Patient Care

The Modern Diabetic: How to handle insulin pumps during emergencies

Issue 5 and Volume 33. Editor’s Note: For exclusive bonus content, read “Think You Know Diabetes?”

Course Objectives

>> Define diabetes mellitus and list its primary causes.

>> Compare and contrast the onset, common causes, risk factors, pathophysiology, signs and symptoms, and complications of Metabolic Syndrome, and type 1 and type 2 diabetes.

>> Identify medications and devices used in the treatment of hyperglycemia, including the insulin pump.

Contrary to how we would like life to be, it is what it is, and thousands of EMS patients present like this: Fifty-seven-year-old female found in bed, unconscious and responding only to painful stimuli. Past medical history (PMH): Diabetes and renal failure. Meds: Alzapam, K-Dur, Lipitor, Nexium, Plavix, Temaz, Gabapentin, Bumetanine. Weight: 285 lbs. Glucose 67.

Fifty-six-year-old female found in bed slightly disoriented with difficulty breathing. PMH: Diabetes type 2; cardiac, hypertension. Meds: Acenorm, Avandia, Betaloc, Glucotrol, Lasix, hydralazine, Taztia. Weight: 400 lbs. Glucose 51. Lungs clear. BP 138/70; P 62; R 14; SpO2 95%; ECG NSR.

Sixty-year-old male found sitting on his couchƒshort of breath. Patient states that upon awakening today, he took 20 steps and became very short of breath. PMH: Diabetes, cardiac. Meds: Cardizem, Zoloft, Humulin N, Humulin R, hydralazine. BP 130/52; P 90; R 32; Glucose 600.

What further assessment and care would be needed for each of these patients based on their history and presentation?

What about this patient:

Thirty-four-year-old male found in his vehicle after a collision with a street light. Patient reports having type 1 diabetes and wears an insulin pump. Skin is warm and dry. Vitals: BP 120/82, P 84, R 16. Glucose 280. Patient does not appear dehydrated and there is no evidence of Kussmaul ventilations. You note that the tubing on his insulin pump has been kinked as a result of the collision.

Diabetes has emerged as one of the world’s greatest health threats. As our government grapples with the challenge of providing care and paying for the billions of dollars that diabetes treatment exacts on the economy, we should renew our efforts to promote healthy lifestyles and advocate optimum wellness strategies for all our citizens.

Equally,„EMS personnel must be familiar with the nature of this disease. How does it present? How is it usually managed day to day? What medications are patients taking and how do they work? What types of appliances may patients be using to treat their disease? How do these patients present when complications are evident?

What is diabetes?

Diabetes mellitus is a group of chronic metabolic diseases characterized by hyperglycemia resulting from defects in insulin secretion or its ability to bind to insulin receptor sites. The deficient action of insulin on target tissues causes an insulin/glucagon ratio imbalance, resulting in abnormal metabolism of carbohydrate, fat and protein. The net result is an impairment in the body’s ability to use glucose.

Diabesity is the largest epidemic the world has faced.1 Modern lifestyles and dietary habits have lead to a global epidemic of obesity and type 2 diabetes, with a rise in multiple cardiometabolic risk factors.2 On Dec. 21, 2006, the United Nations General Assembly unanimously passed a resolution declaring diabetes an international public health issue, only the second disease to attain that status (after HIV/AIDS).1

An estimated 20.8 million Americans have diabetes (14.6 million diagnosed and 6.2 million undiagnosed), which translates to about 7% of the population.3 Perhaps 246 million people worldwide may be diabetic, with projections of 380 million by 2025. Many are hyperglycemic for years before being diagnosed, placing them at risk for unsuspected long-term complications.

Normally, the body fuels metabolic processes from three food sources: carbohydrates, used in the form of glucose; fats, which convert to fatty acids; and proteins, in the form of amino acids.

Glucose is the main source of fuel for the body. Blood glucose levels fluctuate continuously based on the time of day, food or beverage ingested, stress, exercise, and hormone activity. Glucose homeostasis is achieved through the interactions of circulating levels of insulin, glucagon, cortisol, catecholamines, growth hormones, and other counter- regulatory hormones and their effects on liver, fat and muscle cells. To maintain normal blood glucose levels, there must be a balance between insulin and glucagon.

After eating, glucose passes into the bloodstream but is too large to readily diffuse across some cell membranes. As the level of blood sugar rises in a healthy person, the pancreas automatically produces the right amount of insulin to move glucose out of the bloodstream into the cells. Insulin binds with insulin receptors on cell membranes like a key in a lock. This action allows glucose to attach to the bound receptor site so it can be released into the cell (known as “facilitated diffusion”).

