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 patient’s 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 patient’s 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 patient’s plan to be appropriate and approves the patient’s 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.

The CDC estimates that the total costs of diabetes care and management in the United States is approximately $174 billion annually. 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. The extent of complications or lack thereof depends on the patient’s average glucose level and how early in life the disease presents. but there is no cure.10 In order to control the disease. Many patients do not manage the disease adequately. With proper management diabetic patients can lead normal lives and have average life expectancies.7 Insulin enables sugar.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. Diabetes is a major cause of heart disease and stroke. Among residents of the United States ages 65 and older. A preparation of glucagon that has been extracted from beef and pork pancreases is available as a parenteral treatment for hypoglycemic patients.8 million people in the US are affected by diabetes (8. 35% of all US adults older than 20 showed signs of prediabetes. 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. non-traumatic lower limb amputation. 18. it is vital that healthcare systems are adequately prepared to meet the growing trends in these patient populations. The pancreas produces digestive enzymes as well as insulin and glucagon which are the hormones that have primary control of blood glucose levels. and amino acids are the primary source of energy at the cellular level and without insulin they are minimally usable. There are also delta cells but researchers are unsure of their specific purpose. the minority. fatty acids. The glycogen is metabolized into glucose that is then available for cellular consumption. These patients are however. The number of patients who suffer from this condition is expanding rapidly.5 Insulin and glucagon are produced in specialized cells known as the islets of Langerhans within the pancreas. When non-diabetic people eat and food is digested. fatty acids.8 This will be discussed in detail in the treatment section. 26. the Centers for Disease Control (CDC) provided the following statistics: 25. Glucagon also stimulates both the liver and kidneys to produce glucose from non-carbohydrate molecules. Another one of glucagon’s 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. It stimulates the release and subsequent breakdown of glycogen into glucose. By maintaining a strict adherence to dietary regimens. thereby increasing the mortality and morbidity of diabetic related illness in the United States.3% of the population). It serves both endocrine and digestive purposes and it is considered both an endocrine and exocrine gland. 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.9% had diabetes in 2010. In addition to strict regulation of caloric intake. The net effect of these cycles is a reduction in blood glucose level. patients must be willing to adjust their diet and activity. hunger stimulates the release of glucagon which causes the secretion of glycogen from the liver. Diabetes is the 7th leading cause of death in the US. and new cases of blindness. The alpha cells produce glucagon and the beta cells secrete insulin.9 million new diagnoses of diabetes in 2010.2 Some patients are even able to manage the disease without any pharmaceuticals. many patients with diabetes mellitus can control disease mortality/efficacy. as well as exercise/weight loss guidelines. Conversely. There were 215. pharmacological treatment . Diabetes is the leading cause of kidney failure.000 patients with diabetes who were 20 years of age or younger in 2010. The fatty acids are converted into triglycerides and stored as fat.Diabetes has become a costly public health problem. 6 There is further subdivision of specialty within the islets. The amino acids are metabolized into proteins and glucose to be used for energy. 7.0 million people are living with diabetes undiagnosed.3 In their 2011 diabetes fact sheet. 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.8 million people are diagnosed with diabetes. The sugars. 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.4 Because of the increased incidence of uncontrolled diabetes mellitus having reached epidemic proportions. There were 1. and amino acids to be taken up and metabolized by cells. Glucagon has an opposing function to insulin.

