Prehospital Diabetic Emergencies - Basic

Objectives
After reading this article, you will be able to:
1. Describe the anatomy and physiology of the normal pancreas and the associated systems of blood sugar
regulation.
2. Discuss the pathophysiology of diabetes.
3. Describe the day to day management and long term complications of diabetes.
4. Describe the signs and symptoms of hypoglycemia and hyperglycemia.
5. Describe prehospital treatment for common diabetic emergencies.

Case Study
At 06:45 in the morning you and your partner are trying to catch a few minutes of rest before the end of your shift
when dispatch alerts your crew to respond to a private residence where a 32-year-old male has been found
unresponsive. While enroute the dispatcher updates you with information that the patient, while unconscious, has a
pulse and is breathing. It is further reported that the patient is a known diabetic and that his family is present on scene
to let you into the home.
Upon arrival on scene the patient is found supine in bed. He is unconscious, pale, diaphoretic, and only responds to
deep painful stimuli with moaning. He does not exhibit any purposeful movement. There is no sign of traumatic injury
and the patients anxious wife denies any recent drug or alcohol abuse. She states that the patient worked late the
previous evening and missed dinner but did not have any complaint or appear to be ill when he got home. The patient
has a strong and regular radial pulse at 110 beats per minute. He is breathing 16 times per minute with normal chest
rise and clear and equal lung sounds. His pulse oxygenation on room air is 94%, and you immediately place him on
high flow O2 via non-rebreather mask. The patients blood pressure is 128/80 mmHg. A finger stick reveals a blood
glucose level of 30 mg/dL. According to his wife, the patient has been an insulin-dependent diabetic since he was a
child and he has no additional medical problems.
After establishing vascular access with an 18 gauge angiocath placed in the left antecubital vein you and your partner
start an infusion of normal saline solution. Once you make sure that the fluid is flowing well and that there is no sign of
infiltration (such as swelling or redness at the IV site), 25 grams of 50% dextrose solution is administered via IV push.
A few minutes later the patient becomes responsive. At first he seems confused but it quickly passes and he becomes
conscious, alert, and oriented. His vital signs are now: pulse 90 beats per minute, respirations 16 breaths per minute,
SPO2 100% (room air), blood pressure 130/90 mmHg, and his blood glucose is 210 mg/dL.
The patient is very embarrassed and states that it has been years since he has had an episode of hypoglycemia. He
reports that he checks his glucose diligently throughout the day and he is careful with his diet. He admits, however, that
he has been working on an important project and skipped dinner the previous evening. He also states that he took his
evening dose of Lantus, a long acting human insulin, without checking his blood sugar.1
When you ask the patient which one of the local hospitals he would like to be transported to, he informs you that he
feels much better and does not wish to go to the emergency room. You advise him and his wife that the dextrose
solution that was administered through the IV will be metabolized quickly and that he may have unpredictable
fluctuations in his blood glucose throughout the day. They understand the risks and their plan is for the patient to
immediately eat a well-balanced meal that includes complex carbohydrates and to monitor his blood sugar closely
throughout the day as well as to follow up with his endocrinologist.
Your protocol requires consultation with online medical direction for a patient refusal after ALS treatment. The
physician finds the patients plan to be appropriate and approves the patients refusal of transport. The appropriate
documentation is completed and signed. The patient agrees that if anything changes or he becomes ill he will call EMS.
You and your partner return to the station to be relieved by the next shift. It is finally time to go home and get some
sleep.

Introduction
Diabetes Mellitus is a disease of the endocrine system where either the pancreas does not produce adequate insulin or
the body becomes resistant to the insulin that is produced. Both of these pathologies lead to a situation where the body
is unable to metabolize sugars. This metabolic inability can cause the patient to present with low blood sugar
(hypoglycemia), or high blood sugar (hyperglycemia). Diabetic emergencies are a common occurrence for emergency
medical services personnel. In order to recognize and manage these life threatening conditions effectively the provider
must be familiar with the anatomic systems and pathophysiology that are associated with the disease process.

Diabetes has become a costly public health problem. The number of patients who suffer from this condition is expanding
rapidly. With proper management diabetic patients can lead normal lives and have average life expectancies, but there
is no cure.2 Some patients are even able to manage the disease without any pharmaceuticals. By maintaining a strict
adherence to dietary regimens, as well as exercise/weight loss guidelines, many patients with diabetes mellitus can
control disease mortality/efficacy. These patients are however, the minority. Many patients do not manage the disease
adequately, thereby increasing the mortality and morbidity of diabetic related illness in the United States.3 In their
2011 diabetes fact sheet, the Centers for Disease Control (CDC) provided the following statistics:
25.8 million people in the US are affected by diabetes (8.3% of the population).
18.8 million people are diagnosed with diabetes.
7.0 million people are living with diabetes undiagnosed.
Among residents of the United States ages 65 and older, 26.9% had diabetes in 2010.
There were 215,000 patients with diabetes who were 20 years of age or younger in 2010.
There were 1.9 million new diagnoses of diabetes in 2010.
35% of all US adults older than 20 showed signs of prediabetes.
Diabetes is the leading cause of kidney failure, non-traumatic lower limb amputation, and new cases of
blindness.
Diabetes is a major cause of heart disease and stroke.
Diabetes is the 7th leading cause of death in the US.
The CDC estimates that the total costs of diabetes care and management in the United States is approximately
$174 billion annually.4
Because of the increased incidence of uncontrolled diabetes mellitus having reached epidemic proportions, it is vital that
healthcare systems are adequately prepared to meet the growing trends in these patient populations.

