Chemistry Studies
OVERVIEW OF CHEMISTRY STUDIES
Blood chemistry testing identifies many chemical blood constituents. It is often necessary to measure several blood chemicals to establish a pattern of abnormalities. A wide range of tests can be grouped under the headings of enzymes, electrolytes, blood sugars, lipids, hormones, proteins, vitamins, minerals, and drug investigation. Other tests have no common denominator. Selected tests serve as screening devices to identify target organ damage. When collecting specimens for chemistry studies, refer to Standard Precautions for Prevention and Control of Infection in Appendix A, Guidelines for Specimen Transport and Storage in Appendix B, and Effects of Drugs on Laboratory Tests in Appendix E.
General Biochemical Profiles
Profiles are a group of select tests that screen for certain conditions. Some of the more common profiles or panels are listed in Table 6.1.
Use of the Autoanalyzer
Sophisticated automated instrumentation makes it possible to conduct a wide variety of chemical tests on a single sample of blood and to report results in a timely manner. Numerical results may be reported with low, high, panic (or critical values), toxic, or D (i.e., fails Delta check) comments along with normal reference range. Computerized interfaces allow direct transmission of results
between laboratory and clinical settings. Not only does this method of record keeping provide a baseline for future comparisons, but it can also allow unsuspected diseases to be uncovered and can lead to early diagnosis when symptoms are vague or absent. Chemistry tests may be grouped into lipid, basic metabolic, comprehensive metabolic, hepatic, or electrolyte panels. A list of standard panels appears in Table 6.2.
between laboratory and clinical settings. Not only does this method of record keeping provide a baseline for future comparisons, but it can also allow unsuspected diseases to be uncovered and can lead to early diagnosis when symptoms are vague or absent. Chemistry tests may be grouped into lipid, basic metabolic, comprehensive metabolic, hepatic, or electrolyte panels. A list of standard panels appears in Table 6.2.
TABLE 6.1 Common Screening Profiles | ||||||||||||||||||
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NOTE
Normal or reference values (intervals) for any chemistry determination vary with the method or assay used. For example, differences in substrates or temperature at which the assay is run will alter the normal range. Thus, normal ranges vary from laboratory to laboratory.
DIABETES TESTING, BLOOD GLUCOSE, BLOOD SUGAR, AND RELATED TESTS
• Fasting Blood Glucose (FBG); Fasting Blood Sugar (FBS); Fasting Plasma Glucose (FPG); Casual Random Plasma Glucose (PG)
Glucose is formed from carbohydrate digestion and conversion of glycogen to glucose by the liver. The two hormones that directly regulate blood glucose are glucagon and insulin. Glucagon accelerates glycogen breakdown in the liver and causes the blood glucose level to rise. Insulin increases cell membrane permeability to glucose, transports glucose into cells (for metabolism), stimulates glycogen formation, and reduces blood glucose levels. Driving insulin into the cells requires insulin and insulin receptors. For example, after a meal, the pancreas releases insulin for glucose metabolism, provided there are enough insulin receptors. Insulin binds to these receptors on the surface of target cells such as are found in fat and muscle. This opens the channels so that glucose can pass into cells, where it can be converted into energy. As cellular glucose metabolism occurs, blood glucose levels fall. Adrenocorticotropic hormone (ACTH), adrenocorticosteroids, epinephrine, and thyroxine also play key roles in glucose metabolism.
TABLE 6.2 Standard Panels | ||||||||||||||||||||||
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There are four categories of diabetes:
Type 1 (formerly known as insulin-dependent diabetes mellitus or juvenile-onset diabetes mellitus), due to destruction of pancreatic β cells which leads to deficiency in insulin, accounts for about 5% to 10% of individuals diagnosed with diabetes.
Type 2 (formerly known as non-insulin-dependent diabetes mellitus or adult-onset diabetes mellitus), a progressive form of insulin deficiency concomitant with insulin resistance, accounts for 90% to 95% of individuals diagnosed with diabetes.
Due to other causes (e.g., genetic defects [see Chapter 11 for genetic causes]), disease of the pancreas, drug- or chemical-induced, and so forth.
Gestational (i.e., diagnosed during pregnancy)
The American Diabetes Association (ADA) uses the term prediabetes, also known as impaired glucose tolerance or impaired fasting glucose. Individuals with prediabetes demonstrate higher levels of blood plasma glucose (PG) (100 to 125 mg/dL or 5.6 to 6.9 mmol/L) than normal subjects
(<100 mg/dL or <5.6 mmol/L) and, if left untreated, go on to develop type 2 diabetes within 10 years.
(<100 mg/dL or <5.6 mmol/L) and, if left untreated, go on to develop type 2 diabetes within 10 years.
Diagnosing latent autoimmune diabetes in adults (LADA) early in the course of the disease process is critical because of the high risk for developing insulin dependency. It has been found that most patients with LADA have at least two of the following: age of onset <50 years, body mass index (BMI) <25 kg/m2, personal history of autoimmune disease, acute symptoms before diagnosis, or family history of autoimmune disease.
Fasting blood glucose is a vital component of diabetes management. The term random/casual is defined as any time of day without regard to time since the last meal. Fasting is defined as no caloric intake for at least 8 hours. Abnormal glucose metabolism may be caused by inability of pancreatic islet β cells to produce insulin, reduced numbers of insulin receptors, faulty intestinal glucose absorption, inability of the liver to metabolize glycogen, or altered levels of hormones (e.g., ACTH) that play a role in glucose metabolism.
In most cases, significantly elevated fasting plasma glucose (FPG) levels (i.e., >140 mg/dL or >7.77 mmol/L; hyperglycemia) are, in themselves, usually diagnostic of diabetes. However, mild, borderline cases may present with normal fasting glucose values. If diabetes is suspected, a glucose tolerance test (GTT) can confirm the diagnosis. Occasionally, other diseases may produce elevated PG levels; therefore, a comprehensive history, physical examination, and workup should be done before a definitive diagnosis of diabetes is established.
CLINICAL ALERT
The National Institutes of Health (NIH) guidelines endorse diabetic testing of all adults ≥45 yr of age every 3 yr. The ADA recommends the following guidelines for testing:
Should be considered if patient is >45 yr of age
Strongly recommended if patient is >45 yr of age and overweight
Considered if patient is <45 yr of age and overweight with another risk factor
Diabetes mellitus, a group of metabolic disorders, is characterized by hyperglycemia and abnormal protein, fat, and carbohydrate metabolism due to defects in insulin secretions—that is, inadequate and deficient insulin action (insulin resistance) on target organs.
Criteria for diagnosing diabetes
Symptoms of diabetes plus random/casual PG concentration of ≥200 mg/dL (≥11.1 mmol/L). Random/casual is defined as any time of day without regard to time since last meal. The classic symptoms of diabetes include polyuria, polydipsia, and unexplained weight loss, or
FPG ≥126 mg/dL (≥7.0 mmol/L) on at least two occasions (fasting is defined as no caloric intake for at least 8 hr), or
Two-hour PG ≥200 mg/dL (≥11.1 mmol/L) during an oral glucose tolerance test (OGTT). The test should be performed as described by the World Health Organization (WHO), using a glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water, or
Hemoglobin A1c ≥6.5% (48 mmol/mol). Method used for testing should be NGSP certified and standardized to Diabetes Control and Complications Trial (DCCT) assay.
In the absence of unequivocal hyperglycemia with acute metabolic decompensation, these criteria should be confirmed by repeat testing of b through d on a different day. OGTT is not recommended for routine clinical use.
Source: American Diabetes Association: Standards of medical care in diabetes: Prevention/delay of type 2 diabetes. Diabetes Care 30:S4-S41, 2007, and Sacks DB, Arnold M, Bakris GL, et al: Guidelines and recommendations for laboratory analysis in the diagnosis and management of diabetes mellitus. Diabetes Care 34:e61-e99, 2011.
Normal Findings
FPG, adults: ≤100 mg/dL or ≤5.6 mmol/L
Fasting, children (2 to 18 years): 60 to 100 mg/dL or 3.3 to 5.6 mmol/L
Fasting, young children (0 to 2 years): 60 to 110 mg/dL or 3.3 to 6.1 mmol/L
Fasting, premature infants: 40 to 65 mg/dL or 2.2 to 3.6 mmol/L
CLINICAL ALERTCritical values for fasting blood glucose (FBG): <40 mg/dL (<2.22 mmol/L) may cause brain damage (women and children), <50 mg/dL (<2.77 mmol/L) (men); >400 mg/dL (>22.2 mmol/L) may cause coma.
Procedure
Draw a 5-mL venous blood sample from a fasting person or a random PG (FPG) (any time of day). In known cases of diabetes, blood drawing should precede administration of insulin or oral hypoglycemic agent. Observe standard precautions. Serum is acceptable if separated from red cells within an hour. A gray-topped tube, which contains sodium fluoride, is acceptable for 24 hours without separation.
Self-monitoring of blood glucose by the person (or healthcare provider) with diabetes can be done by finger-stick blood drop sampling several times per day if necessary. Several devices are commercially available for this procedure; they are relatively easy to use and have been established as a major component in satisfactory diabetes control. Calibration of monitoring devices should be done on a regular basis.
Noninvasive methods using skin pads to check blood glucose level are being developed for selfmonitoring that eliminate the dreaded finger-prick test; for example, a GlucoWatch (Cygnus, Redwood City, CA), worn on the wrist and powered by an AAA battery.
NOTE
When whole blood glucose values are not equivalent to plasma values, plasma values are about 10% to 15% higher than whole blood values. However, most glucose meters convert the whole blood values to plasma equivalent values.
Patient Checklist for Self-Monitoring of Blood Glucose Testing
This list is a general outline. Each brand of meter has its own instructions. Read the instructions on each new meter carefully to get accurate results. Know whether the monitor and strips give whole blood or plasma equivalent results (Fig. 6.1).
General instructions
Make sure hands are clean, dry, and warm.
Prick finger with the lancet.
Squeeze out a drop of capillary blood.
Apply SECOND drop of blood onto the test strip or sensor.
Wait for the test strip or sensor to develop.
Compare the test strip to the chart or insert it into the meter.
Safely dispose of the lancet in an approved sharps container.
Record blood glucose results with date and time.
If type 1 diabetes mellitus is present, also monitor urine for ketones or blood β-hydroxybutyrate for possible dangerous complications such as diabetic ketoacidosis (e.g., during stress or acute illness).
Test more often on days when illness occurs, when blood glucose is too high, when meal or exercise plans change, when traveling, or if it is thought that the blood glucose is low.
FIGURE 6.1. Portable blood glucose analyzer. (Reprinted with permission from HemoCue AB, Angelholm, Sweden.)
If concerned about getting accurate results, consult with the diabetes educator or contact the manufacturer to ensure proper use of the monitor.
Several blood glucose meters currently available are approved by the U.S. Food and Drug Administration (FDA), the agency that approves medical devices, for what is called “alternate site testing.”
Alternate sites (other than fingertips) include forearm, bicep area, palm of hand, between fingers, and sometimes the calf.
Tips for using alternate sites
Rub the site to be used to check blood glucose vigorously before pricking skin. This increases blood flow to the site.
Use one type of monitor; do not alternate between different monitors. This will help to obtain consistent results.
Consistently use the same alternate site. For example, always use forearms. This will also help to obtain consistent results.
CLINICAL ALERTA recent warning was published by the FDA, alerting users of portable glucose monitors to be cognizant of the units of measurement displayed; that is, mg/dL or mmol/L. Reporting a glucose value without reporting the unit of measurement could result in an adverse event.
Clinical Implications
Elevated blood glucose (hyperglycemia) occurs in the following conditions:
Diabetes mellitus: a fasting glucose ≥126 mg/dL (>7.0 mmol/L) or a 2-hour postprandial load PG ≥200 mg/dL (>11.1 mmol/L) during an oral GTT.