These characteristics include excess fat in the abdominal area. Often the diagnosis is made when the child presents with malaise. frequent infections with slow wound healing. excessive thirst.19 Typically the symptoms of type 2 diabetes develop gradually in non-pregnant patients. Some women’s bodies are not able to achieve this and gestational diabetes develops. and seizure activity. elevated blood pressure. experience a chronic lack of physical activity. type 2 diabetes develops later in life although with increasing child obesity there are more and more cases of younger patients being diagnosed. nausea. stroke. and have a hereditary predisposition are more likely to suffer from metabolic syndrome and consequently. meaning that if one’s parents suffer from the disease. The first is a fasting blood glucose level that is greater than 126 mg/dL. excessive urination. These patients must also follow strict dietary guidelines in order to limit their intake of sugars and carbohydrates. The third is an oral glucose tolerance test. Researchers have identified that there is a hereditary predisposition to type 1 diabetes. unexplained weight loss. They include fatigue. than the patient is considered diabetic.20 As was previously noted according to the Centers for Disease Control. women who experience this are 35% to 60% more likely to be diagnosed with type 2 diabetes within the next 10 to 20 years. however. 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. there are at least seven million people living with undiagnosed and untreated diabetes. As early screening and diagnosis improve the incidence of long term complications may be reduced.12 Typically.13 The insulin resistance that is the hallmark of type 2 diabetes develops from a group of characteristics known as metabolic syndrome. Hypoglycemia and hyperglycemia are both common in patients who suffer from gestational diabetes. Cellular starvation occurs even though large quantities of sugar are present because the lack of or resistance to insulin inhibits cellular uptake and metabolization. During pregnancy the fetus requires glucose for energy. Diabetes has two primary causes. The mother’s physiology must adapt to the increased demand for glucose.focuses on maintaining normal glucose levels.16 It is important to note that while uncommon. 21 This is in large part due to the non-specific symptoms and presentation in adult patients.17 Expectant women sometimes develop diabetic symptoms during their pregnancy and this is known as gestational diabetes.22 HbA1C will be further explained later in the module. the children are more likely to also have it. Ninety percent of all diabetic patients in the United States suffer from type 2 diabetes. It also significantly increases the patient’s risk for cardiovascular disease. There are four different criteria that are used to diagnose diabetes. The final diagnostic is a measure of the glycated hemoglobin (HbA1C) level in the blood. Under normal conditions. The second is an exaggerated cellular resistance to the insulin that is produced. The first is an organic malfunction within the pancreas that can be related to autoimmune disease where the beta cells are damaged or destroyed. neuropathy. the pancreas secretes increased amounts of insulin and the maternal cells show decreased sensitivity to it. 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. unresponsiveness. Both pathologies lead to elevated blood glucose levels. Over time.5% or greater. Women who are obese or are otherwise predisposed to diabetes are more likely to suffer from this condition. increased irritability. and peripheral vascular disease. 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. type 2 diabetes. polyuria. confusion. and poor peripheral circulation (eventually amputation). The second is a random blood sample that is found to have glucose levels of 200 mg/dL or greater. and dehydration. excessive thirst. This is type 1 or juvenile diabetes. and if it is found to be 6. Wild fluctuations in blood glucose can occur. if left untreated or poorly managed. There are fetoplacental hormones that are present to regulate glucose levels in the fetus.14 Individuals who are overweight. blindness. 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. This is supplied from the maternal circulation. This is type 2 or adult onset diabetes. chronic hyperglycemia leads to renal failure.15 It is not fully understood why metabolic syndrome leads to insulin resistance. and high levels of blood lipids. during pregnancy. which can be especially challenging for pediatric patients. type 2 diabetes may also be a result of pancreatic malfunction and insufficient insulin production. shakiness. Maternal insulin is too large of a molecule to cross the placental barrier. In healthy women a delicate balance is achieved and homeostasis is maintained with glucose made available to the fetus. Type 1 diabetes is sometimes called juvenile diabetes and it generally strikes children as opposed to adults. 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. blurred vision. Often doctors look for one or more of the four benchmarks to present on more than one occasion to make the diagnosis. If the blood glucose is 200 mg/dL or greater then he or she has met the criteria for diabetes. Insulin production is limited or not present. Day to Day Management and Long Term Complications of Diabetes . Type 2 or adult onset diabetes is the most common form of the disease. 18 Gestational diabetes will often resolve after pregnancy.

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

Poorly controlled hypertension and lifestyle factors such as alcohol abuse. Progressive complications worsen over time. increased disability. The symptoms of DPN are treated with anti-depressants such as duloxetine (Cymbalta) and bupropion (Wellbutrin) as well as with opioid analgesics. and peripheral vascular disease. accounting for 44% of all new cases of kidney failure in 2008. Unfortunately many diabetics do not inspect their feet regularly. it is known that 70% of diabetics also suffer from hypertension or are prescribed antihypertensive medications which in itself increases risk for these pathologies. cigarette smoking.38 The primary risk factor for DPN is chronic hyperglycemia. and elevated cholesterol levels.43 Patients who are forced to have an extremity amputated experience decreased mobility. 48 Over time elevated blood glucose levels damage the tiny blood vessels that supply the retina of the eye.50 Also diabetics are two to four times more likely to suffer from strokes than the general population. At any given time there are approximately 150. hypertension.46 Diabetic retinopathy.36 The second sub category is macrovascular complications. and are generally irreversible. and the presence of peripheral neuropathy. autoimmune dysfunction that causes swelling in the nerves. This can ultimately lead to loss of motor function and subsequent disability. The second set of symptoms is extremity pain that occurs while at rest.44 According to the Centers for Disease Control diabetes is the leading cause of renal failure in the United States.51 When diabetic men suffer from hypertension as well as have other risk factors for cardiovascular disease such as obesity. nephropathy (renal system damage). 