The Anatomy and Physiology of the Normal Pancreas and the Associated Systems of Blood
Sugar Regulation
The pancreas is a small solid organ that lies between the stomach and the duodenum in the anterior chamber of the
retroperitoneal space. It serves both endocrine and digestive purposes and it is considered both an endocrine and
exocrine gland. The pancreas produces digestive enzymes as well as insulin and glucagon which are the hormones that
have primary control of blood glucose levels.5
Insulin and glucagon are produced in specialized cells known as the islets of Langerhans within the pancreas. 6 There is
further subdivision of specialty within the islets. The alpha cells produce glucagon and the beta cells secrete insulin.
There are also delta cells but researchers are unsure of their specific purpose.7
Insulin enables sugar, fatty acids, and amino acids to be taken up and metabolized by cells. The sugars, fatty acids,
and amino acids are the primary source of energy at the cellular level and without insulin they are minimally usable.
Insulin also stimulates storage of un-metabolized food and the conversion of glucose into a long polymer chain called
glycogen which is then stored in the liver for use later. The fatty acids are converted into triglycerides and stored as
fat. The amino acids are metabolized into proteins and glucose to be used for energy. The net effect of these cycles is a
reduction in blood glucose level.
Glucagon has an opposing function to insulin. It stimulates the release and subsequent breakdown of glycogen into
glucose. Glucagon also stimulates both the liver and kidneys to produce glucose from non-carbohydrate molecules.
Another one of glucagons important functions is the activation of the enzyme hormone-sensitive lipase which breaks
down triglycerides into free fatty acids and glycerol which are then metabolized or converted to ketones. A preparation
of glucagon that has been extracted from beef and pork pancreases is available as a parenteral treatment for
hypoglycemic patients.8 This will be discussed in detail in the treatment section.
When non-diabetic people eat and food is digested, their blood sugar will rise but insulin is quickly released which allows
the sugars to be metabolized and the blood glucose level will normalize within a short period of time. Conversely,
hunger stimulates the release of glucagon which causes the secretion of glycogen from the liver. The glycogen is
metabolized into glucose that is then available for cellular consumption. It is important to note that people who are
chronically malnourished may not have adequate glycogen stores within their livers and the glucagon may not be
effective. Under normal circumstances the actions of insulin and glucagon prevent the plasma glucose concentration
from rising over 170 mg/dL after eating and dropping below 50 mg/dL in between meals.9

The Pathophysiology of Diabetes

When insulin is not produced or the cells become resistant to it blood sugar levels rise unchecked and will wreak havoc
on many different body systems over time. The extent of complications or lack thereof depends on the patients
average glucose level and how early in life the disease presents.10 In order to control the disease, patients must be
willing to adjust their diet and activity. In addition to strict regulation of caloric intake, pharmacological treatment

focuses on maintaining normal glucose levels.

Diabetes has two primary causes. The first is an organic malfunction within the pancreas that can be related to
autoimmune disease where the beta cells are damaged or destroyed. Insulin production is limited or not present. This
is type 1 or juvenile diabetes. The second is an exaggerated cellular resistance to the insulin that is produced. This is
type 2 or adult onset diabetes. Both pathologies lead to elevated blood glucose levels. Cellular starvation occurs even
though large quantities of sugar are present because the lack of or resistance to insulin inhibits cellular uptake and
metabolization. Over time, if left untreated or poorly managed, chronic hyperglycemia leads to renal failure, blindness,
neuropathy, and poor peripheral circulation (eventually amputation). It also significantly increases the patients risk for
cardiovascular disease, stroke, and peripheral vascular disease.
Type 1 diabetes is sometimes called juvenile diabetes and it generally strikes children as opposed to adults. Often the
diagnosis is made when the child presents with malaise, excessive thirst, excessive urination, and dehydration.
Researchers have identified that there is a hereditary predisposition to type 1 diabetes, meaning that if ones parents
suffer from the disease, the children are more likely to also have it. They also believe that environmental factors such
as infection can trigger an autoimmune reaction where antibodies destroy or damage the islets of Langerhans within
the pancreas. 11 Most patients who suffer from type 1 diabetes do not produce any insulin at all which is why they must
rely on insulin injections in order to control their blood glucose levels. These patients must also follow strict dietary
guidelines in order to limit their intake of sugars and carbohydrates, which can be especially challenging for pediatric
patients.
Type 2 or adult onset diabetes is the most common form of the disease. Ninety percent of all diabetic patients in the
United States suffer from type 2 diabetes.12 Typically, type 2 diabetes develops later in life although with increasing
child obesity there are more and more cases of younger patients being diagnosed.13 The insulin resistance that is the
hallmark of type 2 diabetes develops from a group of characteristics known as metabolic syndrome. These
characteristics include excess fat in the abdominal area, elevated blood pressure, and high levels of blood lipids.14
Individuals who are overweight, experience a chronic lack of physical activity, and have a hereditary predisposition are
more likely to suffer from metabolic syndrome and consequently, type 2 diabetes.15
It is not fully understood why metabolic syndrome leads to insulin resistance. Some research indicates that metabolic
syndrome causes changes in the insulin receptor sites within the target cells making them unable to receive the insulin
when it arrives.16 It is important to note that while uncommon, type 2 diabetes may also be a result of pancreatic
malfunction and insufficient insulin production.17
Expectant women sometimes develop diabetic symptoms during their pregnancy and this is known as gestational
diabetes. During pregnancy the fetus requires glucose for energy. This is supplied from the maternal circulation.
Maternal insulin is too large of a molecule to cross the placental barrier. There are fetoplacental hormones that are
present to regulate glucose levels in the fetus. The mothers physiology must adapt to the increased demand for
glucose. Under normal conditions, during pregnancy, the pancreas secretes increased amounts of insulin and the
maternal cells show decreased sensitivity to it. Maternal hormones like progesterone and estrogen which are present at
increased levels during pregnancy also blunt the action of insulin and increase the amount of glucose that is produced.
In healthy women a delicate balance is achieved and homeostasis is maintained with glucose made available to the
fetus. Some womens bodies are not able to achieve this and gestational diabetes develops. Wild fluctuations in blood
glucose can occur. Hypoglycemia and hyperglycemia are both common in patients who suffer from gestational
diabetes. Women who are obese or are otherwise predisposed to diabetes are more likely to suffer from this
condition. 18 Gestational diabetes will often resolve after pregnancy; however, women who experience this are 35% to
60% more likely to be diagnosed with type 2 diabetes within the next 10 to 20 years.19
Typically the symptoms of type 2 diabetes develop gradually in non-pregnant patients. They include fatigue, nausea,
polyuria, excessive thirst, unexplained weight loss, blurred vision, frequent infections with slow wound healing,
increased irritability, confusion, shakiness, unresponsiveness, and seizure activity.20 As was previously noted according
to the Centers for Disease Control, there are at least seven million people living with undiagnosed and untreated
diabetes. 21 This is in large part due to the non-specific symptoms and presentation in adult patients. As early screening
and diagnosis improve the incidence of long term complications may be reduced.
There are four different criteria that are used to diagnose diabetes. Often doctors look for one or more of the four
benchmarks to present on more than one occasion to make the diagnosis. The first is a fasting blood glucose level that
is greater than 126 mg/dL. The second is a random blood sample that is found to have glucose levels of 200 mg/dL or
greater. The third is an oral glucose tolerance test. In this test the patient is given a designated amount of oral glucose
solution and then his or her blood glucose level is evaluated two hours later. If the blood glucose is 200 mg/dL or
greater then he or she has met the criteria for diabetes. The final diagnostic is a measure of the glycated hemoglobin
(HbA1C) level in the blood, and if it is found to be 6.5% or greater, than the patient is considered diabetic.22 HbA1C will
be further explained later in the module.