Other conditions that produce elevated PG glucose levels include the following:
Cushing’s disease (increased glucocorticoids cause elevated blood sugar levels)
Acute emotional or physical stress situations (e.g., myocardial infarction [MI], cerebrovascular accident, convulsions)
Pheochromocytoma, acromegaly, gigantism
Pituitary adenoma (increased secretion of growth hormone causes elevated blood glucose levels)
Hemochromatosis
Pancreatitis (acute and chronic), neoplasms of pancreas
Glucagonoma
Advanced liver disease
Chronic renal disease
Vitamin B deficiency: Wernicke’s encephalopathy
Pregnancy (may signal potential for onset of diabetes later in life)
Decreased blood PG (hypoglycemia) occurs in the following conditions:
Pancreatic islet cell carcinoma (insulinomas)
Extrapancreatic stomach tumors (carcinoma)
Addison’s disease (adrenal insufficiency), carcinoma of adrenal gland
Hypopituitarism, hypothyroidism, ACTH deficiency
Starvation, malabsorption (starvation does not cause hypoglycemia in normal persons)
Liver damage (alcoholism, chloroform poisoning, arsenic poisoning)
Premature infant; infant delivered to a mother with diabetes
Enzyme-deficiency diseases (e.g., galactosemia, inherited maple syrup urine disease, von Gierke’s syndrome)
Insulin overdose (accidental or deliberate)
Reactive hypoglycemia, including alimentary hyperinsulinism, prediabetes, endocrine deficiency
Postprandial hypoglycemia may occur after gastrointestinal (GI) surgery and is described with hereditary fructose intolerance, galactosemia, and leucine sensitivity.
According to the ADA criteria, there are four definitive tests for diabetes:
Symptoms of diabetes plus a random/casual PG ≥200 mg/dL (>11.1 mmol/L), or
An FPG ≥126 mg/dL (>6.99 mmol/L; in the absence of unequivocal hyperglycemia, criteria b to d should be confirmed by repeat testing), or
An OGTT with a 2-hour postload (75-g glucose load) level ≥200 mg/dL (>11.1 mmol/L; in the absence of unequivocal hyperglycemia, criteria b to d should be confirmed by repeat testing), or
Hemoglobin A1c (HbA1c) ≥6.5% (in the absence of unequivocal hyperglycemia, criteria b to d should be confirmed by repeat testing)
The classification of diabetes diagnosis reflects a shift to the etiology or pathology of the disease from a classification based on pharmacologic treatment.
Impaired fasting glucose (IFG) or impaired glucose tolerance (IGT) is referred to as prediabetes.
Interfering Factors
Elevated glucose
Steroids, diuretics, other drugs (see Appendix E)
Pregnancy (a slight blood glucose elevation normally occurs)
Surgical procedures, anesthesia, and hospitalization in intensive care unit (ICU)
Obesity or sedentary lifestyle
Parenteral glucose administration (e.g., from total parenteral nutrition)
Intravenous (IV) glucose (recent or current)
Heavy smoking
The dawn phenomenon occurs in both non-insulin-dependent and insulin-dependent diabetes mellitus. There is an increase in blood glucose, typically between 4:00 a.m. and 8:00 a.m., due to counter-regulatory hormones, including growth hormone, cortisol, and glucagon.
Decreased glucose
Hematocrit >55%
Intense exercise
Toxic doses of aspirin, salicylates, and acetaminophen
Other drugs (see Appendix E), including ethanol, quinine, and haloperidol
Interventions
Pretest Patient Care
Explain test purpose (to detect hyperglycemia) and blood-drawing procedure. Note time.
Tell patient that the test requires at least an overnight fast; water is permitted. Instruct the patient to defer insulin or oral hypoglycemics until after blood is drawn, unless specifically instructed to do otherwise.
Note the last time the patient ate in the record and on the laboratory requisition.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Tell the patient that he or she may eat and drink after fasting blood is drawn. Note time.
Review test results; report and record findings. Modify the nursing care plan as needed. Monitor appropriately for hyperglycemia and hypoglycemia. Counsel regarding necessary lifestyle changes (e.g., diet, exercise, glycemic control, medication). Target blood glucose levels: before meals or upon waking, 80 to 120 mg/dL (4.4 to 6.6 mmol/L); and at bedtime, 100 to 140 mg/dL (5.5 to 7.7 mmol/L).
Pharmacologic intervention may include pioglitazone (targets insulin resistance) plus glimepiride (increases amount of insulin) to improve glycemic control in type 2 diabetes.
Treatment regimens
Initial medical treatment includes use of metformin. The addition of other glucose-lowering medications may be necessary.
When target goals are not achieved and glucose and A1c remain elevated, early (basal) insulin therapy may be indicated.
In hospitalized patients (ICU, surgery, critical illnesses), strict glycemic controls, interventions (blood checking at least four times daily and sliding scale insulin administration), and aggressive insulin therapy are indicated.
Glucose may be monitored by three methods: (1) intermittent laboratory analysis, (2) bedside monitor, and (3) continuous glucose monitoring. The continuous glucose monitor system has been used to safely lower blood sugar in children with type 1 diabetes. In this instance, a tiny glucose-sensing device is inserted under the skin of the abdomen. This sensor and computer (attached to a belt) measure and record blood glucose every 10 seconds for 3 days.
Give the patient the following checklist:
Take special care of feet.
Use a lubricant or unscented hand cream on dry, scaly skin.
Look for calluses on soles. Rub them gently with a pumice stone.
Make sure new shoes fit properly; wear freshly washed socks or stockings.
Never go barefoot.
Avoid using hot water bottles, tubs of hot water, or heating pads on the feet.
Trim toenails straight across.
Make sure doctor inspects feet as part of every visit.
Use a team approach to help make decisions about care. The team may include a doctor, nurse diabetes educator, dietitian, pharmacist, ophthalmologist or optometrist, exercise physiologist, podiatrist, psychologist, and the family.
Follow the most healthful lifestyle possible, focusing on diet, exercise, and weight management.
Persons with glucose levels >200 mg/dL (>11.1 mmol/L) should be placed on a strict intake and output program.
In-home test kits are available for patients to evaluate whether they have lost protective sensation in a foot, which would put them at high risk for lower extremity amputation. The lower extremity amputation prevention (LEAP) monofilament test includes a 10-g reusable monofilament that is touched to eight sites on each foot for 1 to 2 seconds. A diagram of each foot with the sites marked is included in the kit for recording whether sensation was felt at each site. The results can then be reviewed by the healthcare provider and further evaluation undertaken if indicated.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
CLINICAL ALERT
If a person with known or suspected diabetes experiences headaches, irritability, dizziness, weakness, fainting, or impaired cognition, a blood glucose test or finger stick test must be done before giving insulin. Similar symptoms may be present for both hypoglycemia and hyperglycemia. If a blood glucose level cannot be obtained and one is uncertain regarding the situation, glucose may be given in the form of orange juice, sugar-containing soda, or candy (e.g., hard candy, jelly beans). Make certain the person is sufficiently conscious to manage eating or swallowing. In the acute care setting, IV glucose may be given in the event of severe hypoglycemia. A glucose gel is also commercially available and may be rubbed on the inside of the mouth by another person if the person with diabetes is unable to swallow or to respond properly. Instruct persons prone to hypoglycemia to carry sugar-type items on their person and to wear a necklace or bracelet that identifies the person as diabetic.
Frequent blood glucose monitoring, including self-monitoring, allows better control and management of diabetes than urine glucose monitoring.
When blood glucose values are >300 mg/dL (>16.6 mmol/L), urine output increases, as does the risk for dehydration.
Diabetes is a “disease of the moment”: Persons living with diabetes are continually affected by fluctuations in blood glucose levels and must learn to manage and adapt their lifestyle within this framework. For some, adaptation is relatively straightforward; for others, especially those identified as being “brittle,” lifestyle changes and management are more complicated, and these patients require constant vigilance, attention, encouragement, and support.
Each person with diabetes may experience certain symptoms in his or her own unique way and in a unique pattern.
CLINICAL ALERT
Infants with tremor, convulsion, or respiratory distress should have STAT glucose done, particularly in the presence of maternal diabetes or with hemolytic disease of the newborn.
Newborns who are too small or too large for gestational age should have their glucose level measured in the first day of life.
Diseases related to neonatal hypoglycemia
Glycogen storage diseases
Galactosemia
Hereditary fructose intolerance
Ketogenic hypoglycemia of infancy
Carnitine deficiency (Reye’s syndrome)
• Hemoglobin A1c (HbA1c); Glycohemoglobin (G-Hb); Glycated Hemoglobin (GhB); Diabetic Control Index; Glycated Serum Protein (GSP)
Glycohemoglobin (G-Hb) is a normal, minor type of hemoglobin. Glycosylated hemoglobin is formed at a rate proportional to the average glucose concentration by a slow, nonenzymatic process within the red blood cells (RBCs) during their 120-day circulating life span. G-Hb is blood glucose bound
to hemoglobin. In the presence of hyperglycemia, an increase in G-Hb causes an increase in HbA1c (formed as a result of irreversible attachment of glucose to an amino acid in the β chain of the adult hemoglobin molecule). If the glucose concentration increases because of insulin deficiency, then glycosylation is irreversible.
to hemoglobin. In the presence of hyperglycemia, an increase in G-Hb causes an increase in HbA1c (formed as a result of irreversible attachment of glucose to an amino acid in the β chain of the adult hemoglobin molecule). If the glucose concentration increases because of insulin deficiency, then glycosylation is irreversible.
Glycosylated hemoglobin values reflect average blood sugar levels for the 2- to 3-month period before the test. This test provides information for evaluating diabetic treatment modalities (every 3 months), is useful in determining treatment for juvenile-onset diabetes with acute ketoacidosis, and tracks control of blood glucose in milder cases of diabetes. It can be a valuable adjunct in determining which therapeutic choices and directions (e.g., oral antihypoglycemic agents, insulin, β-cell transplantation) will be most effective. A blood sample can be drawn at any time. The measurement is of particular value for specific groups of patients: diabetic children; diabetic patients in whom the renal threshold for glucose is abnormal; unstable type 1 diabetic patients (taking insulin) in whom blood sugar levels vary markedly from day to day; type 2 diabetic patients who become pregnant; and persons who, before their scheduled appointments, change their usual habits, dietary or otherwise, so that their metabolic control appears better than it actually is.
Normal Findings
Results are expressed as percentage of total hemoglobin. Values vary slightly by method and laboratory.
G-Hb: 4.0% to 7.0% or 0.04 to 0.07
HbA1c: 5.0% to 7.0% (100 to 170 mg/dL or 5.5 to 9.3 mmol/L)
Plasma blood glucose (mg/dL) = (HbA1c × 35.6) − 77.3
Plasma blood glucose (mmol/L) = (HbA1c × 1.98) − 4.29
CLINICAL ALERTCritical Value
G-Hb: >10.1% (>0.101)
HbA1c: >8.1% (>0.08) corresponds to an estimated average glucose >186 mg/dL (>10.3 mmol/L)
Procedure
Obtain a 5-mL venous blood sample with ethylenediaminetetraacetic acid (EDTA) purple-topped anticoagulant additive. Serum may not be used.
Observe standard precautions. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.
Clinical Implications
Values are frequently increased in persons with poorly controlled or newly diagnosed diabetes.
With optimal control, the HbA1c moves toward normal levels.
A diabetic patient who recently comes under good control may still show higher concentrations of glycosylated hemoglobin. This level declines gradually over several months as nearly normal glycosylated hemoglobin replaces older RBCs with higher concentrations.
Increases in glycosylated hemoglobin occur in the following nondiabetic conditions:
Iron-deficiency anemia
Splenectomy
Alcohol toxicity
Lead toxicity
Decreases in HbA1c occur in the following nondiabetic conditions:
Hemolytic anemia
Chronic blood loss
Pregnancy
Chronic renal failure
Interfering Factors (varies by method)
Presence of HbF and H causes falsely elevated values.
Presence of HbS, C, E, D, G, and Lepore (autosomal recessive mutation resulting in a hemoglobinopathy) causes falsely decreased values.