52 Peripheral artery disease (PAD) also known as peripheral vascular disease (PVD) is another macrovascular complication of diabetes. DPN presents with pain. The incidence of PAD increases with patient age.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. also known as claudication. Cardiovascular disease is the cause of death for as many as 65% of patients with diabetes. foot ulcerations. The first is pain and discomfort that occurs with movement and exercise and resolves with rest. 40 Typically. obesity. or have access to the podiatric care that they require.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. mechanical injury to the nerves. as well as loss of independence. Episodic complications can include such things as foot ulcers or non-healing wounds as a result of peripheral vascular disease.47 It is the most common microvascular complication of diabetes. and inherited traits. This loss of circulation and swelling in the retina will ultimately lead to blurred vision and subsequent vision loss. alcohol consumption. Researchers believe that this nerve damage is the result of a combination of factors including metabolic imbalance (hyperglycemia and low insulin levels). and subsequent infections. Mortality rates due to heart disease are two to four times higher for diabetic patients than for the general population. If they are episodic. duration of disease. 37 Heart disease and renal failure are two examples of progressive disease processes. The first sub category is microvascular complications which include neuropathy (nervous system damage). However.41 Diabetic patients are 10 to 20 times more likely than non-diabetics to have a lower extremity amputation. . 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. and kidneys. and cigarette smoking also increase the risk of renal disease among diabetic patients. Microvascular complications are the most common long term complications of diabetes. Hyperglycemia also causes swelling to the retina. The rest are related to peripheral vascular disease. numbness. The problems associated with complications from diabetes can be either episodic or progressive. 42 More than half of all amputations are caused by worsening DPN. Typically. This is due to tissue ischemia caused by reduced blood flow. Diabetic peripheral neuropathy (DPN). they typically have poorer outcomes and suffer increased mortality and morbidity as compared to the non-diabetic population. is related to prolonged hyperglycemia and results in more than 10. and tingling in the extremities that worsens over time. Peripheral artery disease is a major risk factor for eventual lower extremity amputation. result in increasing organ dysfunction. elevated triglycerides. higher body mass index. Pedal problems can be limited by regular inspection of the feet. that means that they can be treated and can recur numerous times. These disease processes can be divided into two sub categories.45 The relationship between diabetes and nephropathy is poorly understood but researchers believe that it is related to metabolic dysfunction. and retinopathy (eye damage). 53 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. and appropriate footwear. duration of the disease. a progressive microvascular disease. These include cardiovascular disease.000 new cases of blindness every year. damage to the eyes. It is characterized by the narrowing of the blood vessels that supply the extremities. stroke. wear appropriate shoes.The long term complications of diabetes can cause dysfunction in a number of different organ systems. patients suffering from PAD will present with two different types of symptoms. smoking cigarettes. and taller patient height. stomach. The physiological cause of this disproportionate increase in risk is not clear. access to podiatric care. is estimated to affect between 30% and 50% of diabetic patients. Other factors that also increase the patient’s chances for suffering from DPN include age.39 DPN is caused by chronic nerve damage.

insulin pump malfunction.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. 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. 59 Hypoglycemic patients may appear to be intoxicated and can even be highly combative. In the early stages as blood sugar drops the patient may exhibit a sympathetic nervous system response that includes diaphoresis. a fasting blood sugar that is greater than or equal to 130 mg/dL. liver disease.58 Hypoglycemia develops relatively quickly. seizures.56 Make sure that you are familiar with your local protocol that defines the lower limit of acceptable blood glucose level. The onset of symptoms in the diabetic patient with hyperglycemia is variable. When blood sugar is low the brain is unable to function properly causing the telltale confusion that is associated with the condition. and/or stress.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. if the cause of the hyperglycemia is infection or illness it may take several days for the symptoms to develop.61 . There is a multitude of ways in which the diabetic patient can become hypoglycemic.55 Glucose is the primary fuel for the brain. Hyperglycemia Hyperglycemia. salicylates (commonly aspirin and Pepto-Bismol). 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. The signs and symptoms of hypoglycemia depend on how low the patient’s blood sugar is. and even death will follow. and anxiety. If the patient’s blood sugar continues to drop then confusion. illness. 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. infection. and medications such as propranolol. unconsciousness. infections. tachycardia. It is often seen in alcoholics who are chronically malnourished. It is important to note that hypoglycemia can occur in non-diabetic patients. surgery. increased physical activity. insufficient insulin. is caused by excessive food intake. The blood glucose level where the patient becomes symptomatic is variable and depends on his or her own personal physiology. 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.57 Other things that have been known to precipitate hypoglycemia include stressors. liver or kidney malfunction. and some antibiotics. The most common of those is decreased oral intake without concomitant decrease in insulin or antihyperglycemic medication dosage. alcohol use. Conversely.The Signs and Symptoms of Hypoglycemia and Hyperglycemia Hypoglycemia Hypoglycemia is the most common endocrine condition that emergency medical professionals will respond to. as the glucose that is available is quickly metabolized in the insulin rich environment. Certain cancers. antimalarials. and renal failure can also inhibit the natural mechanisms that regulate blood sugar levels and can lead to profound hypoglycemia. usually in a matter of hours.