Day to Day Management and Long Term Complications of Diabetes

Patients whose pancreases do not produce insulin must take subcutaneous insulin injections multiple times throughout
every day in order to maintain normal blood glucose levels. Insulin is available in a number of different forms. In the
1980s scientists were able to derive human insulin from genetically engineered bacteria. Prior to that discovery patients
had to take insulin that was derived from the pancreases of pigs and cows. Today all of the insulin sold in the United
States is made in a laboratory with some being human, some derived from bacteria, and the rest being synthetic.23
Insulin is classified by its onset of action and the categories are rapid acting, regular or short acting, intermediate
acting, and long acting. The actual onset of action and duration of effect is dependent on many factors including the site
of injection, the patients overall circulatory status, and the activity level.24 Many diabetics take a combination of rapid
and long or intermediate acting insulin in order to effectively control their sugar. Some even take formulas of insulin
that are a combination of different kinds. An example would be 70/30 insulin that is 70% intermediate acting insulin and
30% rapid acting insulin.25
In the United States insulin packaged for home use is supplied in a concentration such that 1 mL contains 100 units.26 It
is supplied in prefilled pens, vials, and pumps. Most type 1 diabetics take doses that are variable and are adjusted
based on a sliding scale related to oral intake or blood glucose level.
Insulin pumps are becoming increasingly popular because the patient receives his or her insulin discreetly without
multiple injections. The pumps that are currently in use are approximately the size of a cell phone or pager and are
designed to clip to the patients waist or belt. The insulin is delivered continuously from a reservoir through an
indwelling subcutaneous catheter. An insulin bolus can also be delivered at mealtime with the push of a button.27 At
times there can be increased risk of hypoglycemia with insulin pumps. If the patient forgets to or chooses not to eat he
or she will still receive continuous insulin which can cause the blood sugar to bottom out.
Those diabetics who are insulin resistant will first try and control the disease with diet and exercise. There are some
who are able to effectively manage their blood sugar without any pharmaceuticals but those who are not, take oral
medications. Oral medications that are prescribed to diabetics are divided into six categories. They are sulfonylureas,
meglitinides, biguanides, thiazolidnediones, alphaglucosidase inhibitors, and DPP-4 inhibitors.28
Sulfonylureas were first developed in the 1950s and they activate the beta cells within the islets of Langerhans to
produce more insulin. Meglitinides also stimulate the release of increased amounts of insulin. Glipizide (Glucotrol) and
glyburide (Micronase, Glynase) are common sulfonylureas that prehospital providers will encounter in the field.
Repaglinide (Prandin) is a frequently prescribed meglitinide. Often patients will take these medications once or twice
daily prior to meal times. 29 When these medications are taken without adequate nutrient intake or in conjunction with
the consumption of large amounts of alcohol it can lead to hypoglycemia.
One of the most common oral medications that is used to control blood sugar is metformin (Glucophage). Metformin is
a biguanide that functions primarily by reducing the amount of glucose that is produced by the liver. It also makes the
cells in musculoskeletal tissue more sensitive to insulin which leads to greater uptake of glucose throughout the
body.30 Thiazolidinediones like rosiglitazone (Avandia) and pioglitazone (ACTOS) also increase the insulin sensitivity of
cells throughout the body and reduce glucose production in the liver.31
Alpha-glucosidase inhibitors lower blood glucose levels by inhibiting the digestion of starchy foods like bread, potatoes,
and pasta. They also slow the breakdown of simple sugars during digestion and help to prevent spikes in blood glucose
after eating. Due to their mechanism within the gastric tract, alpha-glucosidase inhibitors have been known to have
side effects like flatulence and diarrhea.32
Finally DPP-4 inhibitors, the most recently developed class of medications, prevent the breakdown of GLP-1 which is a
naturally occurring compound that decreases blood glucose levels. When GLP-1 levels are increased blood glucose
levels decrease. Common DPP-4 inhibitors include sitagliptin (Januvia) and saxagliptin (Onglyza).33
All type 1 diabetics must take insulin injections and most type 2 diabetics control their blood glucose levels with diet,
exercise, and pharmaceuticals. These are not, however, exclusive categories. There are some type 1 diabetics that
must add anti-hyperglycemic medications to their daily regimen and there are type 2 diabetics that must rely on insulin
injections as their disease worsens.
Whether they use insulin injections or oral medications in conjunction with diet and exercise diabetic patients strive to
maintain consistent blood glucose levels throughout the day. The American Diabetes Association reports that blood
glucose levels between 70 and 130 mg/dL are considered normal.34 In order to monitor their blood sugar levels many
patients must prick their fingers and use a glucometer to test blood samples multiple times per day.
The American Diabetes Association also recommends at least biannual testing of A1c. A test of A1c measures average
blood glucose over the past three months. The test determines this by measuring the percentage of glycated
hemoglobin (HbA1c) in blood. Excess glucose leads to increased glycation of hemoglobin. A diabetic patient whose A1c
level is 7% or less is considered well-controlled. An A1c of greater than or equal to 15% would indicate poorly
controlled diabetes. A person who does not have diabetes will have an A1c of approximately 5%.35