Interventions
Pretest Patient Care
Explain test purpose and blood-drawing procedure. Observe standard precautions. Fasting is not required.
Note that this test is not meant for short-term diabetes mellitus management; instead, it assesses the efficacy of long-term management modalities over several weeks or months. It is not useful more often than 4 to 6 weeks.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Review test outcome, with target HbA1c of <5.7%, and counsel patient appropriately for management of diabetes with oral hypoglycemics and insulin. If test results are not consistent with clinical findings, check the patient for HbF, which elevates HbA1c results.
Follow guidelines in Chapter 1 regarding safe, effective, informed posttest care.
CLINICAL ALERTA number of different tests can determine glycosylated hemoglobin levels. The most specific of these measures is HbA1c. There are different expected values for each test. Keep in mind that HbA1 is always 2%-4% higher than HbA1c. When reviewing results, be certain of the specific test used.
• Gestational Diabetes Mellitus (GDM)
Glucose intolerance during pregnancy (gestational diabetes mellitus [GDM]) is associated with an increase in perinatal morbidity and mortality, especially in women who are aged >25 years, overweight, or hypertensive. In addition, more than one half of all pregnant patients with an abnormal GTT do not have any of the same risk factors. It is therefore recommended by the ADA that all pregnant women be screened for GDM as follows: Women with presence of risk factors should be screened at the first prenatal visit, and women with no known prior diabetes should be screened at 24 to 28 weeks.
A diabetes risk assessment should be done at the first prenatal visit. Screening for very-high-risk pregnancies should be done as soon as possible. At this stage, screening can be done using standard criteria. An OGTT is done to detect GDM and screen nonsymptomatic pregnant women. During pregnancy, abnormal carbohydrate metabolism is evaluated by screening all pregnant women at the first prenatal visit and then again at 24 to 28 weeks.
Two approaches may be followed for GDM screening at 24 to 28 weeks:
Two-step approach:
Perform initial screening by measuring plasma or serum glucose 1 hour after a 50-g load of 140 mg/dL identifies 80% of women with GDM, whereas the sensitivity is further increased to 90% by a threshold of 130 mg/dL.
Perform a diagnostic 100-g OGTT on a separate day in women who exceed the chosen threshold on 50-g screening.
One-step approach (may be preferred in clinics with high prevalence of GDM): Perform a diagnostic 100-g OGTT in all women to be tested at 24 to 28 weeks. The 100-g OGTT should be performed in the morning after an overnight fast of at least 8 hours.
Reference Values
To make a diagnosis of GDM, at least two of the following PG values must be found:
FPG >95 mg/dL (>5.3 mmol/L)
1-hour >180 mg/dL (>10.0 mmol/L)
2-hour >155 mg/dL (>8.6 mmol/L)
3-hour >140 mg/dL (>7.8 mmol/L)
Procedure
Draw a 5-mL venous blood sample (sodium fluoride) after an 8- to 14-hour fast, at least 3 days of unrestricted diet and activity, and after glucose load.
Observe standard precautions. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.
Clinical Implications
A positive result in a pregnant woman means she is at much greater risk (seven times) for having GDM.
GDM is any degree of glucose intolerance with onset during pregnancy or first recognized during pregnancy.
Interventions
Pretest Patient Care
Explain test purpose (to evaluate abnormal carbohydrate metabolism and predict diabetes in later life) and procedure. No fasting is usually required. Obtain pertinent history of diabetes and record any signs or symptoms of diabetes.
Instruct the woman about obtaining a urine sample for glucose testing to check before drinking the glucose load. Positive urine glucose should be checked with the healthcare provider before glucose load. Those with glycosuria >250 mg/dL (>13.8 mmol/L) must have a blood glucose test before GDM testing.
Give the patient the appropriate glucose beverage (150 mL dissolved in water or Trutol or Orange DEX).
Explain to the patient that no eating, drinking, smoking, or gum chewing is allowed during the test. The patient should not leave the office. She may void if necessary.
After 1 hour, draw one NaF or EDTA tube (5-mL venous blood) using standard venipuncture technique.
Posttest Patient Care
Normal activities, eating, and drinking may be resumed.
Review test results; report and record findings. Modify the nursing care plan as needed. Explain to the patient what to expect for a normal outcome.
Six to 12 weeks after delivery, the patient should be retested and reclassified. In most cases, glucose will return to normal.
• Glucose Tolerance Test (GTT); Oral Glucose Tolerance Test (OGTT)
In a healthy individual, the insulin response to a large oral glucose dose is almost immediate. It peaks in 30 to 60 minutes and returns to normal levels within 3 hours when sufficient insulin is present to metabolize the glucose ingested at the beginning of the test. The test should be performed according to WHO guidelines using glucose load containing the equivalent of 75 g of anhydrous glucose dissolved in water or other solution.
If fasting and postload glucose test results are borderline, the GTT can support or rule out a diagnosis of diabetes mellitus; it can also be a part of a workup for unexplained hypertriglyceridemia, neuropathy, impotence, renal diseases, or retinopathy. This test may be ordered when there is sugar in the urine or when the fasting blood sugar level is significantly elevated. The GTT/OGTT should not be used as a screening test in nonpregnant adults or children.
Indications for Test
The GTT/OGTT is done on certain patients, with the following indications (few indications still meet wide acceptance):
Family history of diabetes
Obesity
Unexplained episodes of hypoglycemia
History of recurrent infections (boils and abscesses)
In women, history of delivery of large infants, stillbirths, neonatal death, premature labor, and spontaneous abortions
Transitory glycosuria or hyperglycemia during pregnancy, surgery, trauma, stress, MI, and ACTH administration
Normal Findings
FPG
Adults: 100 mg/dL or 5.6 mmol/L
120-Minute (2-Hour GTT Test) 2-Hour PG after 75-g Glucose Load
Adults: ≤200 mg/dL or ≤11.1 mmol/L
Adults: 140 to 199 mg/dL (7.8 to 11.0 mmol/L), IGT
Procedure
This is a timed test for glucose tolerance. A 2-hour PG test is done after glucose load to detect diabetes in individuals other than pregnant women.
Have the patient eat a diet with >150 g of carbohydrates for 3 days before the test.
Ensure that the following drugs are discontinued 3 days before the test because they may influence test results:
Hormones, oral contraceptives, steroids
Salicylates, anti-inflammatory drugs
Diuretic agents
Hypoglycemic agents
Antihypertensive drugs
Anticonvulsants (see Appendix E)
Insulin and oral hypoglycemic agents should be withheld until the test is completed.
Record the patient’s weight.
Pediatric doses of glucose are based on body weight, calculated as 1.75 g/kg not to exceed a total of 75 g.
Nonpregnant adults: 75 g of glucose
A 5-mL sample of venous blood is drawn. Serum or gray-topped tubes are used. The patient should fast 12 to 16 hours before testing. After the blood is drawn, the patient drinks all of a specially formulated glucose solution within a 5-minute time frame.
Blood samples are obtained at fasting and 2 hours after glucose ingestion.
Tolerance tests can also be performed for pentose, lactose, galactose, and D-xylose.
The GTT is not indicated in these situations:
Persistent fasting hyperglycemia >140 mg/dL or >7.8 mmol/L
Persistent fasting normal PG
Patients with overt diabetes mellitus
Persistent 2-hour PG >200 mg/dL or >11.1 mmol/L
Test has limited value in diagnosis of diabetes mellitus in children and is rarely indicated for that purpose.
PROCEDURAL ALERT
GTT is contraindicated in patients with a recent history of surgery, MI, or labor and delivery—these conditions can produce invalid values.
The GTT should be postponed if the patient becomes ill, even with common illnesses such as the flu or a severe cold.
Record and report any reactions during the test. Weakness, faintness, and sweating may occur between the second and third hours of the test. If this occurs, a blood sample for a glucose level should be drawn immediately and the GTT aborted.
Should the patient vomit the glucose solution, the test is declared invalid; it can be repeated in 3 d (˜72 hr).
Clinical Implications
The presence of abnormal GTT values (decreased tolerance to glucose) is based on the International Classification for Diabetes Mellitus and the following glucose intolerance categories:
At least two GTT values must be abnormal for a diagnosis of diabetes mellitus to be validated.
In cases of overt diabetes, no insulin is secreted; abnormally high glucose levels persist throughout the test.
Glucose values that fall above normal values but below the diagnostic criteria for diabetes or IGT should be considered nondiagnostic.
See Table 6.3 for an interpretation of glucose tolerance levels.
Decreased glucose tolerance occurs with high glucose values in the following conditions:
Diabetes mellitus
Postgastrectomy
Hyperthyroidism
Excess glucose ingestion
Hyperlipidemia types III, IV, and V
Hemochromatosis
Cushing’s disease (steroid effect)
Central nervous system (CNS) lesions
Pheochromocytoma
Decreased glucose tolerance with hypoglycemia can be found in persons with von Gierke’s disease, severe liver damage, or increased epinephrine levels.
TABLE 6.3 Glucose Tolerance Test Levels
Conventional Units (mg/dL)
SI Units (mmol/L)
Fasting adult
140
7.8
Adult diabetes mellitus 1-hr glucose
>200
>11.1
and 2-hr glucose
>200
>11.1
Fasting adult
140
7.8
Adult impaired glucose tolerance 1-hr glucose
>200
>11.1
and 2-hr glucose
>140-200
>7.8-11.1
Juvenile diabetes mellitus (fasting glucose)
>140
>7.8
and 1-hr glucose
>200
>11.1
and 2-hr glucose
>200
>11.1
Impaired glucose tolerance in children (fasting glucose)
—
—
and 2-hr glucose
>140
>7.8
Increased glucose tolerance with flat curve (i.e., glucose does not increase but may decrease to hypoglycemic levels) occurs in the following conditions:
Pancreatic islet cell hyperplasia or tumor
Poor intestinal absorption caused by diseases such as sprue, celiac disease, or Whipple’s disease
Hypoparathyroidism
Addison’s disease
Liver disease
Hypopituitarism, hypothyroidism
Interfering Factors
Smoking increases glucose levels.
Altered diets (e.g., weight reduction) before testing can diminish carbohydrate tolerance and suggest “false diabetes.”
Glucose levels normally tend to increase with aging.
Prolonged oral contraceptive use causes significantly higher glucose levels in the second hour or in later blood specimens.
Infectious diseases, illnesses, and operative procedures affect glucose tolerance. Two weeks of recovery should be allowed before performing the test.
Certain drugs impair glucose tolerance levels (this list is not all inclusive; see Appendix E for other drugs):
If possible, these drugs should be discontinued for at least 3 days before testing. Check with the healthcare provider for specific orders.
Insulin
Oral hypoglycemics
Large doses of salicylates, anti-inflammatory drugs
Thiazide diuretics
Oral contraceptives
Corticosteroids
Estrogens
Heparin
Nicotinic acid
Phenothiazines
Lithium
Metyrapone (Metopirone)
Prolonged bed rest influences GTT results. If possible, the patient should be ambulatory. A GTT in a hospitalized patient has limited value.
Interventions
Pretest Patient Care
Explain test purpose and procedure. A written reminder may be helpful.
A diet high in carbohydrates (150 g) should be eaten for 3 days preceding the test. Instruct the patient to abstain from alcohol.
The patient should fast for at least 12 hours but not more than 16 hours before the test. Only water may be ingested during fasting time and test time. Use of tobacco products is not permitted during testing.
Patients should rest or walk quietly during the test period. They may feel weak, faint, or nauseated during the test. Vigorous exercise alters glucose values and should be avoided during testing.
Collect blood specimens at the prescribed times and record exact times collected. Urine glucose testing is no longer recommended.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal diet and activities at the end of the test. Encourage eating complex carbohydrates and protein if permitted.
Administer prescribed insulin or oral hypoglycemics when the test is done. Arrange for the patient to eat within a short time (30 minutes) after these medications are taken.