In people with diabetes, the pancreas either produces little or no insulin, or there’s a problem with the insulin receptors (i.e., the locks are rusty), so muscle, liver and fat cells aren’t able to use the insulin properly. As a result, glucose builds up in the blood, while the cells starve.

The brain must have a “just in time” glucose source. This supply is so important that neural cells don’t need insulin to absorb glucose. As soon as blood glucose levels fall, brain function immediately decreases. Lethargy, confusion or loss of consciousness may rapidly result.

A healthy liver removes circulating insulin within 10-15 minutes from the time of secretion.4 A normal pancreas must constantly produce small amounts to control excess glucose output by the liver and to keep blood glucose levels constant. During fasting states, the secretion rate of basal insulin is about 1 unit/hour.5

When a person hasn’t eaten, blood glucose levels begin to drop. This reduction slows insulin secretion and prompts the release of glucagon. Glucagon (gluco = glucose; agon = to drive) drives an increase in blood glucose and produces the opposite effect of insulin.4 It causes the liver to break down glycogen stores into glucose (glycogenolysis) and the conversion of free fatty acids to glucose (gluconeogenesis) to raise blood sugar. Glucagon also serves as the “on” switch for the ketogenic pathway, where fatty acids convert into ketoacids and ketone bodies that the liver oxidizes for energy.

Individual targets for blood glucose ranges are based on medications, age, general health, activity patterns and the types of complications for which a person is at greatest risk. The goal is to keep blood glucose levels within appropriate ranges to minimize the risk of complications based on an individualized profile (see Table 1, p. 86 of the May issue of JEMS).

Causes & types of diabetes

In 1997, an expert committee of the American Diabetes Association (ADA) recommended adoption of a simplified approach to classifying diabetes. They moved away from basing the names of the two main types on treatment or age at onset.6 The National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) agreed.

So what was once known as “Type I,” “juvenile diabetes” or “insulin-dependent diabetes mellitus (IDDM)” became known simply as type 1 diabetes. What was previously known as “Type II,” “adult-onset diabetes” or “non-insulin-dependent diabetes mellitus (NIDDM)” became type 2 diabetes.

The committee recommended we keep the term “gestational diabetes mellitus (GDM)” to describe DM that develops during pregnancy. Also, they added the terms “impaired glucose tolerance (IGT)” and “impaired fasting glucose (IFG)” to qualify test results showing levels considered at risk for DM.

Type 1: In general, 5Ï10% of diagnosed cases in the„U.S. are type 1. It’s usually first diagnosed in children, teenagers or young adults, but can appear at any age. In this form of the disease, the immune system attacks and destroys the insulin-producing beta cells in the pancreas. Why this happens remains unknown, but scientists believe that autoimmune, genetic and environmental factors, and possibly viruses, are involved.

Symptoms usually develop over a short period, although beta-cell destruction can begin years earlier. Symptoms of both type 1 and type 2 diabetes include frequent urination, increased thirst, constant hunger, extreme fatigue, blurred vision and frequent/persistent infections. Type 1 also presents with weight loss, abdominal pain with vomiting and ketones in the urine.

Type 2: Of all diagnosed cases of diabetes, type 2 accounts for 90-95%. About 600,000 new cases are diagnosed each year, with about 15 million people in the U.S. currently affected. Unlike type 1, this form is usually first diagnosed in adulthood, related to obesity. An alarming new trend is the rising incidence of the disease in children and adolescents; these children are obese, spend more than five hours per day in front of the TV or computer, rarely exercise and eat poor diets (low in fiber)ƒthe same risk factors that lead to type 2 diabetes in adults. Other risk factors include family history of diabetes and certain ethnicities.

These patients produce too little insulin, produce it too late to match the rise in blood glucose or don’t respond correctly to the insulin produced. In time, beta cells fail and the pancreas loses its ability to secrete enough insulin in response to glucose loads. Glucose persistently builds up in the blood, and the body can’t make efficient use of its main source of fuel.

In contrast to the quicker onset of type 1, the signs and symptoms have a gradual onset in type 2. Some people have no symptoms. This type presents with more subtle signs, which may include muscle cramps, impotence and nighttime diarrhea. Also, retinopathy (non-inflammatory disorder of the retina) may begin to develop years before clinical diagnosis.

See Table 2 (p. 88) in the May issue of JEMS for more comparison factors between type 1 and type 2 diabetes.

Pre-diabetes: Patients with blood glucose levels that are higher than normal but not high enough for a diagnosis of diabetes are considered to have pre-diabetes. Pre-diabetes is also referred to as IFG or IGT, depending on the test used to diagnose it. Some people have both IFG and IGT.7 According to the U.S. Department of Health and Human Services, at least 54 million adults had pre-diabetes in 2002. Many people with pre-diabetes go on to develop type 2 diabetes within 10 years and are also at risk for heart disease and stroke.