The long term complications of diabetes can cause dysfunction in a number of different organ systems. These disease
processes can be divided into two sub categories. The first sub category is microvascular complications which include
neuropathy (nervous system damage), nephropathy (renal system damage), and retinopathy (eye damage).
Microvascular complications are the most common long term complications of diabetes.36 The second sub category is
macrovascular complications. These include cardiovascular disease, stroke, and peripheral vascular disease. The
problems associated with complications from diabetes can be either episodic or progressive. If they are episodic, that
means that they can be treated and can recur numerous times. Episodic complications can include such things as foot
ulcers or non-healing wounds as a result of peripheral vascular disease. Progressive complications worsen over time,
result in increasing organ dysfunction, and are generally irreversible. 37 Heart disease and renal failure are two
examples of progressive disease processes.
Diabetic peripheral neuropathy (DPN), a progressive microvascular disease, is estimated to affect between 30% and
50% of diabetic patients.38 The primary risk factor for DPN is chronic hyperglycemia. Other factors that also increase
the patients chances for suffering from DPN include age, duration of disease, cigarette smoking, hypertension, elevated
triglycerides, higher body mass index, alcohol consumption, and taller patient height.39 DPN is caused by chronic nerve
damage. Researchers believe that this nerve damage is the result of a combination of factors including metabolic
imbalance (hyperglycemia and low insulin levels), autoimmune dysfunction that causes swelling in the nerves,
mechanical injury to the nerves, and inherited traits. 40 Typically, DPN presents with pain, numbness, and tingling in the
extremities that worsens over time. This can ultimately lead to loss of motor function and subsequent disability. The
symptoms of DPN are treated with anti-depressants such as duloxetine (Cymbalta) and bupropion (Wellbutrin) as well
as with opioid analgesics. Proper management of blood sugar can slow the progress of the disease but at this time
there is no way to reverse the nerve damage.41
Diabetic patients are 10 to 20 times more likely than non-diabetics to have a lower extremity amputation. 42 More than
half of all amputations are caused by worsening DPN. The rest are related to peripheral vascular disease, foot
ulcerations, and subsequent infections. Pedal problems can be limited by regular inspection of the feet, access to
podiatric care, and appropriate footwear. Unfortunately many diabetics do not inspect their feet regularly, wear
appropriate shoes, or have access to the podiatric care that they require.43 Patients who are forced to have an
extremity amputated experience decreased mobility, increased disability, as well as loss of independence.
At any given time there are approximately 150,000 people in the United States with end stage renal disease that are on
chronic dialysis treatment or who have received a kidney transplant as a result of diabetic nephropathy.44 According to
the Centers for Disease Control diabetes is the leading cause of renal failure in the United States, accounting for 44% of
all new cases of kidney failure in 2008.45 The relationship between diabetes and nephropathy is poorly understood but
researchers believe that it is related to metabolic dysfunction. Poorly controlled hypertension and lifestyle factors such
as alcohol abuse, obesity, and cigarette smoking also increase the risk of renal disease among diabetic patients.46
Diabetic retinopathy, damage to the eyes, is related to prolonged hyperglycemia and results in more than 10,000 new
cases of blindness every year.47 It is the most common microvascular complication of diabetes. Typically, retinopathy is
slow to develop and there are indicators that it may begin to develop years before clinical diagnosis of type 2 diabetes
even occurs. 48 Over time elevated blood glucose levels damage the tiny blood vessels that supply the retina of the
eye. Hyperglycemia also causes swelling to the retina. This loss of circulation and swelling in the retina will ultimately
lead to blurred vision and subsequent vision loss.49
Patients who suffer from both diabetic nephropathy and retinopathy also known as renal retinal syndrome are at much
greater risk of suffering from the macrovascular complications of diabetes such as heart disease and stroke.
Cardiovascular disease is the cause of death for as many as 65% of patients with diabetes. Mortality rates due to heart
disease are two to four times higher for diabetic patients than for the general population.50 Also diabetics are two to
four times more likely to suffer from strokes than the general population. The physiological cause of this
disproportionate increase in risk is not clear. However, it is known that 70% of diabetics also suffer from hypertension
or are prescribed antihypertensive medications which in itself increases risk for these pathologies.51 When diabetic men
suffer from hypertension as well as have other risk factors for cardiovascular disease such as obesity, smoking
cigarettes, and elevated cholesterol levels, they typically have poorer outcomes and suffer increased mortality and
morbidity as compared to the non-diabetic population. 52
Peripheral artery disease (PAD) also known as peripheral vascular disease (PVD) is another macrovascular complication
of diabetes. It is characterized by the narrowing of the blood vessels that supply the extremities, stomach, and
kidneys. The incidence of PAD increases with patient age, duration of the disease, and the presence of peripheral
neuropathy. 53 Typically, patients suffering from PAD will present with two different types of symptoms. The first is pain
and discomfort that occurs with movement and exercise and resolves with rest, also known as claudication. The second
set of symptoms is extremity pain that occurs while at rest. This is due to tissue ischemia caused by reduced blood flow.
Peripheral artery disease is a major risk factor for eventual lower extremity amputation.