When this occurs the cells must find an alternate source of energy. When untreated. When in doubt. Some adult HONK patients may require as much as nine liters of water in order to restore adequate fluid balance. polydipsia. Studies indicate that as many as 25% of DKA cases are in patients without previous diagnosis of diabetes. The patient will typically present with excessive thirst and excessive urination. the patient’s blood glucose level is greater than or equal to 600 mg/dL and dehydration is worse in HONK than DKA. Without insulin the cells of the body are unable to metabolize the glucose that is available and they begin to starve. and finally. visual disturbances.63 DKA is often seen in teenagers and young adult type 1 diabetics and may even occur prior to initial diagnosis.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. all diabetic patients should receive glucose.66 It is surprising but patients suffering from HONK present in coma less than 10% of the time. It is hyperglycemia with similar metabolic derangement to DKA but no ketosis. and death are possible just as with hypoglycemia. and for unknown reasons. 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.61 Differential Diagnosis Diagnosis of a diabetic emergency is sometimes difficult. tachycardia. the fruity odor of ketones on the patient’s breath. coma. The way they achieve this is to break down proteins into amino acids.67 More often these patients have focal neurological deficits in addition to the dehydration. Typically. nausea. seizure. 65 Type 2 diabetics sometimes experience DKA but more often when they have untreated hyperglycemia they experience hyperosmolar non-ketotic coma (HONK). flushed dry skin. and lipids are broken down into free fatty acids and oxidized to ketones. Treatment algorithms are the same for both conditions.As blood glucose levels rise the body attempts to compensate and reduce them by excreting the glucose in urine. Untreated hyperglycemia can progress into diabetic ketoacidosis (DKA). vomiting.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. abdominal pain. this physiological compensation can lead to life-threatening dehydration. This acidosis is exacerbated by the dehydration and blood hyperosmolarity that is related to the excessive urination Symptoms of DKA are altered mental status. 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. weakness.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 . Interestingly. polyuria. System Diabetic Hypoglycemia Ketoacidosis Pulse Rapid Normal to Rapid Blood Pressure Low Normal Respirations Exaggerated Normal to shallow Breath Odor Acetone Normal Sweet . As the patient’s hyperglycemia and dehydration worsen altered mentation. coma. deep rapid respirations (Kussmaul) as the body attempts to correct acidosis by blowing off carbon dioxide. acute myocardial infarctions are frequently seen in conjunction with HONK.

69 When treating hypoglycemia orally be aware that it can sometimes take an extended period of time for the patient’s glucose level to rise because the sugar has to be absorbed through the gastric tract prior to taking effect. Once you have managed the patient’s airway. If the patient wakes up with an endotracheal tube in his or her throat then he or she will likely panic. Patients can be aggressive and combative when their blood glucose is low. Pay close attention to the IV site. If the patient does not regain consciousness after treatment then use whatever means you have available to secure the airway. you must be ready to prepare it . Make sure to follow your local protocol and contact online medical direction when in doubt. alert. It can cause necrosis if it is pushed into a line that has become infiltrated. If the patient is awake. If there is any sign of infiltration stop using the site immediately. There are a number of different preparations of oral glucose in either gel or tablet form. The treatment algorithm for hypoglycemic patients is based on his or her mental status and his or her ability to follow commands. Once your IV is in place. and circulation. It only takes approximately seven ounces of soda to get the patient 25g of sugar. ventilation. breathing.72 For children younger than eight-years-old. and if needed. that you avoid endotracheal intubation or another advanced airway maneuver until after you attempt to correct the hypoglycemia. if there are family members on scene they will be familiar with the patient’s condition and can be a valuable resource to help manage and calm the patient. It is recommended. pull the tube out. 2mL/kg of D25 is the recommended dosage. place ice at the site. 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. The dextrose solution is hypertonic and acidic making it highly caustic to tissue. breathing. over a few minutes. start an infusion of normal saline solution. elevate the extremity. and potentially cause trauma to the airway. Therefore. It is normally packaged as D50 where the sugar is in a solution with 50 mL of saline solution. The glucose solution that is used by EMS providers is thick and viscous. The medication should be pushed slowly. airway support. and can be difficult to push through small catheters and veins. and candy will be metabolized quickly and eating a meal will help to prevent rebound hypoglycemia. and expedite transport to the closest appropriate facility. If a commercial product is not readily available then any food or beverage that is high in sugar will have a similar effect. If the hypoglycemic patient is hypoxic or experiencing respiratory depression then you must provide. and able to follow commands then oral treatment is acceptable. 