagementWhenever treating hyperglycemia the

primary intervention goals are the same: stabilize and normalize blood glucose; rehydrate; maintain electrolyte homeo-stasis; and treat the underlying condition.

The management of diabetic ketoaci-dosis has additional treatment goals of acid-base normalization and early insulin administration.

Suspected or known hyperglycemia is an advanced life support call. BLS management is supportive in nature and includes oxygen via nasal cannula, early access to ALS and rapid transport to an emergency department. Advanced providers need to initiate cardiac moni-toring early during patient care. Perform a 12-lead EKG to rule out STEMI. Additionally, continuous cardiac monitoring is essen-tial to monitor for profound electrolyte abnormalities, particularly hypokalemia.

Manage the airway and breathing carefully. It is common to observe hyper-ventilation in patients with hyperglycemic emergencies, as the patient’s body is eliminating excess carbon dioxide to try to maintain a normal pH. These increased respiratory rates are a critical compen-sation mechanism and need to be supported. As necessary, provide oxygen to maintain an SpO2 between 92%–96%.

As early as possible, advanced providers should establish IV access and initiate a fluid bolus of normal saline. Remember, patients can be dehydrated by as many as 9 liters, and in-hospital care will strive to replace at least half the fluid deficit within 12 hours, and up to 2 liters in the first 2 hours. When patients are experiencing HHS, aggressive fluid

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replacement may be enough to correct hyper-glycemia. When DKA is suspected, first-hour fluid administration can be increased to 3 liters of normal saline. Keep in mind that most patients in DKA are children; for chil-dren, initiate 20 mL/kg of normal saline to be administered over the first hour.

The potential benefit of prehospital insulin by paramedics has been long discussed and rarely implemented. In HHS, all patients will eventually need IV insulin. However, IV insulin is initially contraindicated because if insulin is administered prior to fluid replacement, it is likely to drive glucose, potassium and water into the cells at a rate that can cause circulatory collapse and life-threatening hypokalemia.5 Insulin is administered earlier in DKA than in HHS, typically within an hour of initial fluid therapy. In both emergencies insulin is not initiated prior to determining the patient’s potassium. Several studies have demonstrated that earlier insulin in DKA does not hurt patient outcomes; however, it does not benefit patients either and therefore is not generally recommended in the field.6

For teams that participate in interfacility transports, insulin may regularly be seen. For these transports, check the patient’s blood sugar regularly and keep in mind that when insulin is administered, the rate of blood glucose decline should be limited to a maximum of 100 mg/dL per hour. If the blood sugar is decreased at a faster rate, patients risk developing cerebral edema.

When profound acidosis is suspected or known, administration of sodium bicarbonate may be tempting. Sodium bicarbonate is only indicated when the acidosis appears life-threatening or when associated with severe sepsis or lactic acidosis. Typically this is not done during prehospital care unless the patient is seizing or unresponsive, or if the team is able to perform an arterial blood gas.

Programs managing patients during interfacility transports will have the added benefit of lab data identifying the patient’s electrolyte levels. Patients with hyperglycemia will likely have low potassium and sodium levels. These cannot be managed without known accurate lab data, but when known, it’s common to provide potassium replace-ment while managing the elevated blood glucose. When profound hypokalemia is present, many emergency departments also assume simultaneous hypomagnesemia and initiate IV magnesium replacement.

SummaryDiabetes mellitus is an incredibly

complex disease and impacts millions of Americans. The pancreas and insulin are both key to normal glucose metabolism and glucose control. Nearly any body stressor that alters a patient’s metabolism can impair normal insulin function and trigger hyper-glycemia. It is prudent to check blood sugar in all patients with suspected serious illness, whether or not they have diabetic histories. Hyperglycemia can affect any patient and is a predictor of increased mortality if not treated early. Diabetic ketoacidosis has a more rapid onset than a hyperosmolar hyperglycemic state and often presents with a compara-tively lower blood sugar and the presence of acidosis. HHS does not present with profound acidosis and has a slower onset, yet more profound dehydration and a higher blood sugar. Do not underestimate the need for early prehospital intervention with hypergly-cemia. Early and aggressive IV fluid admin-istration can improve patient outcomes and speed recovery.

REFERENCES1. Bhavsar AR. Diabetic Retinopathy. Medscape, http://emedicine.medscape.com/article/1225122-overview.2. Lin HC. Diabetic Neuropathy. Medscape, http://emedicine.medscape.com/article/1170337-overview.3. Bronze MS. Diabetic Foot Infections. Medscape, http://emedicine.medscape.com/article/237378-overview.4. Schuetz P, Kennedy M, Lucas JM, Howell MD, Aird WC, Yealy DM, Shapiro NI. Initial management of septic patients with hyperglycemia in the noncritical care inpatient setting. Am J Med, 2012 Jul; 125(7): 670–8.5. Hemphill RR. Hyperosmolar Hyperglycemic State. Medscape, http://emedicine.medscape.com/article/1914705-overview.6. Raghavan VA. Diabetic Ketoacidosis. Medscape, http://emedicine.medscape.com/article/118361-overview.7. MacIntyre EJ, Majumdar SR, Gamble JM, Minhas-Sandhu JK, Marrie TJ, Eurich DT. Stress hyperglycemia and newly diagnosed diabetes in 2,124 patients hospitalized with pneumonia. Am J Med, 2012 Oct; 125(10): 1,036.e17–23.8. Sperry JL, Frankel HL, Vanek SL, Nathens AB, Moore EE, Maier RV, Minei JP. Early hyperglycemia predicts multiple organ failure and mortality but not infection. J Trauma, 2007 Sep; 63(3): 487–93, discussion 493–4.9. Mann EA, Pidcoke HF, Salinas J, Wade CE, Holcomb JB, Wolf SE. Accuracy of glucometers should not be assumed. Am J Crit Care, 2007 Nov; 16(6): 531–2.

Kevin T. Collopy, BA, FP-C, CCEMT-P, NREMT-P, WEMT, is performance improvement coordinator for Vitalink/Airlink in Wilmington, NC, and a lead instructor for Wilderness Medical Associates. E-mail [email protected].

Sean M. Kivlehan, MD, MPH, NREMT-P, is an emergency medicine resident at the University of California, San Francisco. E-mail [email protected].

Scott R. Snyder, BS, NREMT-P, is a faculty member at the Public Safety Training Center in the Emergency Care Program at Santa Rosa Junior College, CA. E-mail [email protected].

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