The Signs and Symptoms of Hypoglycemia and Hyperglycemia

Hypoglycemia
Hypoglycemia is the most common endocrine condition that emergency medical professionals will respond to.54 It is so
common that prehospital protocol dictates that any patient who presents with altered mentation gets his or her blood
glucose checked during the initial assessment regardless of whether his or her past medical history includes diabetes or
not.55 Glucose is the primary fuel for the brain. When blood sugar is low the brain is unable to function properly causing
the telltale confusion that is associated with the condition. The Pennsylvania advanced life support protocol states that
any patient whose blood glucose is found to be less than or equal to 60 mg/dL is considered hypoglycemic and he or she
should receive treatment.56 Make sure that you are familiar with your local protocol that defines the lower limit of
acceptable blood glucose level.
There is a multitude of ways in which the diabetic patient can become hypoglycemic. The most common of those is
decreased oral intake without concomitant decrease in insulin or antihyperglycemic medication dosage.57 Other things
that have been known to precipitate hypoglycemia include stressors, increased physical activity, alcohol use, liver or
kidney malfunction, insulin pump malfunction, infections, and medications such as propranolol, salicylates (commonly
aspirin and Pepto-Bismol), antimalarials, and some antibiotics.58 Hypoglycemia develops relatively quickly, usually in a
matter of hours, as the glucose that is available is quickly metabolized in the insulin rich environment.
The signs and symptoms of hypoglycemia depend on how low the patients blood sugar is. In the early stages as blood
sugar drops the patient may exhibit a sympathetic nervous system response that includes diaphoresis, tachycardia, and
anxiety. If the patients blood sugar continues to drop then confusion, unconsciousness, seizures, and even death will
follow. 59 Hypoglycemic patients may appear to be intoxicated and can even be highly combative. They may also
present with slurred speech and unilateral hemiparesis that appears to be stroke-like in nature which is why all stroke
assessment tools include evaluation of blood sugar early in the assessment. The blood glucose level where the patient
becomes symptomatic is variable and depends on his or her own personal physiology.
It is important to note that hypoglycemia can occur in non-diabetic patients. It is often seen in alcoholics who are
chronically malnourished. Poisoning or overdose on medications like aspirin can have a profound effect on the liver and
kidneys which can also cause steep drops in blood glucose levels. Certain cancers, liver disease, and renal failure can
also inhibit the natural mechanisms that regulate blood sugar levels and can lead to profound hypoglycemia.60 It
cannot be stressed enough that any patient who presents with an altered level of consciousness should have his or her
blood glucose level evaluated.

Hyperglycemia
Hyperglycemia, a fasting blood sugar that is greater than or equal to 130 mg/dL, is caused by excessive food intake,
insufficient insulin, infection, illness, surgery, and/or stress. The onset of symptoms in the diabetic patient with
hyperglycemia is variable. If the diabetic patient eats a large sugary meal and does not take any insulin or other
antihyperglycemic medication then his or her blood glucose can rise rapidly. Conversely, if the cause of the
hyperglycemia is infection or illness it may take several days for the symptoms to develop.61