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. adequately protecting his or her airway. If D50 does become infiltrated immediately remove the IV. 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. especially when it is cold. soda. The simple sugars in oral glucose. Most are packaged as individual 25g doses.When responding to assist a patient with hypoglycemia the safety of you and your partner is paramount. Pediatric patients should receive a less concentrated dose of dextrose than adults because the caustic nature of the solution can damage their veins. however. After the patient’s blood glucose level begins to rise it is also important to encourage the patient to eat a full meal with protein and complex carbohydrates. Once the dextrose is administered the patient’s blood sugar should normalize within a few minutes. When possible select a large vein for your site and use at least an 18 gauge angiocatheter. Make sure to take steps to protect yourself and the patient. Often. In the most severe cases you may have to administer additional doses of D50 in order to bring the patient’s sugar level back into normal range. Most EMS services do not carry premixed D25 in their drug boxes.71 Adult patients should receive 25g of dextrose intravenously as per protocol. and circulation obtain vascular access. with constant monitoring of the IV site for signs of infiltration. oxygen.

Often. knows why he or she became hypoglycemic. Once the patient’s 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. has a plan to eat a well-balanced meal. it is common for him or her to wish to refuse further treatment and transport. If you are unable to obtain IV access and the patient will not tolerate oral treatment then you can administer intramuscular glucagon. giving 12.1 mg/kg up to 1 mg.73 If the patient does not respond to your treatment then manage his or her airway. breathing. You will then be able to administer the correct weight-based dosage. Again. Glucagon stimulates the release of glycogen stored in the liver and may take 15-30 minutes to reach full effect. The easiest way to do this is to waste half of an amp of D50.74 .5g of dextrose in 25mL of solution in the syringe. will not be alone. this is acceptable if the patient is a known diabetic. 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. and circulation as best that you can and provide rapid transport to the closest appropriate facility. 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. Then you should draw 25mL of normal saline solution into the syringe.5g of dextrose in 50 mL of solution which is D25. leaving 12. If you are unsure or have questions contact online medical direction. The adult dosage is 1 mg and the pediatric dosage is . 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. and has a plan to follow up with his or her endocrinologist or other physician.yourself. It is recommended that infants receive 2mL/kg of D10. When the patient is awake and alert. most services do not carry this in a premixed form.

and/or starting a group fitness program with coworkers. Copyright CE Solutions. If this has occurred large peaked T waves may be present on the patient’s electrocardiogram. and hyperosmolar non-ketotic acidosis. ventilatory support. 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. suffer from obesity. 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. showing signs of shock. is a growing problem in the general population and it is also a growing problem among EMS providers. and management of diabetes. 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. and make sure the appropriate resources are mobilized. DKA.5 mg of nebulized albuterol. In the field always be diligent in evaluating your patient’s blood glucose levels when indicated. pathophysiology. We owe it to ourselves. 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. Hopefully. if these patients are not protecting their airways do not hesitate to utilize the advanced airway tools that you have available.Hyperglycemia The primary treatment for hyperglycemia is insulin but in most cases that is administered in the hospital as opposed to in the field. packing a lunch with nutritious items. chances are that you have responded to a multitude of diabetic emergencies.78 In the prehospital setting maintaining a systolic blood pressure of at least 90 mmHg is the goal. Be prepared. 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. All Rights Reserved. eat poorly. begin by providing high flow oxygen. and or 2. Please be aware of your personal risk factors and do everything that you can to mitigate them.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. lack in adequate exercise. The patient will likely need at least one liter of fluid per hour for the first few hours. This module provides an expansive description of the etiology. This profession of ours makes astronomical demands on our minds and bodies and if unchecked it will take its toll. and/or experiencing potentially life-threatening electrolyte and metabolic abnormalities. especially type 2.82 We tend to work in high stress environments. 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. and airway management as needed. In contrast with the patient suffering from hypoglycemia. experiencing significantly alerted mentation. and our patients to do everything that we can to prevent health problems like type 2 diabetes. 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. 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. References . 