Review test results; report and record findings. Modify the nursing care plan as needed. Counsel the patient appropriately. Patients newly diagnosed with diabetes will need diet, medication, and lifestyle modification instructions.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
CLINICAL ALERT
If fasting glucose is >140 mg/dL (>7.8 mmol/L) on two separate occasions, or if the 2-hr postprandial blood glucose is >200 mg/dL (>11.1 mmol/L) on two separate occasions, GTT is not necessary for a diagnosis of diabetes mellitus to be established.
The GTT is of limited diagnostic value for children.
• Lactose Tolerance; Breath Hydrogen Test
Lactose intolerance often begins in infancy, with symptoms of diarrhea, vomiting, failure to thrive, and malabsorption. The patient becomes asymptomatic when lactose is removed from the diet. This syndrome is caused by a deficiency of sugar-splitting enzymes (lactase) in the intestinal tract.
This test is actually a GTT done to diagnose intestinal disaccharidase (lactase) deficiency. Glucose is measured, and it is the increase or lack of increase over the fasting specimen that is used for the interpretation. Breath samples reveal increased hydrogen levels, which are caused by lactose buildup in the intestinal tract. Colonic bacteria metabolize the lactose and produce hydrogen gas.
Normal Findings
Change in glucose from normal value >30 mg/dL or >1.7 mmol/L
Inconclusive: 20 to 30 mg/dL or 1.1 to 1.7 mmol/L
Abnormal: <20 mg/dL or <1.1 mmol/L
Hydrogen (breath):
Fasting: <5 ppm or <5 × 10-6
After lactose ingestion: <12 ppm or <12 × 10-6 increase from fasting level
Procedure
Follow instructions given for the GTT.
Draw a blood specimen from a fasting patient. The patient then drinks 50 g of lactose mixed with 200 mL of water (2 g of lactose/kg body weight).
Draw blood lactose samples at 0, 30-, 60-, and 90-minute intervals.
Take breath hydrogen samples at the same time intervals as the blood specimens. Contact your laboratory for collection procedures.
Clinical Implications
Lactose intolerance occurs as follows:
A “flat” lactose tolerance finding (i.e., no rise in glucose) points to a deficiency of sugar-splitting enzymes, as in irritable bowel syndrome. This type of deficiency is more prevalent in American Indians, African Americans, Asians, and Jews.
A monosaccharide tolerance test such as the glucose/galactose tolerance test should be done as a follow-up.
The patient ingests 25 g of both glucose and galactose.
A normal increase in glucose indicates a lactose deficiency.
Secondary lactose deficiency found in:
Infectious enteritis
Bacterial overgrowth in intestines
Inflammatory bowel disease, Crohn’s disease
Giardia lamblia infestation
Cystic fibrosis of pancreas
The breath hydrogen test is abnormal in the lactose deficiency test because:
Malabsorption causes hydrogen (H2) production through the process of fermentation of lactose in the colon.
The H2 formed is directly proportional to the amount of test dose lactose not digested by lactase.
In diabetes:
Blood glucose values may show increases >20 mg/dL (>1.11 mmol/L) despite impaired lactose absorption.
There may be an abnormal lactose tolerance curve due to faulty metabolism, not necessarily from lactose intolerance.
Interventions
Pretest Patient Care
Explain test purpose and procedure. The patient must fast for 8 to 12 hours before the test.
Do not allow the patient to eat dark bread, peas, beans, sugars, or high-fiber foods within 24 hours of the test.
Do not permit smoking during the test and for 8 hours before testing; no gum chewing.
Do not allow antibiotics to be taken for 2 weeks before the test unless specifically ordered.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal diet and activity.
Review test results; report and record findings. Modify the nursing care plan as needed. Counsel the patient appropriately. Patients with irritable bowel syndrome with gas, bloating, abdominal pain, constipation, and diarrhea have lactose deficiency. Restricting milk intake relieves symptoms.
Follow guidelines in Chapter 1 regarding safe, effective, informed posttest care.
• Related Tests That Influence Glucose Metabolism
C-PEPTIDE
C-peptide is formed during the conversion of proinsulin to insulin. Proinsulin is cleaved (holds α- and β-insulin chains together in the proinsulin molecule) into insulin and biologically inactive C-peptide. C-peptide assay provides distinction between exogenous and endogenous circulating insulin.
The main use of C-peptide is to evaluate hypoglycemia. C-peptide levels provide reliable indicators for pancreatic and secretory functions and insulin secretions. In a patient with type 1 diabetes mellitus, C-peptide measurements can be an index of insulin production and mark endogenous β-cell activity. C-peptide levels can also be used to confirm suspected surreptitious insulin injections (i.e., factitious hypoglycemia). Findings in these patients reveal that insulin levels are usually high, insulin antibodies may be high, but C-peptide levels are low or undetectable. This test also monitors the patient’s recovery after excision of an insulinoma. Rising C-peptide levels suggest insulinoma tumor recurrence or metastases.
Normal Findings
Fasting: 0.51 to 2.72 ng/mL or 0.17 to 0.90 mmol/L
Values vary with laboratory.
Procedure
Draw a 1-mL venous blood sample from a fasting patient using a red-topped chilled tube. Serum is needed for test. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Date and time must be correct. Centrifuge blood for 30 minutes. Follow standard precautions.
Separate the blood at 4°C and freeze if it will not be tested until later.
A sample for glucose testing is usually drawn at the same time.
Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place specimen in a biohazard bag.
Clinical Implications
Increased C-peptide values occur in the following conditions:
Endogenous hyperinsulinism (insulinemia)
Oral hypoglycemic drug ingestion
Pancreas or β-cell transplantation
Insulin-secreting neoplasms (islet cell tumor)
Type 2 diabetes mellitus (non-insulin-dependent)
Decreased C-peptide values occur in the following conditions:
Factitious hypoglycemia (surreptitious insulin administration)
Radical pancreatectomy
Type 1 diabetes mellitus
C-peptide stimulation test can determine the following:
Distinguish between type 1 and type 2 diabetes mellitus.
Identify patients with diabetes whose C-peptide stimulation values are >1.8 ng/mL (>0.59 nmol/L) who can be managed without insulin treatment.
Interfering Factors
Increased C-Peptide
Renal failure
Ingestion of sulfonylurea
CLINICAL ALERTTo differentiate insulinoma from factitious hypoglycemia, an insulin-to-C-peptide ratio can be performed.
<1.0 ratio: increased endogenous insulin secretion
>1.0 ratio: exogenous insulin
Interventions
Pretest Patient Care
Explain the test purpose and blood-drawing procedure. Obtain history of signs and symptoms of hypoglycemia.
Ensure that the patient fasts, except for water, for 8 to 12 hours before blood is drawn.
If a radioisotope test is necessary, it should take place after blood is drawn for C-peptide levels.
If the C-peptide stimulation test is done, give IV glucagon after a baseline value blood sample is drawn.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
GLUCAGON
Glucagon is a peptide hormone that originates in the α cells of the pancreatic islets of Langerhans. This hormone promotes glucose production in the liver. Normally, glucagon is a counterbalance to insulin. Glucagon provides a sensitive, coordinated control mechanism for glucose production and storage. For example, low blood glucose levels cause glucagon to stimulate glucose release into the bloodstream, whereas elevated blood glucose levels reduce the amount of circulating glucagon to about 50% of that found in the fasting state. The kidneys also affect glucagon metabolism. Elevated fasting glucagon levels in the presence of renal failure return to normal levels following successful renal transplantation. Abnormally high glucagon levels drop toward normal once insulin therapy effectively controls diabetes. However, when compared with a healthy person, glucagon secretion in the person with diabetes does not decrease after eating carbohydrates. Moreover, in healthy persons, arginine infusion causes increased glucagon secretion.
This test measures glucagon production and metabolism. A glucagon deficiency reflects pancreatic tissue loss. Failure of glucagon levels to rise during arginine infusion confirms glucagon deficiency. Hyperglucagonemia (i.e., elevated glucagon levels) occurs in diabetes, acute pancreatitis, and situations in which catecholamine secretion is stimulated (e.g., pheochromocytoma, infection).
Normal Findings
Adults: 20 to 100 pg/mL or 20 to 100 ng/L
Children: 0 to 148 pg/mL or 0 to 148 ng/L
Newborns: 0 to 1750 pg/mL or 0 to 1750 ng/L
Normal ranges vary with different laboratories.
CLINICAL ALERTDuring a GTT in healthy persons, glucagon levels will decline significantly compared with baseline fasting levels because normal hyperglycemia takes place during the first hour of testing.
Procedure
Draw a 5-mL blood sample from a fasting person into a chilled EDTA Vacutainer tube containing aprotinin (Trasylol) proteinase inhibitor. Special handling is required because glucagon is very prone to enzymatic degradation. Tubes used to draw blood must be chilled before the sample is collected and placed on ice afterward, and plasma must be frozen as soon as possible after centrifuging.
Observe standard precautions. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.
Clinical Implications
Increased glucagon levels are associated with the following conditions:
Acute pancreatitis (e.g., pancreatic α-cell tumor)
Diabetes mellitus: Persons with severe diabetic ketoacidosis are reported to have fasting glucagon levels five times normal despite marked hyperglycemia.
Glucagonoma (familial), which may be manifested by three different syndromes:
The first syndrome exhibits a characteristic skin rash, necrolytic migratory erythema, diabetes mellitus or IGT, weight loss, anemia, and venous thrombosis. This form usually shows elevated glucagon levels (>1000 pg/mL or >1000 ng/L) (diagnostic).
The second syndrome occurs with severe diabetes.
The third form is associated with multiple endocrine neoplasia syndrome and can show relatively lower glucagon levels as compared with the others.
Chronic renal failure
Hyperlipidemia
Stress (trauma, burns, surgery)
Uremia
Hepatic cirrhosis
Hyperosmolality
Acute pancreatitis
Hypoglycemia
Reduced levels of glucagon are associated with the following conditions:
Loss of pancreatic tissue
Pancreatic neoplasms
Pancreatectomy
Chronic pancreatitis
Cystic fibrosis
NOTE
After glucose load, there is no suppression of glucagon in patients with glucagonoma.
Interventions
Pretest Patient Care
Explain purpose of test and blood-drawing procedure. A minimum 8-hour fast (no calorie intake for at least 8 hours) is necessary before the test.
Promote relaxation in a low-stress environment; stress alters normal glucagon levels.
Do not administer radiopharmaceuticals within 1 week before the test.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal activities.
Review the test outcome and monitor for the three different syndromes of glucagonoma.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
INSULIN
Insulin, a hormone produced by the pancreatic β cells of the islets of Langerhans, regulates carbohydrate metabolism together with contributions from the liver, adipose tissue, and other target cells. Insulin is responsible for maintaining blood glucose levels at a constant level within a defined range. The rate of insulin secretion is primarily regulated by the level of blood glucose perfusing the pancreas; however, it can also be affected by hormones, the autonomic nervous system, and nutritional status.
Insulin levels are valuable for establishing the presence of an insulinoma (i.e., tumor of the islets of Langerhans). This test is also used for investigating the causes of fasting hypoglycemic states and neoplasm differentiation. The insulin study can be done in conjunction with a GTT or FBG test or a FPG test.
Normal Findings
Immunoreactive
Adults: 0 to 35 µIU/mL or 0 to 243 pmol/L
Children: 0 to 10 µIU/mL or 0 to 69 pmol/L
Free
Adults: 0 to 17 µIU/mL or 0 to 118 pmol/L
Children (prepubertal): 0 to 13 µIU/mL or 0 to 90 pmol/L
CLINICAL ALERTCritical range: >35 µIU/mL or >243 pmol/L (fasting)
Procedure
Obtain a 5-mL blood sample (red-topped tube) from a fasting (8 hours) person; serum is preferred. Observe standard precautions. Heparinized blood may be used.
If done in conjunction with a GTT, draw the specimens before administering oral glucose, at ingestion, and 120 minutes after glucose ingestion (the same times as the GTT).