As blood glucose levels rise the body attempts to compensate and reduce them by excreting the glucose in urine. When
untreated, this physiological compensation can lead to life-threatening dehydration. The patient will typically present
with excessive thirst and excessive urination. As the patients hyperglycemia and dehydration worsen altered
mentation, coma, seizure, and death are possible just as with hypoglycemia.
Untreated hyperglycemia can progress into diabetic ketoacidosis (DKA). Without insulin the cells of the body are unable
to metabolize the glucose that is available and they begin to starve. When this occurs the cells must find an alternate
source of energy. The way they achieve this is to break down proteins into amino acids, and lipids are broken down into
free fatty acids and oxidized to ketones.62 This process provides a source for cellular metabolism but it is highly
inefficient and there are significant amounts of toxic byproducts which lead to a state of metabolic acidosis. This
acidosis is exacerbated by the dehydration and blood hyperosmolarity that is related to the excessive urination
Symptoms of DKA are altered mental status, weakness, visual disturbances, nausea, vomiting, polyuria, polydipsia,
abdominal pain, tachycardia, flushed dry skin, the fruity odor of ketones on the patients breath, deep rapid respirations
(Kussmaul) as the body attempts to correct acidosis by blowing off carbon dioxide, and finally, coma.63
DKA is often seen in teenagers and young adult type 1 diabetics and may even occur prior to initial diagnosis. Studies
indicate that as many as 25% of DKA cases are in patients without previous diagnosis of diabetes.64 DKA is diagnosed
when the patient presents with the previously described signs and symptoms (not every patient has every sign and
symptom) and a blood glucose level greater than or equal to 300 mg/dL. 65
Type 2 diabetics sometimes experience DKA but more often when they have untreated hyperglycemia they experience
hyperosmolar non-ketotic coma (HONK). It is hyperglycemia with similar metabolic derangement to DKA but no
ketosis. It is believed that the small amount of insulin that is retained by type 2 diabetics provides a metabolic blockade
that inhibits the ketosis and acidosis that are present in DKA. Typically, the patients blood glucose level is greater than
or equal to 600 mg/dL and dehydration is worse in HONK than DKA. Some adult HONK patients may require as much as
nine liters of water in order to restore adequate fluid balance.66
It is surprising but patients suffering from HONK present in coma less than 10% of the time.67 More often these
patients have focal neurological deficits in addition to the dehydration. Interestingly, and for unknown reasons, acute
myocardial infarctions are frequently seen in conjunction with HONK. The symptoms that are associated with HONK are
very similar to that of DKA and it may be impossible to differentiate between them in the field. Treatment algorithms
are the same for both conditions.61

Differential Diagnosis
Diagnosis of a diabetic emergency is sometimes difficult. When in doubt, all diabetic patients should receive glucose.
System

Diabetic
Hypoglycemia
Ketoacidosis

Pulse

Rapid

Normal to Rapid

Blood
Pressure

Low

Normal

Respirations Exaggerated

Normal to
shallow

Breath Odor

Acetone Normal
Sweet - Fruity

Headache

Absent

Present

Mental State

Restless Unconscious

Irritable Unconscious

Tremors

Absent

Present

Convulsion

None

In late stages

Mouth

Dry

Drooling

Thirst

Intense

Absent

Vomiting

Common

Uncommon

Abdominal
Pain

Common

Absent

Vision

Dim

Double Vision

Prehospital Treatment for Common Diabetic Emergencies

When responding to assist a patient with hypoglycemia the safety of you and your partner is paramount. Patients can
be aggressive and combative when their blood glucose is low. Make sure to take steps to protect yourself and the
patient. If you must restrain a hypoglycemic patient make sure to do so as gently as possible and do not forget that
the patient is not trying to harm you intentionally. If law enforcement personnel are on scene make sure it is clear to
them that the patient is suffering from a medical emergency as well. Often, if there are family members on scene they
will be familiar with the patients condition and can be a valuable resource to help manage and calm the patient.
The treatment algorithm for hypoglycemic patients is based on his or her mental status and his or her ability to follow
commands. If the patient is awake, alert, adequately protecting his or her airway, and able to follow commands then
oral treatment is acceptable. There are a number of different preparations of oral glucose in either gel or tablet form.
Most are packaged as individual 25g doses. If a commercial product is not readily available then any food or beverage
that is high in sugar will have a similar effect. It only takes approximately seven ounces of soda to get the patient 25g
of sugar.69 When treating hypoglycemia orally be aware that it can sometimes take an extended period of time for the
patients glucose level to rise because the sugar has to be absorbed through the gastric tract prior to taking effect. After
the patients blood glucose level begins to rise it is also important to encourage the patient to eat a full meal with
protein and complex carbohydrates. The simple sugars in oral glucose, soda, and candy will be metabolized quickly and
eating a meal will help to prevent rebound hypoglycemia. 70
If the patient is experiencing an altered level of consciousness or is comatose you must make sure to immediately
manage his or her airway, breathing, and circulation. If the hypoglycemic patient is hypoxic or experiencing respiratory
depression then you must provide, oxygen, ventilation, and if needed, airway support. It is recommended, however,
that you avoid endotracheal intubation or another advanced airway maneuver until after you attempt to correct the
hypoglycemia. If the patient wakes up with an endotracheal tube in his or her throat then he or she will likely panic,
pull the tube out, and potentially cause trauma to the airway. If the patient does not regain consciousness after
treatment then use whatever means you have available to secure the airway.
Once you have managed the patients airway, breathing, and circulation obtain vascular access. When possible select a
large vein for your site and use at least an 18 gauge angiocatheter. The glucose solution that is used by EMS providers
is thick and viscous, especially when it is cold, and can be difficult to push through small catheters and veins. Once your
IV is in place, start an infusion of normal saline solution. Pay close attention to the IV site. If there is any sign of
infiltration stop using the site immediately. The dextrose solution is hypertonic and acidic making it highly caustic to
tissue. It can cause necrosis if it is pushed into a line that has become infiltrated.71 Adult patients should receive 25g of
dextrose intravenously as per protocol. It is normally packaged as D50 where the sugar is in a solution with 50 mL of
saline solution. The medication should be pushed slowly, over a few minutes, with constant monitoring of the IV site for
signs of infiltration. If D50 does become infiltrated immediately remove the IV, elevate the extremity, place ice at the
site, and expedite transport to the closest appropriate facility. Once the dextrose is administered the patients blood
sugar should normalize within a few minutes. In the most severe cases you may have to administer additional doses of
D50 in order to bring the patients sugar level back into normal range. Make sure to follow your local protocol and
contact online medical direction when in doubt.