Types of insulin

Before the discovery of insulin in 1921, everyone with type 1 diabetes died within a few years after diagnosis. The goal of diabetes management today is to keep levels of blood glucose, blood pressure and cholesterol as close to normal ranges as safely possible. Blood glucose levels must be closely monitored through frequent checks.

For type 1 diabetes, patients are required to take insulin. Other management tools include healthy eating and physical activity. The amount of insulin must be balanced with food intake and daily activities. For type 2 diabetes, the keys to disease management are diet, exercise, weight loss, oral anti-hyperglycemic agents and possibly insulin.

More than 20 types of insulin products are available. The decision as to which insulin to choose is based on the patient’s lifestyle (including type and amount of exercise), a physician’s preference and experience, and the person’s blood sugar levels. Many people take at least two types, typically one during the day and one at nighttime.

Among the criteria considered in choosing insulin are onset, peak time and duration of action. Onset is the length of time before insulin reaches the bloodstream and begins lowering blood glucose. This factor can be affected by the place on the body where the injection is given. Peak time is when insulin is at maximum strength.

For years, the insulin used by diabetics was produced from the pancreases of pigs (porcine) and cows (bovine). Because it was not exactly like human insulin, some patients had trouble using it or created antibodies to it. Animal insulin is being phased out by the manufacturers and is no longer produced in the„U.S. However, the FDA allows individuals to import animal insulin for their own personal use.

The„U.S. standard for insulin therapy involves synthetic human insulin derived from genetically engineered bacteria, which first became available in 1982. Although it’s synthetic, it’s exactly like human insulin, so no antibodies are formed. Common examples of synthetic insulin are Humulin and Novolin.

The insulin pump & other delivery routes

Currently, patients can deliver insulin by syringe, pen, inhaled dry spray, infusions set and insulin pump. Most common is the subcutaneous injection, which allows insulin to be absorbed gradually. An infusion set involves a catheter (a flexible hollow tube) that’s inserted into the tissue just beneath the skin and remains in place for three to six days. Insulin is then injected into the infuser instead of through the skin.

Absorption rates vary by site; the abdomen absorbs fastest, followed by the arms, thighs and buttocks. Regular insulin may also be given via IV at the hospital to treat emergencies, such as severe hyperglycemia.

A device that’s becoming more common, especially in younger adults with type 1 diabetes, is the external insulin pump. This small electronic device is attached to the body through long (60-100 cm), narrow, flexible tubing with a needle or Teflon catheter inserted into the abdominal subcutaneous tissues. A 3-mL refillable cartridge holds enough rapid- or short-acting insulin for two days. The needle and tubing are changed every two to three days.

The pump is set to deliver a steady basal amount of insulin continuously during 24 hours, mimicking normal pancreatic function to keep blood glucose levels in range between meals and overnight. Users (aka, “pumpers”) can program different amounts of insulin at different times of the day and night. They can also inject bolus doses at meals or at times when blood sugar is too high. Frequent glucose monitoring is necessary to determine insulin doses and to ensure that insulin has been injected.8

The biggest advantages for patients using an insulin pump are more accurate insulin delivery than injections and tighter control of blood glucose levels. The pump eliminates unpredictable effects of intermediate- or long-acting insulin and reduces severe low blood glucose episodes. Also, it allows a person to exercise without having to eat large amounts of carbohydrates. Some disadvantages include cost, weight gain, and disruptions in insulin delivery due to kinks, disconnects or malfunctions.

Insulin pumps & EMS care

Because these electronic devices are becoming more common and are often hidden from view,„EMS providers must be aware of how to handle them during emergencies. A few notes on pump function and how to disconnect it will prepare you for managing these patients.

If a patient is hypoglycemic and symptomatic to the point that they require IV/IO dextrose or IM glucagon, it’s usually appropriate to stop the pump’s insulin infusion. Because there’s significant variability from manufacturer to manufacturer with regard to the controls on the pump and the connection between the pump and the tubing, it’s easiest to stop the infusion by withdrawing the device’s insertion point at the skin. Precaution must be taken to guard against accidental needle sticks from the device’s free needle after its removal from the patient’s skin.

When a pump is disconnected or stopped, remember the following: > If the pump is stopped while in the middle of delivering any bolus, it will not be resumed. The patient may need to program a new bolus.

> If blood glucose is under 150, the patient can wait an hour to bolus.

> The patient should not go longer than one to two hours without any insulin.

