Objectives

At the conclusion of this chapter you should be able to:

  1. Describe the different types of diabetes.
  2. Describe the signs, symptoms and treatment of hypoglycemia and hyperglycemia.
  3. Describe the signs, symptoms and treatment of diabetic ketoacidosis.

Case:
You are dispatched to an "unknown medical emergency" at 1022 Burke Street. Upon arrival you find a 43 year-old male lying unconscious in the living room. His landlord discovered him while doing routine maintenance. During your initial assessment you discover:

You begin your focused assessment while your partner administers oxygen, applies a cardiac monitor and sets up an IV. During your focused assessment you find:

You rapidly package the patient, draw a blood sample, establish an IV of NS en route to the hospital, rapidly infuse 2 liters per protocol, then decrease rate to TKO and contact the receiving hospital with a detailed report. You complete a detailed assessment and continue the ongoing assessment during the 25 minute transport. The patient's condition remained the same during the transport.

Diabetes Mellitus
Diabetes mellitus is characterized by a deficiency of insulin or the inability of the body to respond to insulin. Diabetes mellitus is generally classified as Type I - insulin dependent, or Type II non-insulin dependent.

Patients with type I diabetes mellitus (DM), also known as insulin-dependent DM (IDDM) or juvenile-onset diabetes, may develop diabetic ketoacidosis (DKA). Patients with type II DM, also known as non-insulin-dependent DM (NIDDM), may develop nonketotic hyperglycemic-hyperosmolar coma (NKHHC). Common late microvascular complications include retinopathy, nephropathy, and peripheral and autonomic neuropathies. Macrovascular complications include atherosclerotic coronary and peripheral arterial disease.

Type I Diabetes Mellitus
Type I diabetes is characterized by inadequate production of effective insulin by the pancreas. This form of diabetes affects 1 in every 10 diabetics, and may occur any time after birth. This form usually presents itself in the teen years or young adult years. Type I diabetes requires lifelong treatment with insulin injections, exercise, and diet regulation. The symptoms of Type I diabetes can present suddenly, and can include, polyuria, polydipsia, dizziness, blurred vision, and rapid, unexplained weight loss.

Type II Diabetes Mellitus
Type II diabetes is characterized by a decrease production of insulin by the beta cells of the pancreas, and diminished tissue sensitivity to insulin. The disease occurs most often in people over 40 years old and in those who are overweight. Most people with Type II diabetes require an oral hyperglycemic medication, exercise, and dietary regulation to help control their illness. A small number of Type II diabetics require insulin injections. Symptoms of Type II diabetes include fatigue, changes in appetite, numbness, tingling, and pain in the extremities.

What are Normal Blood Glucose Levels?
The amount of glucose (sugar) in your blood changes throughout the day and night. Your levels will vary depending upon when, what and how much you have eaten, and whether or not you have exercised. The American Diabetes Association categories for normal blood sugar levels are the following, based on how your glucose levels are tested:

Effects of Diabetes Mellitus
Most effects of diabetes mellitus can be attributed to the following effects of insulin levels.

Diabetes attributed to pancreatic disease: Chronic pancreatitis, particularly in alcoholics, is frequently associated with diabetes. Such patients lose both insulin-secreting and glucagon-secreting islets. Therefore, they may be mildly hyperglycemic and sensitive to low doses of insulin. Given the lack of effective counterregulation (exogenous insulin that is unopposed by glucagon), they frequently suffer from rapid onset of hypoglycemia. In Asia, Africa, and the Caribbean, DM is commonly observed in young, severely malnourished patients with severe protein deficiency and pancreatic disease; these patients are not DKA-prone but may require insulin.

Diabetes associated with other endocrine diseases: Type II DM can be secondary to:

Most of these disorders are associated with peripheral or hepatic insulin resistance. Many patients will become diabetic once insulin secretion is also decreased. The prevalence of type I DM is increased in patients with certain autoimmune endocrine diseases, e.g., Graves' disease, Hashimoto's thyroiditis, and idiopathic Addison's disease.

Loss of Glucose in the Urine
When the glucose quantity entering the kidney tubules rises above the glomerular filtration rate, the glucose spills into the urine. The spilling of glucose into the urine causes diuresis because the osmotic effect of glucose in the tubules prevents tubular reabsorption of fluid. This causes dehydration of the extracellular and intracellular spaces.

Acidosis in Diabetes
When carbohydrate metabolism shifts to fat metabolism, ketoacidosis occurs. Ketoacidosis is the formation of ketone bodies. Ketone bodies are strong acids, and if they continue to produce, can lead to metabolic acidosis. Metabolic acidosis is often compensated by respiratory alkalosis that causes kussmauls respirations. The body's mechanism to clear the acid by the kidneys is overwhelmed by the continuous production of ketone bodies, therefore, profound acidosis eventually occurs. The acidosis along with the severe dehydration can lead to death.

Diabetes mellitus is a systemic disease that can have many long-term complications.

These include:

Anatomy and Physiology of the Pancreas
The pancreas is important in the absorption and use of carbohydrates, fat, and protein. The pancreas is a principal regulator of blood glucose concentration.

Insulin
The primary function of insulin is to increase glucose transport into cells, increase glucose metabolism, increase liver glycogen levels, and decrease blood glucose concentration toward a normal level.

