1elsevier items and derived items © 2007 by saunders, an imprint of elsevier, inc. chapter 46...

1Elsevier items and derived items © 2007 by Saunders, an imprint of Elsevier, Inc.

Chapter 46

Diabetes Mellitus and Hypoglycemia


Learning Objectives

• Describe the role of insulin in the body.• Explain the pathophysiology of diabetes mellitus and

hypoglycemia.• Describe the signs and symptoms of diabetes mellitus

and hypoglycemia.• Explain tests and procedures used to diagnose diabetes

mellitus and hypoglycemia.• Discuss treatment of diabetes mellitus and

hypoglycemia.• Explain the difference between type 1 and type 2 diabetes mellitus.


Learning Objectives

• Differentiate between acute hypoglycemia and diabeticketoacidosis.

• Describe the treatment of a patient experiencing acutehypoglycemia or diabetic ketoacidosis.

• Describe the complications of diabetes mellitus.• Identify nursing interventions for a patient diagnosed

with diabetes mellitus or hypoglycemia.• Identify nursing interventions for a patient diagnosed

with ketoacidosis.


Diabetes Mellitus


Pathophysiology

• Chronic disorder of impaired metabolism with vascular and neurologic complications

• Key feature is elevated blood glucose, called hyperglycemia • Blood glucose level normally regulated by insulin, a

hormone produced by beta cells in the islets of Langerhans located in the pancreas


Type 1

• Absence of endogenous insulin • Formerly called juvenile-onset diabetes because it most

commonly occurs in juveniles and young adults

• An autoimmune process, possibly triggered by a viral infection, destroys beta cells, the development of insulin antibodies, and the production of islet cell antibodies (ICAs)

• Affected people require exogenous insulin for the rest of their lives


Type 2

• Inadequate endogenous insulin and body’s inability to properly use insulin

• Beta cells respond inadequately to hyperglycemia; results in chronically elevated blood glucose

• Continuous high glucose level in the blood desensitizes the beta cells; they become less responsive to the elevated glucose

• More common in adults; increasing in children • Controlled by diet and exercise; may require oral

hypoglycemic agents or exogenous insulin


Role of Insulin

• Glucose • Insulin stimulates active transport of glucose into cells • If insulin absent, glucose remains in the bloodstream • Blood becomes thick, which increases its osmolality • Increased osmolality stimulates the thirst center• Increased fluid does not pass into body tissues; high serum

osmolality retains fluid in the bloodstream • As blood passes through the kidneys, some glucose

eliminated • Osmotic force created by glucose draws extra fluid and

electrolytes with it, causing abnormally increased urine volume


Role of Insulin

• Fatty acids• Promotes fatty acid synthesis and conversion of fatty acids

into fat, which is stored as adipose tissue • Also spares fat by inhibiting breakdown of adipose tissue and

mobilization of fat and by inhibiting the conversion of fats to glucose

• Without adequate insulin, fat stores break down and increased triglycerides are stored in the liver

• Increased fatty acids in the liver can triple the production of lipoproteins; promotes atherosclerosis


Role of Insulin

• Protein• Enhances protein synthesis in tissues and inhibits the

conversion of protein into glucose • Amino acids are admitted into cells; enhances rate of protein

formation while preventing protein degradation • Without adequate insulin, protein storage halts; large amounts

of amino acids dumped into the bloodstream • High levels of plasma amino acids place people with diabetes

at risk for development of gout • Changes in protein metabolism lead to extreme weakness and

poor organ functioning


Etiology

• An autoimmune malfunction may cause complete destruction of the islets of Langerhans in the pancreas, creating type 1 diabetes

• Islet cell antibodies are identified in more than 80% of all people with type 1 diabetes at the time of diagnosis