Clinical Implications
Increased insulin values are associated with the following conditions:
Insulinoma (pancreatic islet tumor). Diagnosis is based on the following findings:
Hyperinsulinemia with hypoglycemia (glucose <30 mg/dL or <1.66 mmol/L)
Persistent hypoglycemia together with hyperinsulinemia (>20 µIU/mL or >139 pmol/L) after tolbutamide injection (rapid rise and rapid fall)
Failed C-peptide suppression with a PG level <30 mg/dL or <1.66 mmol/L and insulin/glucose ratio >0.3.
Type 2 diabetes mellitus, untreated
Acromegaly
Cushing’s syndrome
Endogenous administration of insulin (factitious hypoglycemia)
Obesity (most common cause)
Pancreatic islet cell hyperplasia
Decreased insulin values are found in the following conditions:
Type 1 diabetes mellitus, severe
Hypopituitarism
Interfering Factors
Surreptitious insulin or oral hypoglycemic agent ingestion or injection causes elevated insulin levels (with low C-peptide values).
Oral contraceptives and other drugs cause falsely elevated values.
Recently administered radioisotopes affect test results.
In the second to third trimester of pregnancy, there is a relative insulin resistance with a progressive decrease of PG and immunoreactive insulin.
Interventions
Pretest Patient Care
Explain test purpose and procedure.
Ensure that the patient fasts from all food and fluid, except water, unless otherwise directed.
Insulin release from an insulinoma may be erratic and unpredictable; therefore, it may be necessary for the patient to fast for as long as 72 hours before the test.
Follow guidelines in Chapter 1 regarding safe, effective, informed pretest care.
Posttest Patient Care
Have patient resume normal activity and diet.
Review test results; report and record findings. Modify the nursing care plan as needed. Obese patients may have insulin resistance and unusually high fasting and postprandial (after eating) insulin levels. Explain possible need for further testing and treatment.
Follow guidelines in Chapter 1 regarding safe, effective, informed posttest care.
CLINICAL ALERTA potentially fatal situation may exist if the insulinoma secretes unpredictably high levels of insulin. In this case, the blood glucose may drop to such dangerously low levels as to render the person comatose and unable to self-administer oral glucose forms. Patients and their families must learn how to deal with such an emergency and to be vigilant until the problem is treated.
END PRODUCTS OF METABOLISM AND OTHER TESTS
• Ammonia (NH3)
Ammonia, an end product of protein metabolism, is formed by bacteria acting on intestinal proteins together with glutamine hydrolysis in the kidneys. The liver normally removes most of this ammonia through the portal vein circulation and converts the ammonia to urea. Because any appreciable level of ammonia in the blood affects the body’s acid-base balance and brain function, its removal from the body is essential. The liver accomplishes this by synthesizing urea so that it can be excreted by the kidneys.
Blood ammonia levels are used to diagnose Reye’s syndrome, to evaluate metabolism, and to determine the progress of severe liver disease and its response to treatment. Blood ammonia measurements are useful in monitoring patients on hyperalimentation therapy.
Normal Findings
When Measured as NH3
Adults: 15 to 60 µg/dL or 11 to 35 µmol/L
10 days to 2 years: 70 to 135 µg/dL or 41 to 80 µmol/L
Birth to 10 days: 170 to 340 µg/dL or 100 to 200 µmol/L
When Measured as N
Adults: 15 to 45 µg/dL or 11 to 32 µmol/L
>1 month of age: 30 to 70 µg/dL or 21 to 50 µmol/L
Birth to 14 days: 80 to 130 µg/dL or 57 to 93 µmol/L
Values test somewhat higher in capillary blood samples. Values can vary with testing method used.
Procedure
Obtain a 5-mL venous plasma sample from a fasting patient. A green-topped (heparin) or purpletopped (EDTA) tube may be used. Observe standard precautions.
Place the sample in an iced container. The specimen must be centrifuged at 4°C. Promptly remove plasma from cells. Perform the test within 20 minutes or freeze plasma immediately.
Note all antibiotics the patient is receiving; these drugs lower ammonia levels.
Clinical Implications
Increased ammonia levels occur in the following conditions:
Reye’s syndrome (a potentially fatal disease associated with aspirin use secondary to viral infections primarily in children)
Liver disease, cirrhosis
Hepatic coma (does not reflect degree of coma)
GI hemorrhage
Renal disease
HHH syndrome: hyperornithinemia, hyperammonemia, homocitrullinuria
Transient hyperammonemia of newborn
Certain inborn errors of metabolism of urea except for argininosuccinic aciduria
GI tract infection with distention and stasis
Total parenteral nutrition
Ureterosigmoidostomy
Interfering Factors
Ammonia levels vary with protein intake and many drugs.
Exercise may cause an increase in ammonia levels.
Ammonia levels may be increased by use of a tight tourniquet or by tightly clenching the fist while samples are drawn.
Ammonia levels can rise rapidly in the blood tubes.
Hemolyzed blood gives falsely elevated levels.
Interventions
Pretest Patient Care
Explain test purpose and procedure. Instruct the patient to fast (if possible) for 8 hours before the blood test. Water is permitted.
Do not allow the patient to smoke for several hours before the test (raises levels).
Follow guidelines in Chapter 1 regarding safe, effective, informed pretest care.
Posttest Patient Care
Review test results; report and record findings. Modify the nursing care plan as needed. Begin treatment.
In patients with impaired liver function demonstrated by elevated ammonia levels, the blood ammonia level can be lowered by reduced protein intake and by use of antibiotics to reduce intestinal bacteria counts.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
CLINICAL ALERTAmmonia should be measured in all cases of unexplained lethargy and vomiting, in encephalitis, or in any neonate with unexplained neurologic deterioration.
• Bilirubin
Bilirubin results from the breakdown of hemoglobin in the RBCs and is a byproduct of hemolysis (i.e., RBC destruction). It is produced by the reticuloendothelial system. Removed from the body by the liver, which excretes it into the bile, bilirubin gives the bile its major pigmentation. Usually, a small amount of bilirubin is found in the serum. A rise in serum bilirubin levels occurs when there is excessive destruction of RBCs or when the liver is unable to excrete the normal amounts of bilirubin produced.
There are two major forms of bilirubin in the body: conjugated bilirubin and unconjugated bilirubin, sometimes termed direct and indirect bilirubin, respectively. Unconjugated bilirubin circulates freely in the blood until it reaches the liver, where it is conjugated with glucuronide transferase and then excreted into the bile. An increase in unconjugated bilirubin is more frequently associated with increased destruction of RBCs (hemolysis) as well as in neonatal jaundice. An increase in freeflowing bilirubin is more likely seen in dysfunction or blockage of the liver. A routine examination measures only the total bilirubin. A normal level of total bilirubin rules out any significant impairment of the excretory function of the liver or excessive hemolysis of red cells. Only when total bilirubin levels are elevated will there be a call for differentiation of the bilirubin levels by conjugated and unconjugated types.
The measurement of bilirubin allows evaluation of liver function and hemolytic anemias. For infants younger than 15 days of age, a neonatal, or more specifically an unconjugated, bilirubin measurement may be necessary.
Normal Findings
Adults
Total: 0.3 to 1.0 mg/dL or 5 to 17 µmol/L
Conjugated (direct): 0.0 to 0.2 mg/dL or 0.0 to 3.4 µmol/L
CLINICAL ALERTCritical Value for Bilirubin in Adults
12 mg/dL or >200 µmol/L
Procedure
Obtain a 5-mL nonhemolyzed sample (red-topped tube) from a fasting patient. Observe standard precautions. Serum is used.
Protect the sample from ultraviolet light (sunlight).
Avoid air bubbles and unnecessary shaking of the sample during blood collection.
If the specimen cannot be examined immediately, store it away from light and in a refrigerator.
Clinical Implications
Total bilirubin elevations accompanied by jaundice may be due to hepatic, obstructive, or hemolytic causes.
Hepatocellular jaundice results from injury or disease of the parenchymal cells of the liver and can be caused by the following conditions:
Viral hepatitis
Cirrhosis
Infectious mononucleosis
Reactions to certain drugs such as chlorpromazine (antipsychotic medication used to treat manic depression or schizophrenia)
Obstructive jaundice is usually the result of obstruction of the common bile or hepatic ducts due to stones or neoplasms. The obstruction produces high conjugated bilirubin levels due to bile regurgitation.
Hemolytic jaundice is due to overproduction of bilirubin resulting from hemolytic processes that produce high levels of unconjugated bilirubin. Hemolytic jaundice can be found in the following conditions:
After blood transfusions, especially those involving many units
Pernicious anemia
Sickle cell anemia
Transfusion reactions (ABO or Rh incompatibility)
Crigler-Najjar syndrome (a severe disease that results from a genetic deficiency of a hepatic enzyme needed for the conjugation of bilirubin)
Erythroblastosis fetalis (see Neonatal Bilirubin, Total and Fractionated [“Baby Bili”])
Miscellaneous diseases
Dubin-Johnson syndrome (autosomal recessive disorder resulting in an increase in the serum levels of conjugated bilirubin)
Gilbert’s disease (familial hyperbilirubinemia)
Nelson’s disease (with acute liver failure)
Pulmonary embolism/infarct
Congestive heart failure
Elevated indirect (unconjugated) bilirubin levels occur in the following conditions:
Neonatal jaundice
Hemolytic anemias due to a large hematoma
Trauma in the presence of a large hematoma
Hemorrhagic pulmonary infarcts
Crigler-Najjar syndrome (rare)
Gilbert’s disease (conjugated hyperbilirubinemia; rare)
Elevated direct (conjugated) bilirubin levels occur in the following conditions:
Cancer of the head of the pancreas
Choledocholithiasis
Dubin-Johnson syndrome
Interfering Factors
A 1-hour exposure of the specimen to sunlight or high-intensity artificial light at room temperature will decrease the bilirubin content.
No contrast media should be administered 24 hours before measurement; a high-fat meal may also cause decreased bilirubin levels by interfering with the chemical reactions.
Air bubbles and shaking of the specimen may cause decreased bilirubin levels.
Certain foods (e.g., carrots, yams) and drugs (see Appendix E) increase the yellow hue in the serum and can falsely increase bilirubin levels when tests are done using certain methods (e.g., spectrophotometry).
Prolonged fasting and anorexia raises the bilirubin level.
Nicotinic acid increases unconjugated bilirubin.
Interventions
Pretest Patient Care
Explain test purpose and procedure and relation of results to jaundice.
Ensure that the patient is fasting, if possible.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
NOTE
Excessive amounts of bilirubin eventually seep into the tissues, which assume a yellow hue as a result. This yellow color is a clinical sign of jaundice. In newborns, signs of jaundice may indicate hemolytic anemia or congenital icterus. Total bilirubin must be >2.5 mg/dL (>41.6 mmol/L) to detect jaundice in adults.
Posttest Patient Care
Review test results; report and record findings. Modify the nursing care plan as needed.
Have the patient resume normal activities.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
• Neonatal Bilirubin, Total and Fractionated (“Baby Bili”)
In newborns, signs of jaundice may indicate hemolytic anemia or congenital icterus. If bilirubin levels reach a critical point in the infant, damage to the CNS may occur in a condition known as kernicterus. Therefore, in these infants, the level of bilirubin is the deciding factor in whether or not to perform an exchange transfusion.
Neonatal bilirubin is used to monitor erythroblastosis fetalis (hemolytic disease of the newborn), which usually causes jaundice in the first 2 days of life. All other causes of neonatal jaundice, including physiologic jaundice, hematoma or hemorrhage, liver disease, and biliary disease, should also be monitored. Normal, full-term neonates experience a normal, neonatal, physiologic, transient hyperbilirubinemia by the 3rd day of life, which rapidly falls by the 5th to 10th day of life.
Normal Findings
Newborns (0 to 7 days)
Interpretation of newborn bilirubin concentrations should be done using a nomogram comparing the age of the infant in hours to the bilirubin concentration. This nomogram provides the risk for a subsequent bilirubin result to be consistent with hyperbilirubinemia. See Figure 6.2.