Types of Insulin
The fastest acting insulins are called lispro (Humalog)and insulin aspart (Novolog). They should be injected under the skin within 15 minutes before eating. Patients  have to remember to eat within 15 minutes after the injection.  These insulins start working in five to 15 minutes and lower the blood sugar most in 45 to 90 minutes. It finishes working in three to four hours. With regular insulin you have to wait 30 to 45 minutes before eating. Many people like using lispro because it's easier to coordinate eating with this type of insulin.

Insulin Injection Locations
Fast acting - The fast acting insulin is called regular insulin. It lowers blood sugar most in 2 to 5 hours and finishes its work in 5 to 8 hours.

Intermediate acting - NPH (N) or Lente (L) insulin starts working in one to three hours, lowers your blood sugar most in six to 12 hours and finishes working in 20 to 24 hours.

Glucagon
Glucagon is a protein released by the alpha cells when the blood glucose level falls. Glucagon increases the blood glucose level by stimulating the liver to release glucose stores from glycogen and other glucose storage sites. Glucagon also stimulates glucose formation by breaking down the fats and fatty acids.

Diabetic Emergencies
There are three life-threatening emergencies that may result from diabetes. These include:

Hypoglycemia
Hypoglycemia also known as Insulin Shock is a syndrome related to the blood glucose levels below 60. Symptoms of hypoglycemia usually develop after the blood glucose level falls below 60. Symptoms may develop sooner if the fall in blood glucose level rapidly drops. Hypoglycemia is usually caused by too much insulin, a delayed or missed meal, vigorous physical activity, and emotional stress.

Signs and symptoms of hypoglycemia usually occur rapidly, and the patient may complain of extreme hunger, or other symptoms including:

Hyperglycemia (Diabetic Coma)
Symptoms of hyperglycemia distress develops gradually and include:

Treatment
Take the person to an emergency room as quickly as possible. Any acute change in alertness, consciousness, or mental status in a diabetic warrants immediate medical attention.

Diabetic Ketoacidosis
Diabetic ketoacidosis results from an absence of or resistance to insulin. The low insulin level prevents glucose from entering the cells and causes glucose to accumulate in the blood. The cells then become starved for glucose and begin to use other sources of energy usually fat. When fat is metabolized, it produces fatty acids and glycerol. The glycerol provides energy to the cells, but the fatty acids are further metabolized to form ketoacids, which results in acidosis.

Common Causes of Diabetic Ketoacidosis:

As blood sugar rises, the patient undergoes massive osmotic diuresis, which when combined with vomiting causes dehydration and shock. The electrolyte imbalance may cause cardiac dysrhythmias, and seizures. Signs and symptoms of diabetic ketoacidosis include:

Hyperosmolar Hyperglycemic Nonketotic Coma
HHNK coma is a life threatening emergency that occurs frequently in older patients who have Type II diabetes. It also occurs in patients who have undiagnosed diabetes. This syndrome differs from DKA in that residual insulin may be adequate to prevent ketogenesis and ketoacidosis but not enough to permit glucose use by the peripheral tissues or decrease gluconeiogenesis to the liver. The hyperglycemia produces a hyperosmolar state followed by an osmotic diuresis, dehydration, and electrolyte losses. Signs, symptoms, and precipitating factors include:

Assessment of the Diabetic Patient
Patients with a diabetic emergency often have various signs and symptoms. Many of these mimic other common conditions. You should always suspect a diabetic related illness. Always be alert for medical alert information, the presence of insulin syringes, and diabetic medications. Diabetic medications are often kept in the refrigerator. In assessing the patient's history, you should assess the:

Management of the Conscious Diabetic Patient
High concentration oxygen should be administered, and if appropriate, glucose should be given. Obtain a blood sample for laboratory testing before administering glucose. Some field EMS services utilize Dextrostix, Chemstrips, or glucometers for this purpose. If your patient's glucose level is below 60, and he/she is experiencing signs and symptoms of hypoglycemia, glucose should be given. While transporting the patient, monitor the patient's LOC, vital signs, and ECG continuously.

Management of the Unconscious Diabetic Patient
Prehospital management of any unconscious patient should be directed at maintaining an airway, high concentration oxygen administration, and ventilatory support. Depending on your particular protocol, an IV should be started using lactated Ringer's or a saline solution to replenish fluids and electrolytes. If alcohol or drug use is suspected your medical direction may recommend administration of Narcan before administering glucose. If you are unable to obtain a blood glucose level you should administer glucose. This additional glucose load will not adversley effect the hyperglycemic patient but it may save the life of a hypoglycemic patient. 

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

System Diabetic Ketoacidosis Hypoglycemia
Pulse Rapid Normal to Rapid
Blood Pressure Low Normal
Respirations Exaggerated Normal to shallow
Breath Odor Acetone - Sweet - Fruity Normal
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

Summary
Diabetic emergencies are metabolic disorders often encountered in the prehospital care setting. The illness may be life threatening, but a proper assessment, a thorough history, and appropriate drug therapy can often reverse the immediate pathological process. Volume replacement is the primary goal in treating DKA and HHNK coma. Glucose is the primary goal of therapy for the hypoglycemic patient.

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References
Mosby’s Paramedic Textbook, Revised Second Edition, 2001,Sanders M, pp. 946-65
Brady Paramedic Emergency Care Third Edition, 1997, Bledsoe et. al, pp.730-36
Brady Emergency Care 9th Edition, 2001 Limmer, O'keefe, et. al, pp. 371-378