Figure 46-1


Risk Factors

• Obesity • Sedentary lifestyle • Family history of diabetes • Age 40 years and older • History of gestational DM • History of delivering infant weighing more than 10 lb • African American (33% higher risk for type 2 DM) • Latin American/Hispanic (>300% higher risk for type 2 DM)• American Indians (33%-50% higher risk for type 2 DM)


Risk Factors

• Metabolic syndrome • Thought to be a precursor to diabetes • Impaired glucose tolerance, high serum insulin, hypertension,

elevated triglycerides, low HDL cholesterol, altered size and density of LDL cholesterol

• Believed that metabolic syndrome is a chronic low-grade inflammatory process affecting endothelial tissue

• Long-term effects: atherosclerosis, ischemic heart disease, left ventricular hypertrophy, type 2 DM

• Research directed at learning how to detect this syndrome early and what interventions might slow or arrest the progress


Long-Term Complications


Microvascular Complications

• Retinopathy • Pathological changes in the retina that are

associated with DM

• Nephropathy • Kidney damage


Macrovascular Complications

• Accelerated atherosclerotic changes in the person with diabetes

• Associated with coronary artery disease (CAD), cerebral vascular accidents (CVA or stroke), and peripheral vascular disease (PVD)


Neuropathic Complications

• Neuropathy: pathologic changes in nerve tissue• Mononeuropathy affects a single nerve or group of

nerves • Polyneuropathy involves both sensory and

autonomic nerves • Autonomic neuropathy affects the sympathetic and

parasympathetic nervous systems


Hypoglycemic Unawareness

• The usual symptoms of tachycardia, palpitations, tremor, sweating, and nervousness may be absent

• Patient may suddenly have changes in mental status as the first sign of hypoglycemia



• Foot complications of diabetes• May have foot problems associated with

neuropathy, inadequate blood supply, or a combination

• Mechanical irritation • Thermal injury • Chemical irritation


Long-Term Complications: Prevention

• Diabetes Control and Complications Trial (DCCT): intensive treatment of type 1 DM delayed the onset or slowed the progress of diabetic retinopathy, nephropathy, and neuropathy

• Outcome of United Kingdom Prospective Diabetes Study (UKPDS): similar benefits of tight control with type 2 DM


Long-Term Complications: Prevention

• ADA recommends • Blood pressure: <130 systolic, <80 diastolic • Total cholesterol: <200 mg/dL • LDL: <100 mg/dL • HDL: >45 mg/dL for men (>55 mg/dL for women) • Triglyceride: <150 mg/dL


Acute Emergency Complications


Acute Hypoglycemia

• Dangerous drop in blood glucose• Causes

• Taking too much insulin, not eating enough food or not eating at the right time, an inconsistent pattern of exercise

• Gastroparesis, renal insufficiency, and certain drugs including aspirin and beta-adrenergic blockers


Acute Hypoglycemia

• Signs and symptoms• Adrenergic: shakiness, nervousness, irritability, tachycardia,

anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, and diaphoresis

• Neuroglucopenia: drowsiness, irritability, impaired judgment, blurred vision, slurred speech, headaches, and mood swings progressing to disorientation, seizures, and unconsciousness


Acute Hypoglycemia

• Treatment• Give patient 10 to 15 g of quick-acting

carbohydrates• Repeat every 15-30 minutes until blood glucose is

>70 mg/dL for adults, 80 to 100 mg/dL for older adults and children

• If patient is unable to swallow, an IM or subcutaneous injection of 1 mg of glucagon or an IV dose of 50 mL of 50% dextrose should be given as ordered or per protocol


Diabetic Ketoacidosis (DKA)

• Life-threatening emergency caused by a relative or absolute deficiency of insulin

• Early signs and symptoms• Anorexia, headache, and fatigue• As condition progresses, classic symptoms of polydipsia,

polyuria, and polyphagia develop

• If untreated, patient becomes dehydrated, weak, and lethargic with abdominal pain, nausea, vomiting, fruity breath, increased respiratory rate, tachycardia, blurred vision, and hypothermia