Cord Blood Total
Full term: <2.5 mg/dL or <43 µmol/L
Premature: <2.9 mg/dL or <50 µmol/L
CLINICAL ALERTCritical Value for Neonatal Bilirubin
>15 mg/dL or >256 µmol/L (mental retardation can occur)
 FIGURE 6.2. Nomogram for designation of risk in 2840 well newborns at 36 or more weeks’ gestational age with birth weight of 2000 g or more, or at 35 or more weeks’ gestational age and birth weight of 2500 g or more, based on the hour-specific serum bilirubin values. The serum bilirubin level was obtained before discharge, and the zone in which the value fell predicted the likelihood of a subsequent bilirubin level exceeding the 95th percentile (high-risk zone). (Used with permission from Bhutani VK, Johnson L, Sivieri EM: Predictive ability of a predischarge hour-specific serum bilirubin for subsequent significant hyperbilirubinemia in healthy term and near-term newborns. Pediatrics 103:6-14, 1999. Reprinted from American Academy of Pediatrics: Management of hyperbilirubinemia in the newborn infant 35 or more weeks of gestation. Pediatrics 114:297-316, 2004.) |
See Table 6.4 for a comparison of premature and full-term infants.
NOTE
The American Academy of Pediatrics recommends that total bilirubin values for normal-term newborns be assessed for risk for developing hyperbilirubinemia using the Bhutani nomogram (Fig. 6.2).
Procedure
Draw blood from heel of newborn using a capillary pipette and amber Microtainer tube; 0.5 mL of serum is needed. Cord blood may also be used.
Protect sample from light.
TABLE 6.4 Total Bilirubin Comparison | ||||||||||||||||||||||||||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|---|
| ||||||||||||||||||||||||||||||
Clinical Implications
Elevated total bilirubin (neonatal) is associated with the following conditions:
Erythroblastosis fetalis occurs as a result of blood group incompatibility between mother and fetus.
Rh (D) antibodies and other Rh factors
ABO antibodies
Other blood groups, including Kidd, Kell, and Duffy (see Chapter 8)
Galactosemia
Sepsis
Infectious diseases (e.g., syphilis, toxoplasmosis, cytomegalovirus)
RBC enzyme abnormalities
Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Pyruvate kinase (PK) deficiency
Spherocytosis (autohemolytic anemia causing the RBCs to become sphere-shaped and not the typical biconcave shape)
Subdural hematoma, hemangiomas
Elevated unconjugated (indirect) neonatal bilirubin is associated with the following conditions:
Erythroblastosis fetalis
Hypothyroidism
Crigler-Najjar syndrome
Obstructive jaundice
Infants of diabetic mothers
Elevated conjugated (direct) neonatal bilirubin is associated with the following conditions:
Biliary obstruction
Neonatal hepatitis
Sepsis
Interventions
Pretest Patient Care
Explain test purpose and procedure and its relation to jaundice to the mother.
See Chapter 1 guidelines for safe, informed, effective pretest care.
Posttest Patient Care
Review test results; report and record findings. Modify the nursing care plan as needed.
For slight elevations (i.e., <10.0 mg/dL or <170 µmol/L), phototherapy may be initiated.
Monitor neonatal bilirubin levels to determine indications for exchange transfusion. Tests should be done every 12 hours in jaundiced newborns. See Table 6.5 for exchange transfusion indications.
TABLE 6.5 Indications for Exchange Transfusion
Birth Weight (g)
Serum Bilirubin (mg/dL)
Serum Bilirubin (µmol/L)
<1000
10.0
170
1001-1250
13.0
222
1251-1500
15.0
256
1501-2000
17.0
291
2001-2500
18.0
309
>2500
20.0
>342
Transfuse at one step earlier in the presence of the following conditions:
Coombs’ test positive
Serum protein <5 g/dL
Metabolic acidosis (pH <7.25)
Respiratory distress (with O2 <50 mm Hg or 6.6 kPa)
Certain clinical findings (e.g., hypothermia, CNS or other clinical deterioration, sepsis, hemolysis)
Other criteria for exchange transfusion are suddenness and rate of bilirubin increase and when such an increase occurs; for example, an increase of 3 mg/dL (51 µmol/L) in 12 hours, especially after bilirubin has already leveled off, must be followed by frequent serial determinations, especially if it occurs on the first or seventh day of life rather than on the third day. Be cognizant of a rate of bilirubin increase of >1 mg/dL (>17 µmol/L) during the first day of life. Serum bilirubin of 10 mg/dL (170 µmol/L) after 24 hours or 15 mg/dL (256 µmol/L) after 48 hours despite phototherapy usually indicates that serum bilirubin will reach 20 mg/dL (342 µmol/L).
• Blood Urea Nitrogen (BUN, Urea Nitrogen)
Urea forms in the liver and, along with CO2, constitutes the final product of protein metabolism. The amount of excreted urea varies directly with dietary protein intake, increased excretion in fever, diabetes, and increased adrenal gland activity.
The test for blood urea nitrogen (BUN), which measures the nitrogen portion of urea, is used as an index of glomerular function in the production and excretion of urea. Rapid protein catabolism and impairment of kidney function will result in an elevated BUN level. The rate at which the BUN level rises is influenced by the degree of tissue necrosis, protein catabolism, and the rate at which the kidneys excrete the urea nitrogen. A markedly increased BUN is conclusive evidence of severe impaired glomerular function. In chronic renal disease, the BUN level correlates better with symptoms of uremia than does the serum creatinine.
Normal Findings
Adults: 6 to 20 mg/dL or 2.1 to 7.1 mmol/L
Older adults (>60 years): 8 to 23 mg/dL or 2.9 to 8.2 mmol/L
Children: 5 to 18 mg/dL or 1.8 to 6.4 mmol/L
CLINICAL ALERTCritical value for BUN is >100 mg/dL (>35 mmol/L).
Procedure
Obtain a 5-mL venous blood sample (red-topped tube). Serum is preferred.
Observe standard precautions.
Clinical Implications
Increased BUN levels (azotemia) occur in the following conditions:
Impaired renal function caused by the following conditions:
Congestive heart failure
Salt and water depletion
Shock
Stress
Acute MI
Chronic renal disease such as glomerulonephritis and pyelonephritis
Urinary tract obstruction
Hemorrhage into GI tract
Diabetes mellitus with ketoacidosis
Excessive protein intake or protein catabolism as occurs in burns or cancer
Anabolic steroid use
Decreased BUN levels are associated with the following conditions:
Liver failure (severe liver disease), such as that resulting from hepatitis, drugs, or poisoning
Acromegaly
Malnutrition, low-protein diets
Impaired absorption (celiac disease)
Nephrotic syndrome (occasional)
Syndrome of inappropriate antidiuretic hormone (SIADH)
Interfering Factors
A combination of a low-protein and high-carbohydrate diet can cause a decreased BUN level.
The BUN is normally lower in children and women because they have less muscle mass than adult men.
Decreased BUN values normally occur in late pregnancy because of increased plasma volume (physiologic hydremia).
Older persons may have an increased BUN when their kidneys are not able to concentrate urine adequately.
IV feedings only may result in overhydration and decreased BUN levels.
Many drugs may cause increased or decreased BUN levels.
Interventions
Pretest Patient Care
Explain test purpose and blood-drawing procedure. Assess dietary history.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Review test outcome and monitor as appropriate for impaired kidney function. Modify the nursing care plan as needed.
In patients with an elevated BUN level, fluid and electrolyte regulation may be impaired.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
CLINICAL ALERTIf a patient is confused, disoriented, or has convulsions, the BUN level should be checked. If the level is high, it may help to explain these signs and symptoms.
• Albumin
Albumin (along with total protein) is a part of a diverse microenvironment. Its primary function is the maintenance of colloidal osmotic pressure (COP) in the vascular and extravascular spaces (e.g., urine, cerebrospinal fluid, amniotic fluid). Albumin is a source of nutrition and a part of a complex buffer system. It is a “negative” acute-phase reactant. It decreases in response to acute inflammatory infectious processes.
Albumin is used to evaluate nutritional status, albumin loss in acute illness, liver disease and renal disease with proteinuria, hemorrhage, burns, exudates or leaks in the GI tract, and other chronic diseases. Hypoalbuminuria is an independent risk factor for older adults for mortality—admission serum albumin in geriatric patients is a predictor of outcome.
Normal Findings
Using Bromcresol Green Dye
Children: 3.8 to 5.4 g/dL or 38 to 54 g/L
Adults: 3.5 to 5.2 g/dL or 35 to 52 g/L
Older than age 40 years and in persons living in subtropics and tropics (secondary to parasitic infections), level slowly declines.
CLINICAL ALERTCritical Range
<1.5 g/dL or 15 g/L
Procedure
Obtain 5 mL of serum in a light green tube. Fasting is not necessary.
Centrifuge within 30 minutes of blood draw. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place specimen in a biohazard bag.
Observe standard procedures.
Urine specimens may also be collected (see Chapter 3).
Clinical Implications
Increased albumin is not associated with any naturally occurring condition. When albumin is increased, the only cause is decreased plasma water that increases the albumin proportionally: dehydration.
Decreased albumin is associated with the following conditions:
Acute and chronic inflammation and infections
Cirrhosis, liver disease, alcoholism
Nephrotic syndrome, renal disease (increased loss in urine)
Crohn’s disease, colitis
Congenital albuminemia
Burns, severe skin disease
Heart failure
Starvation, malnutrition, malabsorption, anorexia (decreased synthesis)
Thyroid diseases: Cushing’s disease, thyrotoxicosis
Interfering Factors
Albumin is decreased in:
Pregnancy (last trimester, owing to increased plasma volume)
Oral birth control (estrogens) and other drugs (see Appendix E)
Prolonged bed rest
IV fluids, rapid hydration, overhydration
CLINICAL ALERTLevels at 2.0-2.5 g/dL or 20-25 g/L may be the cause of edema.
Low levels occur with prolonged hospital stay.
Lipemic specimens with a high fat content interfere.
Interventions
Pretest Patient Care
Explain test purpose and specimen collection procedure. No fasting is required.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Review test results; report and record findings. Modify the nursing care plan as needed. Explain possible need for treatment (replacement therapy).
Low levels are associated with edema. Assess the patient for these signs and symptoms.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
Further tests may be indicated:
Total protein
Protein electrophoresis
24-Hour urine protein
• Prealbumin (PAB)
The proteins most often used in nutrition assessment include albumin, prealbumin (PAB), C-reactive protein, and retinol-binding protein. When used in combination, they can very accurately reflect a subclinical deficit and assess response to restorative therapy.
For years, albumin was the widely accepted marker for malnutrition. However, mounting evidence points to PAB as the better choice. Because albumin has a half-life of 21 days, it is slow to respond to a patient’s recent increase in nutrients and, therefore, is not a good indicator of recent changes in protein levels. In contrast, PAB responds more rapidly and gives a timelier picture of a change in dietary status. Because of its short half-life (2 days), PAB responds quickly to a decrease in nutritional intake and nutritional restoration. It reflects the current nutritional status within a patient’s body, not the status from 3 weeks ago.
Normal Findings
19 to 38 mg/dL (190 to 380 mg/L) by nephelometry
Procedure
Collect a 7-mL blood serum sample in a red-topped tube. Observe standard precautions.
Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag for transport to the laboratory.
Clinical Implications
Hospital laboratories, in conjunction with dietitians, administration, pharmacists, nurses, physicians, and other healthcare providers, may develop a clinical pathway that includes running a PAB upon admission of each surgical, ICU, and medical patient.
Values of 0 to 5, 5 to 10, and 10 to 15 mg/dL (0 to 50, 50 to 100, and 100 to 150 mg/L) indicate severe, moderate, and mild protein depletion, respectively.
Interventions
Pretest Patient Care
Explain test purpose. PAB is useful in assessing nutritional status, especially in monitoring the response to nutritional support in the acutely ill patient.