Pediatric patients should receive a less concentrated dose of dextrose than adults because the caustic nature of the
solution can damage their veins.72 For children younger than eight-years-old, 2mL/kg of D25 is the recommended
dosage. Most EMS services do not carry premixed D25 in their drug boxes. Therefore, you must be ready to prepare it

yourself. The easiest way to do this is to waste half of an amp of D50, leaving 12.5g of dextrose in 25mL of solution in
the syringe. Then you should draw 25mL of normal saline solution into the syringe, giving 12.5g of dextrose in 50 mL of
solution which is D25. You will then be able to administer the correct weight-based dosage. It is recommended that
infants receive 2mL/kg of D10. Again, most services do not carry this in a premixed form. The least complicated way to
make D10 is to waste 40 mL of solution from your amp of D50 and then draw 40 mL of normal saline back into the
syringe. If you are unsure or have questions contact online medical direction.

If you are unable to obtain IV access and the patient will not tolerate oral treatment then you can administer
intramuscular glucagon. The adult dosage is 1 mg and the pediatric dosage is .1 mg/kg up to 1 mg. Glucagon stimulates
the release of glycogen stored in the liver and may take 15-30 minutes to reach full effect.73 If the patient does not
respond to your treatment then manage his or her airway, breathing, and circulation as best that you can and provide
rapid transport to the closest appropriate facility.

Once the patients blood glucose level normalizes he or she will return to his or her baseline level of consciousness
unless there is an underlying illness or injury that is affecting them. When the patient is awake and alert, it is common
for him or her to wish to refuse further treatment and transport. Often, this is acceptable if the patient is a known
diabetic, knows why he or she became hypoglycemic, has a plan to eat a well-balanced meal, will not be alone, and has
a plan to follow up with his or her endocrinologist or other physician. When declining transport all patients should be
made aware of the risks of rebound hypoglycemia and have a plan to deal with it appropriately should it occur. Be
aware that patients who take long acting insulin or oral medications like gliburide and glipizide (sulfonylureas) are at a
much greater risk of rebound hypoglycemia and should be treated and transported accordingly.74

Hyperglycemia
The primary treatment for hyperglycemia is insulin but in most cases that is administered in the hospital as opposed to
in the field. Upon encountering a symptomatic hyperglycemic patient in the field treatment will focus on supporting his
or her vital signs as needed and providing aggressive rehydration. 75 Many patients will seek medical attention when
they begin to feel sick as their blood glucose rises above normal and will only need fluids and supportive care. You will
on occasion encounter patients suffering from severe hyperglycemia, DKA, and hyperosmolar non-ketotic acidosis, that
are comatose, experiencing significantly alerted mentation, showing signs of shock, and/or experiencing potentially
life-threatening electrolyte and metabolic abnormalities.76 These patients will require aggressive and thorough care.
When caring for the very ill patient, begin by providing high flow oxygen, ventilatory support, and airway management
as needed. In contrast with the patient suffering from hypoglycemia, if these patients are not protecting their airways
do not hesitate to utilize the advanced airway tools that you have available. The likelihood that the patient will improve
to the point of pulling the tube out in the field is slim to none. Once the patient is intubated, if waveform end-tidal
capnography is available, then it should be applied. Not only has it become the gold standard for confirmation of correct
placement of the endotracheal tube but it will also help to support the conclusion of severe hyperglycemia and/or
DKA/HONK. Remember that these patients are suffering from severe metabolic acidosis and will be attempting to
excrete or blow off excess CO2 via the respiratory system. In this situation one would expect the patients end-tidal
CO2 level to be significantly elevated. If the patient is protecting his or her airway you can also use the nasal waveform
end-tidal capnography detectors to gain valuable diagnostic information.
Once the patients airway and breathing are managed appropriately establish large bore IV access and start fluid
resuscitation with normal saline solution.77 It is appropriate to administer as much as one liter of normal saline solution
in the first half hour of treatment or at the rate that medical control orders. The patient will likely need at least one liter
of fluid per hour for the first few hours.78 In the prehospital setting maintaining a systolic blood pressure of at least 90
mmHg is the goal. While providing fluids make sure to monitor the patient closely for signs of flash pulmonary edema.
Pediatric patients should receive at least 20 mL/kg boluses and should be monitored closely because over aggressive
fluid administration can lead to cerebral edema.79
Continuous cardiac monitoring is essential for these patients due to the metabolic derangement that has been
previously discussed. The patients serum potassium may be dangerously high due to the fluid loss associated with this
condition and this can cause myocardial instability. If this has occurred large peaked T waves may be present on the
patients electrocardiogram.80 If you suspect hyperkalemia then consider interventions such as calcium chloride 8 to 16
mg/kg, sodium bicarbonate 1 mEq/kg, and or 2.5 mg of nebulized albuterol. 81 Make sure to enlist the help of online
medical command when treating complex metabolic conditions and make sure to follow local protocols.
After you have stabilized the hyperglycemic patient to the best of your ability you must provide rapid transport to the
closest appropriate facility. The patient must receive definitive care in order to mitigate the crisis at hand.