• Late signs • Air hunger (Kussmaul’s respirations), coma, and

shock • Death can result without prompt medical care



• Treatment aimed at correction of three main problems• Dehydration• Electrolyte imbalance• Acidosis


Hyperglycemic Hyperosmolar Nonketotic Syndrome

• Patient goes into a coma from extremely high glucose levels (>600 mg/dL)• There is no evidence of elevated ketones • Pancreas produces enough insulin to prevent breakdown of

fatty acids and formation of ketones, but not enough to prevent hyperglycemia

• Persistent hyperglycemia causes osmotic diuresis, resulting in loss of fluid and electrolytes

• Dehydration and hypernatremia develop • May be caused by the same factors that trigger

ketoacidosis


Medical Diagnosis

• One or more of the following criteria on two separate occasions is considered DM• Polyuria, polydipsia, polyphagia, unexplained weight loss plus

random glucose level >200 mg/dL • Fasting serum glucose level >126 mg/dL (after at least an 8-

hour fast)• Two-hour postprandial glucose level >200 mg/dL during oral

glucose tolerance test (OGTT) under specific guidelines. Test must use a glucose load of 75 g of anhydrous glucose dissolved in water


Medical Diagnosis

• Prediabetes• Individuals with impaired fasting glucose (IFG)

and/or impaired glucose tolerance (IGT)• Individuals should receive education on weight

reduction and increasing physical activity


Medical Diagnosis

• Oral glucose tolerance test• Diet of 150 to 300 g carbohydrate for 3 days before test • Night before test, patient fasts after midnight • Morning of test, blood drawn for fasting serum glucose • Patient then given a drink (Glucola) containing 75 g of

carbohydrates and instructed to remain quiet • Blood drawn at 30 minutes and 1 hour after the ingestion of

glucose. After these two samples, blood is drawn at hourly intervals until the test is completed


Medical Treatment

• Nutritional management• Medical nutrition therapy (MNT) is an important part

of diabetes management; should be included in diabetes self-management education

• Because of complexity of nutritional management, a registered dietitian should be part of the diabetes management team, and the individual with diabetes should be included in decision making


Medical Treatment

• Exercise• Effective adjunct for people with diabetes • Aids in weight loss, improves cardiovascular

conditioning, improves insulin sensitivity, and promotes a sense of well-being

• Exercising muscle uses glucose at 20 times the rate of a muscle at rest and does not require insulin


Insulin Therapy

• All patients with type 1 disease need insulin injections; some patients with type 2 disease may eventually need insulin

• Insulins classified by source and course of action • Source: human, pork, or beef (beef is being phased

out)• Course of action: rapid acting, short acting,

intermediate acting, and long acting • All rapid-acting and short-acting insulins are clear• The other insulins are cloudy


Figure 46-2


Insulin Therapy

• Route• Oral: insulin cannot be given orally because it is rendered

useless in the gastrointestinal tract • Subcutaneously: all insulins can be given subcutaneously • Intravenously: ONLY regular insulin can be given

intravenously • Inhalation: a form of insulin that can be taken by inhalation has

recently been approved, but it is not yet widely used


Insulin Therapy

• Concentrations• U-100 insulin has 100 units/mL

• Most commonly used

• U-500 insulin has 500 units/mL• Used only in emergencies and for patients who are

extremely insulin resistant

• U-40 insulin has 40 units/mL• Not available in the United States


Insulin Therapy

• Premixed insulin products• Contain both Regular and NPH insulin• 70% NPH and 30% Regular insulin• 50% NPH and 50% Regular insulin• 75% NPH and 25% Lispro


Insulin Therapy

• Dosing schedules• Conventional therapy

• Typically uses a combination of a short-acting and an intermediate- or long-acting insulin

• Intensive therapy • To achieve tight control; may require 3 or 4 injections daily