Follow guidelines in Chapter 1 regarding safe, effective, informed, pretest care.
Posttest Patient Care
Review test outcomes and determine the need for possible follow-up testing. Hospital protocol may require patients to be retested twice a week until discharge if their PAB level is less than 18 mg/dL (<180 mg/L). Possible treatment includes replacement and restorative therapy. Modify the nursing care plan as needed.
Follow guidelines in Chapter 1 regarding safe, effective, informed posttest care.
• Cholinesterase, Serum (Pseudocholinesterase); Cholinesterase, Red Blood Cell (Acetylcholinesterase)
The cholinesterase of serum is referred to as pseudocholinesterase to distinguish it from the true cholinesterase of the RBC. Both of these enzymes act on acetylcholine and other cholinesters. Alkylphosphates are potent inhibitors of both serum and RBC cholinesterase.
Patients who are homozygous for the atypical gene that controls serum cholinesterase activity have low levels of cholinesterase that are not inhibited by dibucaine. Persons with normal serum cholinesterase activity show 70% to 90% inhibition by dibucaine (an amino amide). The red cell (true cholinesterase) enzyme is specific for the substrate acetylcholine.
These are two separate tests. The primary use of serum cholinesterase measurement (pseudocholinesterase) is to monitor the effect of muscle relaxants (e.g., succinylcholine), which are used in surgery. Patients for whom suxamethonium anesthesia is planned should be tested using the dibucaine inhibition test for the presence of atypical cholinesterase variants that are incapable of hydrolyzing this widely used muscle relaxant.
The RBC cholinesterase test is used when poisoning by pesticides such as parathion or malathion is suspected. Severe insecticide poisoning causes headaches, visual distortions, nausea, vomiting, pulmonary edema, confusion, convulsions, respiratory paralysis, and coma.
Normal Findings
Acetylcholinesterase: 7 ± 3.8 (SD) U/g Hb or 2 ± 0.2 mU/mol Hb
Serum cholinesterase: 4.9 to 11.9 U/mL or 4.9 to 11.9 kU/L
Dibucaine inhibition: 79% to 84% or 0.79 to 0.84
Fluoride inhibition: 58% to 64% or 0.58 to 0.64
RBC cholinesterase: 30 to 40 U/g Hb
Values vary with substrate and method. These are two different tests. Values are low at birth and for the first 6 months of life.
Procedures
For serum cholinesterase, obtain a 5-mL blood sample; 3 mL of serum is needed. This is stable for 1 week at 39°F to 77°F or 4°C to 25°C. Observe standard precautions.
For RBC cholinesterase, draw a blood sample using sodium heparin as an anticoagulant; do not use serum. Observe standard precautions. This is stable for 1 week at 39°F to 77°F or 4°C to 25°C.
Clinical Implications
Decreased or no serum cholinesterase occurs in the following conditions:
Congenital inherited recessive disease. These patients are not able to hydrolyze drugs such as muscle relaxants used in surgery. These patients may have a prolonged period of apnea and may die if they are given succinylcholine.
Poisoning from organic phosphate insecticides
Liver diseases, hepatitis, cirrhosis with jaundice
Conditions that may have decreased blood albumin, such as malnutrition, anemia, infections, skin diseases, and acute MI
Congestive heart failure
Decreased RBC cholinesterase levels occur in the following conditions:
Congenital inherited recessive disease
Organic phosphate poisoning
Paroxysmal nocturnal hemoglobinemia
Megaloblastic anemia (returns to normal with therapy)
Increased serum cholinesterase is associated with:
Type IV hyperlipidemia
Nephrosis
Obesity
Diabetes
Increased RBC cholinesterase is associated with:
Reticulocytosis (increase in immature RBCs or reticulocytes)
Sickle cell anemia
Hemolytic anemias
Increased RBC cholinesterase in amniotic fluid, along with elevated α-fetoprotein (AFP), is presumptive evidence of open neural tube defect (not normally present in amniotic fluid).
Interventions
Pretest Patient Care
Explain test purpose and procedure.
Draw blood for serum cholinesterase 2 days before surgery.
Be aware that blood should not be drawn in the recovery room; prior administration of surgical drugs and anesthesia invalidates the test results.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Review test results; report and record findings. Modify the nursing care plan as needed.
Consider patients exhibiting <70% inhibition to have an atypical cholinesterase variant and be aware that the administration of succinylcholine or similar type drugs may pose a risk.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
CLINICAL ALERT
In industrial exposure, workers should not return to work until cholinesterase values rise to at least 75% of normal. RBC cholinesterase regenerates at the rate of 1% per day. Plasma cholinesterase regenerates at the rate of 25% in 7-10 d and returns to baseline in 4-6 wk.
Cholinesterase activity is completely and irreversibly inhibited by organophosphate pesticides.
• Creatinine and Estimated Glomerular Filtration Rate
Creatinine is a byproduct in the breakdown of muscle creatine phosphate resulting from energy metabolism. It is produced at a constant rate depending on the muscle mass of the person and is removed from the body by the kidneys. Production of creatinine is constant as long as muscle mass remains constant. A disorder of kidney function reduces excretion of creatinine, resulting in increased blood creatinine levels. Thus, creatinine levels give an approximation of the glomerular filtration rate (GFR).
An estimated GFR (eGFR) can be calculated using the Modification of Diet in Renal Disease (MDRD) study equation, which requires a serum creatinine result, gender, age, and race.
An estimated GFR (eGFR) can be calculated using the Modification of Diet in Renal Disease (MDRD) study equation, which requires a serum creatinine result, gender, age, and race.
eGFR (mL/min/1.73 m2) = 186 × (Scr)-1.154 × (age)-0.203 × (0.742 if female) × (1.210 if African American) (conventional units)
Many labs are reporting the eGFR with the creatinine result.
This test diagnoses impaired renal function. It is a more specific and sensitive indicator of kidney disease than BUN, although in chronic renal disease, both BUN and creatinine are ordered to evaluate renal problems because the BUN-to-creatinine ratio provides more information.
Normal Findings
Adult men: 0.9 to 1.3 mg/dL or 80 to 115 µmol/L
Adult women: 0.6 to 1.1 mg/dL or 53 to 97 µmol/L
Children (3 to 18 years): 0.5 to 1.0 mg/dL or 44 to 88 µmol/L
Young children (0 to 3 years): 0.3 to 0.7 mg/dL or 27 to 62 µmol/L
BUN-to-creatinine ratio: 10:1 to 20:1
CLINICAL ALERTCritical value is 10 mg/dL or 890 µmol/L in nondialysis patients.
Procedure
Obtain a 5-mL venous blood sample. Serum is preferred, but heparinized blood can be used. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.
Observe standard precautions.
Clinical Implications
Increased blood creatinine levels occur in the following conditions:
Impaired renal function
Chronic nephritis
Obstruction of urinary tract
Muscle disease
Gigantism
Acromegaly
Myasthenia gravis
Muscular dystrophy
Poliomyelitis
Congestive heart failure
Shock
Dehydration
Rhabdomyolysis (skeletal muscle tissue breakdown)
Hyperthyroidism
Decreased creatinine levels occur in the following conditions:
Small stature
Decreased muscle mass
Advanced and severe liver disease
Inadequate dietary protein
Pregnancy (0.4 to 0.6 mg/dL or 36 to 53 µmol/L is normal; >0.8 mg/dL or >71 µmol/L is abnormal and should be noted)
Increased ratio (>20:1) with normal creatinine occurs in the following conditions:
Increased BUN (prerenal azotemia), heart failure, salt depletion, dehydration
Catabolic states with tissue breakdown
GI hemorrhage
Impaired renal function plus excess protein intake, production, or tissue breakdown
Increased ratio (>20:1) with elevated creatinine occurs in the following conditions:
Obstruction of urinary tract
Prerenal azotemia with renal disease
Decreased ratio (<10:1) with decreased BUN occurs in the following conditions:
Acute tubular necrosis
Decreased urea synthesis as in severe liver disease or starvation
Repeated dialysis
SIADH
Pregnancy
Decreased ratio (<10:1) with increased creatinine occurs in the following conditions:
Phenacemide therapy (accelerates conversion of creatine to creatinine)
Rhabdomyolysis (releases muscle creatinine)
Muscular patients who develop renal failure
Interfering Factors
High levels of ascorbic acid and cephalosporin antibiotics can cause a falsely increased creatinine level; these agents also interfere with the BUN-to-creatinine ratio.
Drugs that influence kidney function plus other medications can cause a change in the blood creatinine level (see Appendix E).
A diet high in meat can cause increased creatinine levels.
Creatinine is falsely decreased by bilirubin, glucose, histidine, and quinidine compounds.
Ketoacidosis may increase serum creatinine substantially.
CLINICAL ALERTCreatinine level should always be checked before administering nephrotoxic chemotherapeutics such as methotrexate, cisplatin, cyclophosphamide, mithramycin, and semustine.
Interventions
Pretest Patient Care
Explain test purpose and procedure.
Assess diet for meat and protein intake.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Review test results and monitor as appropriate for impaired renal function. Modify nursing care plan as needed.
Possible treatment includes hemodialysis and renal replacement therapy, including kidney transplant.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
• Cystatin C
Cystatin C is a low-molecular-weight protein inhibitor found in blood serum and is an indicator of glomerular filtration in kidney function.
This test is done to assess GFR. Cystatin C may be a more reliable indicator of renal function than creatinine. Cystatin C is independent of muscle mass and age and is not reabsorbed in the kidney. Measurements of cystatin C are not as common as creatinine measurements.
Normal Findings
Young adults: <0.70 mg/mL (<2.9 µmol/mL)
Older adults (>60 years): <0.85 mg/mL (<3.5 µmol/mL)
NOTE
Cystatin C can be used to estimate the GFR:
GFR (mL/min/1.73 m2) = −4.32 + 80.35/cys C
Source: Hoek FJ, Kemperman FAW, Krediet RT: A comparison between cystatin C, plasma creatinine and the Cockcroft and Gault formula for the estimation of glomerular filtration rate. Nephrol Dial Transplant 18:2024-2031, 2003.
Procedure
No fasting is required.
Obtain a 5-mL venous blood sample (heparin or EDTA).
Clinical Implications
Cystatin C levels abnormally increase in association with impaired renal function and loss of kidney homeostasis, as in acute renal failure, chronic renal failure, diabetic nephropathy, and infections.
Interventions
Pretest Patient Care
Explain purpose and sampling procedure for cystatin C.
Assess for signs of abnormal kidney function (hypertension, pain, edema, uremia, disorders of urination, and urine composition). Some conditions have no symptoms of nephrotic syndrome.
Follow Chapter 1 guidelines for safe, effective, informed pretest care.
Posttest Patient Care
Review outcomes and provide the patient with support and counseling.
Explain follow-up testing and possible treatment for kidney disease.
See Chapter 1 guidelines for safe, effective, informed posttest care.
• Uric Acid
Uric acid is formed from the breakdown of nucleonic acids and is an end product of purine metabolism. Uric acid is transported by the plasma from the liver to the kidney, where it is filtered and where about 70% is excreted. The remainder of uric acid is excreted into the GI tract and degraded. A lack of the enzyme uricase allows this poorly soluble substance to accumulate in body fluids.
The basis for this test is that an overproduction of uric acids occurs when there is excessive cell breakdown and catabolism of nucleonic acids (as in gout), excessive production and destruction of cells (as in leukemia), or an inability to excrete the substance produced (as in renal failure). Measurement of uric acid is used most commonly in the evaluation of renal failure, gout, and leukemia. In hospitalized patients, renal failure is the most common cause of elevated uric acid levels, and gout is the least common cause.
Normal Findings
Men: 3.4 to 7.0 mg/dL or 202 to 416 µmol/L
Women: 2.4 to 6.0 mg/dL or 143 to 357 µmol/L
Children: 2.0 to 5.5 mg/dL or 119 to 327 µmol/L
Procedure
Obtain a 5-mL venous blood sample. Serum is preferred; heparinized blood is acceptable. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.