Conclusion
If you work in the field, chances are that you have responded to a multitude of diabetic emergencies. They are
common calls but they can be challenging when you have a patient who is hypoglycemic and combative or is in severe
DKA and is unresponsive. Be prepared, stay safe, and make sure the appropriate resources are mobilized.
Diabetes, especially type 2, is a growing problem in the general population and it is also a growing problem among EMS
providers.82 We tend to work in high stress environments, lack in adequate exercise, suffer from obesity, eat poorly,
and have incredibly irregular sleep patterns. Please be aware of your personal risk factors and do everything that you
can to mitigate them. This profession of ours makes astronomical demands on our minds and bodies and if unchecked it
will take its toll. We owe it to ourselves, our families, and our patients to do everything that we can to prevent health
problems like type 2 diabetes. We should all strive to lead by example by doing things like eating healthy snacks while
on shift, packing a lunch with nutritious items, and/or starting a group fitness program with coworkers. We are also
primary care ambassadors for many of our patients and we ought to try and live the advice that we hand out on a daily
basis while on the job.
This module provides an expansive description of the etiology, pathophysiology, and management of diabetes.
Hopefully, a broader understanding of these topics will make it easier for you to evaluate and treat your patients as
efficiently and as effectively as possible. In the field always be diligent in evaluating your patients blood glucose levels
when indicated. Treat the patient according to your protocols and remember that diabetic patients may suffer from a
multitude of secondary pathologies as a result of their disease which can complicate their treatment.
Author Simon Taxel, Copyright CE Solutions. All Rights Reserved.
References

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20. Ibid
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general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: U.S. Department of
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22. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
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25. Ibid
26. Ibid
27. Ibid
28. Website: Living with Diabetes. What Are My Options. American Diabetes Association website.
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29. Ibid
30. Ibid
31. Ibid
32. Ibid
33. Ibid
34. Website: Living with Diabetes. Checking Your Blood Glucose. American Diabetes Association website.
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35. Ibid
36. Journal article: Deshpande, Anjail. Hayes-Harris, Marcie. Schootman, Mario. Epidemology of Diabetes an
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37. Ibid
38. Ibid
39. Ibid
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45. Document: Centers for Disease Control and Prevention. National diabetes fact sheet: national estimates and
general information on diabetes and prediabetes in the United States, 2011. Atlanta, GA: U.S. Department of
Health and Human Services, Centers for Disease Control and Prevention, 2011.
46. Journal article: Deshpande, Anjail. Hayes-Harris, Marcie. Schootman, Mario. Epidemology of Diabetes an
Diabetes-Related Complications. Physical Therapy. 2008; 88:1254-1264.
47. Ibid
48. Ibid
49. Website: Diabetic Retinopathy. Mayo Clinic website. http://www.mayoclinic.com/health/diabetic-retinopathy
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50. Journal article: Deshpande, Anjail. Hayes-Harris, Marcie. Schootman, Mario. Epidemology of Diabetes an
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51. Ibid
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56. Ibid
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58. Ibid
59. Ibid
60. Book Chapter: Pollak, Andrew N. Endocrine Emergencies. IN: Nancy Carolines Emergency Care in The Streets
sixth ed. New York, Ny: Jones and Bartlett; 2007:29.1-29.25.
61. Ibid
62. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
Challenge EMS Providers. Journal Of Emergency Medical Services Website. http://www.jems.com/article/patientcare/acute-complications-linked-dm-challenge. Accessed February 6, 2013
63. Book Chapter: Pollak, Andrew N. Endocrine Emergencies. IN: Nancy Carolines Emergency Care in The Streets
sixth ed. New York, Ny: Jones and Bartlett; 2007:29.1-29.25.
64. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
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66. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
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68. Ibid
69. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
Challenge EMS Providers. Journal Of Emergency Medical Services Website. http://www.jems.com/article/patientcare/acute-complications-linked-dm-challenge. Accessed February 6, 2013
70. Ibid
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72. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
Challenge EMS Providers. Journal Of Emergency Medical Services Website. http://www.jems.com/article/patientcare/acute-complications-linked-dm-challenge. Accessed February 6, 2013
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75. Book chapter: Traynor, Owen. Diabetic Ketoacidosis And Hyperglycemia. In: Traynor, Owen. Coonan, Patrick.
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76. Ibid
77. Ibid
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sixth ed. New York, Ny: Jones and Bartlett; 2007:29.1-29.25.
79. Website: Locasto, Donald. Calhoun, Dustin. Meek, Robbie. Trimarco, Thomas. Acute Complications Linked to DM
Challenge EMS Providers. Journal Of Emergency Medical Services Website. http://www.jems.com/article/patientcare/acute-complications-linked-dm-challenge. Accessed February 6, 2013
80. Book Chapter: Pollak, Andrew N. Endocrine Emergencies. IN: Nancy Carolines Emergency Care in The Streets
sixth ed. New York, Ny: Jones and Bartlett; 2007:29.1-29.25.
81. Book chapter: Traynor, Owen. Diabetic Ketoacidosis And Hyperglycemia. In: Traynor, Owen. Coonan, Patrick.
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Learning; 2005: 121-126.
82. Website: Smith Elizabeth. Study Finds that Many EMS Providers are Over Weight or Obese. Journal Of Emergency
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