Also, remember to look for where the pump is secured to the patient’s clothing. They’re typically secured to a waistband, pocket, undergarments or sock. Excess tubing can be tucked into the waistband of underwear or pants. When the patient is sleeping, the pump can be placed next to them on the bed. Some wear it on an armband, legband, or clip it to a blanket, sheet, pajamas, stuffed toy or pillow with a belt clip.

If a disruption occurs, insulin will not be delivered and the patient may be unaware until their blood glucose is discovered to be high. Because the type of insulin used in insulin pumps is short-acting, any disruption in delivery would pose an immediate risk. Within a few hours of being disconnected, the patient will have no functional insulin in the body, resulting in a rapidly increasing blood glucose level that could turn into an episode of ketoacidosis if not rapidly corrected. See Table 3 for more on detecting hypoglycemia.

A dose of dextrose?

Should all hypoglycemic patients get dextrose IV? Not necessarily. If your patient is awake and able to swallow, administering 10Ï15 g of rapidly acting oral carbohydrates will increase blood glucose effectively. Examples include:„

> Three or four glucose tablets to add up to 15 g of carbohydrate;

> One serving of glucose gel (Insta-Glucose, Glutose, Dextrasol or gel frosting) to equal 15 g of carbohydrate;

> Half cup (4 oz.) fruit juice, one cup (8 oz.) milk, or half cup (4 oz.) regular (not diet) soft drink;

> Six to eight jelly beans, five to seven pieces of hard candy or five small sugar cubes; or

> 1 Tbs. of sugar or honey.

Do not use chocolate or ice cream to reverse hypoglycemia; the large fat content slows absorption of the sugar and blood glucose levels rise more slowly. This places the patient at risk of prolonged hypoglycemia. When the sugar is finally absorbed, the patient may become hyperglycemic due to excessive ingestion of sugar-containing substances and stimulation of cortisol and epinephrine.

Dextrose should be administered IV/IO per local protocols. When dextrose administration seems likely, start the IV in a large, more proximal vein (not in the hand). Confirm patency of the vascular access line before infusing hypertonic dextrose. Lower the IV bag and look for a flashback in the chamber. Hypertonic dextrose will cause tissue necrosis if it infiltrates. Notify ED staff immediately if the IV infiltrates while dextrose is being pushed.

If dextrose is given to a known alcoholic, either give thiamine per local protocols or alert the ED staff that you did not give thiamine. Without thiamine, dextrose may cause severe neurological signs and symptoms in alcoholics. In neonates, it may also cause intracranial hemorrhage and vein sclerosis if not diluted prior to administration.

If no IV/IO dextrose is available, administer glucagon 1 mg IM. Observe and record responses to treatment. Recheck glucose level in five minutes. Remember that IM glucagon raises glucose more slowly than IV dextrose. Contact medical control if needed.

Going forward

By 2025, a projected 380 million people worldwide will have diabetes — a scary future. However, medicine continues to evolve in order to better manage this disease and its many short- and long-term complications, and EMS providers must remain aware of the progressive technology our patients are using at home.

Delivery methods under development include surgically implanted pumps (which would be refilled every two to three months), a patch, pills and an oral spray. In addition, scientists are developing an artificial pancreas (a surgically implanted device) that imitates the action of the pancreas by sensing blood glucose levels and secreting insulin in response; the user could also release insulin using a remote control.

External insulin pumps are just one example of an innovation we’re seeing more often in the field. By understanding the basics of diabetes and the mechanics of this device, you’ll be more prepared to manage these patients on your next call.


1. Zimmet P, Alberti G, Kaufman F. “The metabolic syndrome in children and adolescents.” Lancet 2007;370:1541-1542.

2. Mason CC, Hanson RL, Knowler WC. “Progression to type 2 diabetes characterized by moderate then rapid glucose increases.” Diabetes 2007;56:2054-2061.

3. Centers for Disease Control and Prevention. “Diabetes Data & Trends: 2005 Fact Sheet.”„

4. Bledsoe BE, Porter RS, Cherry RA. “Endocrinology.” In Paramedic Care: Principles & Practice Medical Emergencies, eds Brady: Upper Saddle River; 2006. p. 322-333.

5. Nath C, Ponte CD. “Lessons learned about insulin therapy.” Nursing 2002;32:10.

6. American Diabetes Association. “Report of the expert committee on the diagnosis and classification of diabetes mellitus.” Diabetes Care 1997;20:1183-1197.

7. Campos C. “Treating the whole patient for optimal management of type 2 diabetes: considerations for insulin therapy.” South Med J 2007;100:804-811.

8. National Diabetes Information Clearinghouse.

Additional Resources

American Diabetes Association

Centers for Disease Control and Prevention

National Institute of Diabetes and Digestive and Kidney Diseases of the NIH