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. that are comatose. our families. Diabetes. While providing fluids make sure to monitor the patient closely for signs of flash pulmonary edema. You will on occasion encounter patients suffering from severe hyperglycemia. Once the patient’s airway and breathing are managed appropriately establish large bore IV access and start fluid resuscitation with normal saline solution. sodium bicarbonate 1 mEq/kg. 81 Make sure to enlist the help of online medical command when treating complex metabolic conditions and make sure to follow local protocols.76 These patients will require aggressive and thorough care. The patient’s serum potassium may be dangerously high due to the fluid loss associated with this condition and this can cause myocardial instability. if waveform end-tidal capnography is available. 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. In this situation one would expect the patient’s end-tidal CO2 level to be significantly elevated. After you have stabilized the hyperglycemic patient to the best of your ability you must provide rapid transport to the closest appropriate facility.79 Continuous cardiac monitoring is essential for these patients due to the metabolic derangement that has been previously discussed. then it should be applied. When caring for the very ill patient. and have incredibly irregular sleep patterns. Conclusion If you work in the field. We should all strive to lead by example by doing things like eating healthy snacks while on shift.80 If you suspect hyperkalemia then consider interventions such as calcium chloride 8 to 16 mg/kg. 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. The patient must receive definitive care in order to mitigate the crisis at hand. Author Simon Taxel. stay safe.

2007:29. Ibid 14. 19. http://diabetes. Ibid 15. 2004: 254-269. Ibid 32. Website: Living with Diabetes. GA: U. 4. 3. Accessed January 30. New York. Atlanta.S. Marcie. 2013 24. GA: U. Jones and Bartlett.S. Physical Therapy. Ibid 28. Obsterics. 2006: 624-661. Andrew N. Document: Centers for Disease Control and Prevention. Checking Your Blood Glucose. 2008. Website: Living with Diabetes. 2011.rxlist. Dustin. Endocrine Emergencies. Ny: Jones and Bartlett.com/lantus-drug. Calhoun.com/article/patientcare/acute-complications-linked-dm-challenge. Website: Locasto. Website: Lantus. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States. IN: Human Physiology ninth edition. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. GA: U. New York.html. Book Chapter: Pollak. 29 2013. Ibid 27. http://www. Mikel. Ibid 33. Meek. 2011. American Diabetes Association website. 5. New York. Journal article: Deshpande. 2001: 240-255. Department of Health and Human Services. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. http://www. Endocrine System. Bob. 22. 6. Atlanta. 2007:29. Andrew N. New Jersey. 9. Document: Centers for Disease Control and Prevention. Ibid 38. Andrew N. Trimarco. Accessed February 6. 2013 35. Robbie. Ibid 13. New York. 20. 2011. Accessed February 14.html.html.org/living-with-diabetes/treatment-and-care/medication/oral-medications/what-are-myoptions. Website: Living with Diabetes. 2013 25. IN: Prehospital Emergency Pharmacology fifth edition. Accessed January. Bryan. Hayes-Harris. Website: Locasto. Calhoun. Ibid 31. Acute Complications Linked to DM Challenge EMS Providers. Endocrine Emergencies. Epidemology of Diabetes an Diabetes-Related Complications.gov/dm/pubs/neuropathies/. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. 2013 29. Dustin.1. Ny: Jones and Bartlett. Ny: Jones and Bartlett. Kristen.25. Ibid 34. New York. Book Chapter: Fox.1-29. Mario. Ibid 40. http://www. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States. Rothenberg. Marcie. Epidemology of Diabetes an Diabetes-Related Complications. American Diabetes Association website. Regulation of Metabolism. Frank. Thomas. Book Chapter: Pollak. Book Chapter: Bledsoe. Endocrine Emergencies.37. Papa. 88:1254-1264. http://www.diabetes. Dwayne. Brady. Ibid 26. Centers for Disease Control and Prevention.nih. 2007:39. Acute Complications Linked to DM Challenge EMS Providers. Drugs Used in the Treatment of MetabolicEndocrine Emergencies.com/article/patientcare/acute-complications-linked-dm-challenge.diabetes. Accessed February 6. What Are My Options. Ibid 21. Document: Centers for Disease Control and Prevention. Hayes-Harris.25. 11.25. Andrew N. 2011. Donald. Robbie. Physical Therapy.org /living-with-diabetes/treatment-andcare/medication/insulin/insulin-basics. 2011. Ibid 8.jems. McGraw-Hill International Edition. American Diabetes Association website. Book Chapter: Pollak. Massachusetts. Ibid 18. Schootman. 2011.S.1-29. Book Chapter: Elling. Ibid 17. Ibid 16. Donald. Centers for Disease Control and Prevention. Atlanta. Ibid 36. Accessed January 30. 2013.htm. Journal article: Deshpande.1-39. 2. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States. Anjail. In: Anatomy and Physiology Paramedic. American Academy of Orthopaedic Surgeons.1-29. Prentice Hall.diabetes. 12. Elling. Thomas. http://www. 10. Ny: Jones and Bartlett. 2008. Anjail.org/living-with-diabetes/treatment-and-care/blood-glucose-control/checking-your-bloodglucose. 88:1254-1264. Stuart Ira.jems. Mario. Accessed January 30. Trimarco. Book Chapter: Pollak. Meek. 37. Department of Health and Human Services. Journal Of Emergency Medical Services Website.niddk. Clayden. Centers for Disease Control and Prevention. Department of Health and Human Services. . Ibid 7. Insulin Basics. Ibid 39. 2007:29. http://www. Ibid 30. Journal Of Emergency Medical Services Website. National Diabetes Information Clearing House Website. Schootman. 2013 23. Website: Diabetic Neuropathies: The Nerve Damage of Diabetes.