• Continuous subcutaneous insulin infusion • Patient has indwelling subcutaneous catheter connected to

an external portable infusion pump; pump delivers Regular insulin continuously


Insulin Therapy

• Insulin mixing• Two types can be mixed in one syringe to avoid two injections

• Insulin injection• Site rotation helps prevent lipohypertrophy or lipoatrophy • Absorption rate varies with different body sites • American Diabetes Association recommends rotating sites

within one anatomic area rather than moving among all areas • See Figure 46-3


Figure 46-3


Insulin Therapy

• Insulin pump• Needle is inserted subcutaneously in an appropriate

part of the anatomy• Pump is programmed to deliver a steady trickle of

insulin throughout the day and can provide a bolus of insulin at mealtimes


Figure 46-4


Insulin Therapy

• Intranasal route • Only 10% of the drug is absorbed through the nasal mucosa,

making it relatively expensive to use • Nasal irritation is a frequent side effect • Only Regular insulin is given intranasally

• Insulin catheter• Indwelling subcutaneous catheters may be placed in the

abdomen to permit repeated insulin injections without repeated needlesticks


Oral Hypoglycemic Agents

• If patients with type 2 DM unable to control blood glucose with nutrition and exercise, physician may prescribe oral hypoglycemics

• Sulfonylureas (three generations), alpha-glucosidase inhibitors, biguanides, thiazolidinediones, D-phenylalanines, meglitinides

• Combination oral medications• ACTOplus met (pioglitazone and metformin), Avandamet

(rosiglitazone and metformin), Avandaryl (rosiglitazone and glimepiride), Glucovance (glyburide and metformin), Metaglip (glipizide and metformin)


Self-Monitoring of Blood Glucose

• Allows patients to monitor blood glucose levels to regulate their diet, exercise, and medication regimens to remain euglycemic

• Portable electronic glucose meters have largely replaced other methods of self-monitoring


Glycosylated Glucose Levels

• Glycosylated hemoglobin (HbA1c) reflects glucose levels over the past few months

• Fructosamine levels reflect those over several weeks


Complications of Therapy

• Hypoglycemia• A person injects too much insulin, does not eat enough, eats at

the wrong time, or exercises inconsistently: glucose levels may suddenly drop

• Somogyi phenomenon• Rebound hyperglycemia in response to hypoglycemia

• Dawn phenomenon• An increase in fasting blood glucose levels between 5 and 9 AM

that is not related to hypoglycemia


Assessment

• Ketoacidosis: ketonuria, Kussmaul’s respirations, orthostatic hypotension, hypertension, nausea, vomiting, lethargy, or change in level of consciousness

• Hypoglycemic patient: expect to find tachycardia, anxiety, trembling, and decreasing level of consciousness

• Be alert for indications of hyperosmolar nonketotic coma


Assessment

• Attempt to determine the following• Type of diabetes• Hypoglycemic agents: name, dosage, when last

dose was taken• Food and fluid intake for the past 3 days• Relevant laboratory values: blood glucose, blood

pH, bicarbonate levels, electrolytes, and osmolality and urine osmolality


Health History

• Chief complaint and history of present illness• Signs/symptoms that prompted patient to seek medical care

• Past medical history • Type and duration of DM • Name and dosage of prescribed medications and when they

were last taken• If patient monitors blood glucose, record type of equipment

used, testing schedule, recent test results • Family history

• Diabetes, heart disease, stroke, hypertension, hyperlipidemia


Health History

• Review of systems • Description of the patient’s general health • Changes in skin moisture or turgor• Inquire whether the patient has had floaters, diplopia (double

vision), or blurred vision, or has seen white halos around objects

• Abdominal symptoms: diarrhea, abdominal bloating, and gas • Problems passing or holding urine • If any pain in the legs, note when it occurs • Numbness, tingling, or burning in the extremities • Changes in mental alertness or seizures


Health History

• Functional assessment • Explore factors that can affect patient’s ability to perform

self-care, including literacy, financial resources such as health insurance, and family support