Marcie. Journal article: Deshpande. 55. 2013 58. 2013 73. 2007:29. Rubens. Journal article: Deshpande. Vaccaro.jems. Rubens. Ibid 48. Book Chapter: Shurgot. Robbie. Thomas. Epidemology of Diabetes an Diabetes-Related Complications. Calhoun. Thomas. Rahilly.dsf. Website: Locasto.jems. Website: Locasto. Book Chapter: Pollak. http://www. Andrew N. 53. Journal Of Emergency Medical Services Website. 2013 56. Thomas. In: Traynor. Et al. Physical Therapy. 72. Trimarco. Ny: Jones and Bartlett. Hayes-Harris. Book Chapter: Pollak. 2011.25. 2008. Andrew N. Manufactured Shoes In the Prevention of Diabetic Foot Ulcers. The Streetmedic’s Handbook. Acute Complications Linked to DM Challenge EMS Providers. Andrew N. Journal Article: Stamler. Trimarco. Anjail. Accessed February 6. Thomas. 2013 70. Neaton. 2005: 212-215. Schootman. http://www. 88:1254-1264. Ibid 59. New York. Mario. Anjail. Andrew N. Schootman.25. O. Calhoun. Trimarco. Journal Of Emergency Medical Services Website.1-29. Anjail. Physical Therapy. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. 51. Journal article: Deshpande. Hayes-Harris. Dustin. Steve. 50. Donald.com/article/patientcare/acute-complications-linked-dm-challenge. Dustin. Marcie. http://www. Rahilly. 2013. Mario. Robbie. Hayes-Harris. Marcie. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. Ibid 60. Accessed February 14. Trimarco. Mayo Clinic website. Patrick. Website: Locasto.com/health/diabetic-retinopathy /DS00447/DSECTION=causes. Website: Locasto. 2008. Coonan.com/article/patient- . Robbie. Luigi. Steve. 2013 67. 18 no. Donald. Meek. Centers for Disease Control and Prevention. New York. Ibid 62. Hypoglycemia. Ibid 49. Endocrine Emergencies. 2013 65. Meek. Robbie. http://www.us/health/lib/health/ems/als_protocols-effective_07-01-07. Second Edition. Diabetes. Ibid 52. Other Risk Factors. Owen. Ezio. Ibid 69. Acute Complications Linked to DM Challenge EMS Providers.pdf Accessed February 6. Dustin. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. Dustin. 1993.1-29. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. Book Chapter: Pollak. Calhoun. 16: 434-444. Physical Therapy. Donald. Donald. Journal article: Deshpande. Hypoglycemia. Donald.jems. Ny: Jones and Bartlett. Trimarco.jems. 43. 44. 74. Acute Complications Linked to DM Challenge EMS Providers. Robbie. Jonathan. Website: Diabetic Retinopathy. Robbie. Journal Of Emergency Medical Services Website. Document: Centers for Disease Control and Prevention. Marcie. Book Chapter: Shurgot. Dustin. Thomas. Schootman. Meek. Acute Complications Linked to DM Challenge EMS Providers. Journal Of Emergency Medical Services Website. Ny: Jones and Bartlett. 45. Hayes-Harris. Accessed February 6. Robbie. 54. Canada: Thomson Delmar Learning. Website: Locasto.25. Coonan. Journal article: Deshpande. Epidemology of Diabetes an Diabetes-Related Complications. 61. Ibid 57. 46.25. Acute Complications Linked to DM Challenge EMS Providers.1-29. 2011. http://www. 2007:29. Endocrine Emergencies. 88:1254-1264. Physical Therapy. Mario. Journal Of Emergency Medical Services Website. In: Traynor. Journal Of Emergency Medical Services Website.1-29. 66. 89-89. Et al.S. Schootman. Meek. Website: Locasto.25. Mario.com/article/patientcare/acute-complications-linked-dm-challenge.com/article/patientcare/acute-complications-linked-dm-challenge.1-29. New York. Calhoun. Epidemology of Diabetes an Diabetes-Related Complications.com/article/patientcare/acute-complications-linked-dm-challenge. JD. Anjail. Endocrine Emergencies. Andrew N. Thomas. Physical Therapy. Faglia. Book Chapter: Pollak. http://www. Ny: Jones and Bartlett. 64. 88:1254-1264.jems. Mario. Book Chapter: Pollak.state. Trimarco. 2008. Meek. Department of Health and Human Services. Ny: Jones and Bartlett. Atlanta. Thomas. Diabetes Care. Owen. New York. Ibid 71. 2013 63. 2007:29. Journal Of Emergency Medical Services Website.mayoclinic.jems. Journal article: Uccioli. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed.health. Hayes-Harris. Endocrine Emergencies. Calhoun. 88:1254-1264. Accessed February 6. Document: Altered Mental Status statewide ALS protocol. Website: Locasto. Monticone. Meek. 68. Ibid 42.jems. 7002A. Meek. Accessed February 6. Jonathan. http://www. Trimarco. Accessed February 6. 2008. Epidemology of Diabetes an Diabetes-Related Complications. Marcie. 10: 1376-1378. 2008. October 1995. 2005: 212-215. Giovanna. Epidemology of Diabetes an Diabetes-Related Complications. GA: U.41.com/article/patientcare/acute-complications-linked-dm-challenge. Calhoun. Thomas. The Streetmedic’s Handbook. New York. and 12 year Cardiovascular Mortality for Men Screened in the Multiple Risk Factor Trial. Accessed February 6. Endocrine Emergencies. Patrick. Schootman.com/article/patientcare/acute-complications-linked-dm-challenge. Dustin. Acute Complications Linked to DM Challenge EMS Providers. National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States. 47. Available at http://www. Calhoun. Thomas. Pennsylvania Department of Health: 2008. Acute Complications Linked to DM Challenge EMS Providers.pa. Donald. 2007:29. Anjail. 2007:29. Dustin. 88:1254-1264. Donald. Diabetes Care. J. http://www. Second Edition. Canada: Thomson Delmar Learning.

Rubens. 82. Meek. New York. Diabetic Ketoacidosis And Hyperglycemia.com/article/health-and-safety/study-finds-many-ems-providersare-overw Accessed February 17. http://www. Rahilly. Canada: Thomson Delmar Learning. Canada: Thomson Delmar Learning. Owen. Donald. Accessed February 6. Robbie. Jonathan. Rahilly.25. Owen. Thomas. Patrick. 2005: 121-126. Dustin. Andrew N. Book Chapter: Pollak.com/article/patientcare/acute-complications-linked-dm-challenge. 2007:29. Book chapter: Traynor. Coonan. New York. 2013 75. http://www. 79. Endocrine Emergencies.25. Thomas. Patrick. Accessed February 6. 2013. The Streetmedic’s Handbook. 81. Coonan. Ny: Jones and Bartlett. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. Jonathan. 2007:29.jems. Website: Locasto. Ibid 77.jems.1-29. Calhoun. Owen. The Streetmedic’s Handbook. IN: Nancy Caroline’s Emergency Care in The Streets sixth ed. Endocrine Emergencies. . Diabetic Ketoacidosis And Hyperglycemia. In: Traynor. Website: Smith Elizabeth. Acute Complications Linked to DM Challenge EMS Providers. Book chapter: Traynor.care/acute-complications-linked-dm-challenge. Second Edition.1-29. 2005: 121-126. 76. Thomas. 2013 80. Ny: Jones and Bartlett. Andrew N. Book Chapter: Pollak. Rubens. Journal Of Emergency Medical Services Website. Ibid 78. Study Finds that Many EMS Providers are Over Weight or Obese. Second Edition. Trimarco. In: Traynor. Owen. Journal Of Emergency Medical Services Website.