Health History

• Physical examination• Level of consciousness, posture and gait, and apparent well-

being • Vital signs, height, and weight • Skin color, warmth, turgor, and lesions noted • Inspect eye grounds for evidence of diabetic retinopathy or

cataracts• Be alert for a sweet, fruity odor to the patient’s breath that is

common with ketoacidosis • Carefully assess the feet• Test gait, balance, and motor coordination


Interventions

• Ineffective Health Maintenance• Ineffective Therapeutic Regimen Management• Risk for Deficient Fluid Volume• Risk for Injury• Activity Intolerance • Chronic Pain• Disturbed Sensory Perception or Impaired Skin

Integrity• Disturbed Thought Processes• Ineffective Coping


Hypoglycemia


Pathophysiology

• Develops when the blood glucose level falls to less than 45 to 50 mg/dL

• Symptoms occur at different blood levels according to individual tolerances and how rapidly the level falls


Causes

• Exogenous hypoglycemia • Results from outside factors acting on the body to

produce a low blood glucose • Include insulin, oral hypoglycemic agents, alcohol,

or exercise


Causes

• Endogenous hypoglycemia • Occurs when internal factors cause an excessive

secretion of insulin or an increase in glucose metabolism

• These conditions may be related to tumors or genetics


Causes

• Functional hypoglycemia • From a variety of causes, including gastric surgery,

fasting, or malnutrition


Signs and Symptoms

• Glucose level falls rapidly, causes epinephrine, cortisol, glucagon, and growth hormone to be secreted in an attempt to increase glucose levels • Symptoms: weakness, hunger, diaphoresis, tremors, anxiety,

irritability, headache, pallor, and tachycardia

• A blood glucose level that falls over several hours: symptoms attributed to lack of essential glucose to brain tissue • Symptoms: confusion, weakness, dizziness, blurred or double

vision, seizure, and in severe cases, coma


Medical Diagnosis

• The diagnosis of hypoglycemia not associated with diabetes can be based on fasting blood glucose, OGTT, intravenous glucose tolerance test, and 72-hour inpatient fasting

• Whipple’s triad • The presence of symptoms • Documentation of low blood glucose when symptoms occur• Improvement of symptoms when blood glucose rises


Medical Treatment

• In an unconscious patient who has diabetes, hypoglycemia should be suspected until it is ruled out • 50 mL of 50% glucose solution should be administered

immediately

• The patient with a milder form of hypoglycemia• Treated with 15 g carbohydrate• If the patient’s condition does not improve, another

15 g of carbohydrate should be given after 10 minutes


Medical Treatment

• Prevention of hypoglycemia by proper food intake • The diet is directed by the underlying cause • If overproduction of insulin after carbohydrate ingestion, a low-

carbohydrate, high-protein diet• Restriction of carbohydrates to no more than 100 g/day is

recommended • Simple sugars avoided; complex carbohydrates encouraged • Patients may tolerate smaller, more frequent meals. Alcohol

should be avoided


Assessment

• Present illness: shakiness, nervousness, irritability, tachycardia, anxiety, lightheadedness, hunger, tingling or numbness of the lips or tongue, nightmares, and crying out during sleep

• Note when episodes occur in relation to meals and particular food intake

• The past medical history documents diabetes, previous gastric surgery, abdominal cancer, or adrenal insufficiency

• Medications, paying particular attention to hypoglycemic agents


Assessment

• Note hypoglycemic agents, prescribed dose, and the time last dose taken

• Functional assessment: information about current diet, exercise, alcohol intake, and the effects of symptoms on daily activities

• Important aspects of the physical examination include general behavior, appearance, pulse, and blood pressure


Interventions

• Deficient Knowledge• Risk for Injury• Impaired Adjustment

1elsevier items and derived items © 2007 by saunders, an imprint of elsevier, inc. chapter 46...

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