Observe standard precautions.
Clinical Implications
Elevated uric acid levels (hyperuricemia) occur in the following conditions:
Gout (the amount of increase is not directly related to the severity of the disease)
Renal diseases and renal failure, prerenal azotemia
Alcoholism (ethanol consumption)
Down syndrome
Lead poisoning
Leukemia, multiple myeloma, lymphoma
Lesch-Nyhan syndrome (hereditary gout)
Starvation, weight-loss diets
Metabolic acidosis, diabetic ketoacidosis
Toxemia of pregnancy (serial determination to follow therapy)
Liver disease
Hyperlipidemia, obesity
Hypoparathyroidism, hypothyroidism
Hemolytic anemia, sickle cell anemia
Following excessive cell destruction, as in chemotherapy and radiation treatment (acute elevation sometimes follows treatment)
Psoriasis
Glycogen storage disease (G6PD deficiency)
Decreased levels of uric acid occur in the following conditions:
Fanconi’s syndrome (disease of the proximal renal tubules)
Wilson’s disease (autosomal recessive disorder resulting in the accumulation of copper in tissues)
SIADH
Some malignancies (e.g., Hodgkin’s disease, multiple myeloma)
Xanthinuria (deficiency of xanthine oxidase)
Interfering Factors
Stress and strenuous exercise will falsely elevate uric acid.
Many drugs cause increase or decrease of uric acid (see Appendix E).
Purine-rich diet (e.g., liver, kidney, sweetbreads) increases uric acid levels.
High levels of aspirin decrease uric acid levels.
Low purine intake, coffee, and tea decrease uric acid levels.
Interventions
Pretest Patient Care
Advise the patient of test purpose and blood-drawing procedure; fasting is preferred.
Promote relaxation; avoid strenuous exercise.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal activities.
Review test results and monitor appropriately for renal failure, gout, or leukemia. Uric acid level should fall in patients who are treated with uricosuric drugs such as allopurinol, probenecid, and sulfinpyrazone. Modify the nursing care plan as needed.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
CLINICAL ALERT
Monitor uric acid levels during treatment of leukemia.
Acute, dangerous levels may occur following administration of cytotoxic drugs.
• Lead (Pb)
Lead is absorbed into the body through both the respiratory and GI tracts. It also moves transplacentally to the fetus. Absorption through these different routes varies and is affected by age, nutritional status, particle size, and chemical form of the lead. Absorption is inversely proportional to particle size; this factor makes lead-bearing dust important. Adults absorb 6% to 10% of dietary lead and retain very little of it; however, children from birth to 2 years of age have been shown to absorb 40% to 50% and to retain 20% to 25% of dietary lead. Spontaneous excretion of lead in urine by infants and young toddlers is normally about 1 µg/kg/24 hours, which may increase somewhat in cases of acute poisoning. Dietary intake of lead is <1 µg/kg of lead, which provides a margin of safety in the sense that a child goes into positive lead balance when intake exceeds 5 µg/kg of body weight. Early symptoms of lead poisoning include anorexia, apathy or irritability, fatigue, and anemia. Toxic effects include GI distress, joint pain, colic, headache, stupor, convulsions, and coma. Another, less sensitive test that may be used to evaluate lead intoxication is free erythrocyte protoporphyrin. However, a blood lead assay is the definitive test.
The blood lead assay is used to screen adults and children for lead poisoning (plumbism). In adults, high levels are caused mainly by industrial exposure to lead-based paints, gasoline, and ceramics. Highrisk children usually are ages 3 to 12 years and live in or visit old or dilapidated housing with lead-based paint. A single paint chip can contain as much as 10,000 µg of lead.
Normal Findings
Blood
0 to 10 µg/dL or 0 to 0.48 µmol/L
24-hour urine: <80 µg/L or <0.39 µmol/L
Hair
Adult: <155 µg/g dry weight or <0.75 µmol/g dry weight
Child: <70 µg/g dry weight or <0.34 µmol/g dry weight
CLINICAL ALERTCritical Values
<15 yr of age, >20 µg/dL or >0.97 µmol/L; ≥15 yr of age, >30 µg/dL or >1.45 µmol/L
Patients with blood lead concentrations >80 µg/dL or >3.86 µmol/L (panic value) should be hospitalized immediately and treated as a medical emergency.
A single lead determination cannot distinguish between chronic and acute exposure.
Procedure
Obtain a sample by finger stick using lead-free heparinized capillary tubes (capillary specimens are not considered diagnostic) or venous blood drawn in a 3-mL trace element-free tube. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a lead-free biohazard bag or container.
Do not separate plasma from cells. Refrigerate the sample.
24-Hour urine specimens can also be collected.
Hair may also be used.
Observe standard precautions.
Clinical Implications
Blood lead levels in adults
<10 µg/dL or <0.48 µmol/L: normal without occupational exposure
<20 µg/dL or <0.97 µmol/L: acceptable with occupational exposure
>40 µg/dL or >1.9 µmol/L: report to state occupational agency
>60 µg/dL or >2.9 µmol/L: remove from occupational exposure and begin chelation therapy
Interfering Factors
Failing to use lead-free Vacutainer tubes invalidates results.
An elevated level should be confirmed with a second specimen to ensure that the first specimen was not contaminated.
TABLE 6.6 U.S. Centers for Disease Control and Prevention Classifications of Blood Lead Levels | ||||||||||||||||||||||||
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TABLE 6.7 Effects of Increased Blood Lead Levels on Children | ||||||||||||||||||||
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CLINICAL ALERT
Following chelation therapy, lead levels are assessed at varying intervals, and it is not unusual to see a slight increase due to lead leaching from bones.
Pregnant women with blood lead level (BLL) >10 µg/dL or >0.48 µmol/L are at risk for delivering a child with a BLL also >10 µg/dL or >0.48 µmol/L.
Interventions
Pretest Patient Care
Explain test purpose and procedure.
Explain the importance of follow-up if lead levels are elevated.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal activities.
Review test results, counsel, and monitor appropriately for elevated lead levels. Explain chelation therapy and possible need for further testing, such as iron deficiency and blood protoporphyrins. Modify the nursing care plan as needed.
Parental compliance is necessary. Parent education about lead poisoning can be given face to face, by pamphlet distribution, or in both ways.
The most important component of medical management is to facilitate reduction in the child’s exposure to the environmental lead. In providing intervention for the child with an elevated blood lead level, the initial step is to obtain a detailed environmental history. The causes of childhood lead poisoning are multiple and must take into account potential environmental hazards as well as characteristics of the individual child. Once a child is found to have lead intoxication, all potential sources must be identified and removed from the child’s environment.
The recommended diet for a child with lead toxicity is simply a good diet with adequate protein and mineral intake and limitation of excess fat. It is no longer necessary to exclude canned foods and beverages when the cans are manufactured in the United States because the manufacture of cans with lead-soldered seams ended in the United States in 1991.
Iron deficiency can enhance absorption and toxicity of lead and often coexists with overexposure to lead. All children with a blood lead concentration >20 µg/dL or >0.97 µmol/L whole blood should have appropriate testing for iron deficiency.
In class IV lead intoxication, chelation is necessary. Chelation therapy must be done in conjunction with eliminating the source of the lead poisoning. Chelation therapy, when promptly administered, can be life-saving and can reduce the period of morbidity associated with lead toxicity.
Additional follow-up tests may be ordered, including free erythrocyte protoporphyrin, erythrocyte protoporphyrin, or zinc protoporphyrin.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
• Osteocalcin (Bone G1a Protein)
Osteocalcin, also referred to as bone G1a protein, is a protein produced by the osteoblasts and dentin and has a function in bone mineralization and calcium ion homeostasis. A small amount of osteocalcin, an integral part in bone formation, is released into the blood and therefore can serve as a marker for recent bone formation. Osteocalcin levels are influenced by age (rapid growth) and gender (males somewhat higher) and are increased during menopause. This test is used to screen for osteoporosis in postmenopausal women, assess risk for fractures, and determine eligibility for treatment for osteoporosis. The U.S. Preventive Task Force recommends screening for osteoporosis in women over the age of 65 years, and in women under age 65 years who have a risk of fracture that is equal to or greater than that of a 65-year-old white woman. Screening is not recommended for men. Osteocalcin is a specific marker for bone formation and is regulated by 1,25-dehydroxyvitamin D.
Normal Findings
Osteocalcin: 8.1 ± 4.6 µg/L or 1.4 ± 0.8 nmol/L
Carboxylated osteocalcin: 9.9 ± 0.5 µg/L or 1.7 ± 0.1 nmol/L
Undercarboxylated osteocalcin: 3.7 ± 1.0 µg/L or 0.6 ± 0.2 nmol/L
Normal Using RIA
Adult male: 3.0 to 13.0 ng/mL or 3.0 to 13.0 µg/L
Premenopausal female: 0.4 to 8.2 ng/mL or 0.4 to 8.2 µg/L
Postmenopausal female: 1.5 to 11.0 ng/mL or 1.5 to 11.0 µg/L
There is a diurnal variation, a peak during the night and a decrease in the morning.
Procedure
Collect a venous blood sample of serum on ice, separate within 1 hour, and immediately freeze. Avoid a freeze-thaw cycle.
Interfering Factors
Increased during bed rest and no increase in bone formation.
Increased with impaired renal function and no increase in bone formation.
Clinical Implications
Abnormally increased levels indicate increased bone formation in persons with hyperparathyroidism, fractures, and acromegaly.
Decreased levels are associated with hypoparathyroidism, a deficiency of growth hormone, and medications such as glucocorticoids, bisphosphonates, and calcitonin.
Interventions
Pretest Patient Care
Explain purpose and procedure of test. Record age and menopausal state. Tell the patient that the risk for osteoporosis increases steadily with age. Also, obtain pertinent personal and family history of osteoporotic fractures, history of falls, and so forth.
Follow Chapter 1 guideline for safe, effective, informed pretest care.
Posttest Patient Care
Review test outcomes, report and record findings, and counsel regarding further tests (e.g., dualenergy x-ray absorptiometry [DXA], bone density of the femoral neck, or quantitative ultrasound) and possible treatment (e.g., medical: alendronate, raloxifene). Sixteen percent of postmenopausal women will be found to have lumbar spine osteoporosis. Other blood test markers of bone resorption include pyridinolines, telopeptides, acid phosphatase, and urine tests of hydroxyproline and galactosyl hydroxylysine. These markers are known as collagen crosslinks. Modify the nursing care plan as needed.
See Chapter 1 for safe, effective, informed posttest care.
HORMONE TESTS
• Androstenedione
Androstenedione is one of the major androgens produced by the ovaries in females and, to a lesser extent, in the adrenal gland in both genders. This hormone is converted to estrogens by hepatic enzymes. Levels rise sharply after puberty and peak at age 20 years.
This hormone measurement is helpful in the evaluation of conditions characterized by hirsutism (excessive hair growth in women) and virilization. In females, there is poor correlation of plasma levels with clinical severity.
Normal Findings
Newborns: 20 to 290 ng/dL or 0.7 to 10.1 mmol/L
Prepuberty: 8 to 50 ng/dL or 0.3 to 1.7 mmol/L
Women: 75 to 205 ng/dL or 2.6 to 7.2 mmol/L
Men: 85 to 275 ng/dL or 3.0 to 9.6 mmol/L
Postmenopausal women: <10 ng/dL or 0.35 mmol/L (abrupt decline at menopause)
Different laboratories may have variation in reference values.
Procedure
Obtain a 5-mL venous blood sample in the morning and place on ice. Serum or EDTA can be used. Observe standard precautions. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place specimen in a biohazard bag.
In women, collect this specimen 1 week before or after the menstrual period. Record date of last menstrual period on the laboratory form.
Clinical Implications
Increased androstenedione values are associated with the following conditions:
Polycystic ovary syndrome (Stein-Leventhal syndrome)
Cushing’s syndrome
Atypical ovarian tumors
Ectopic ACTH-producing tumor
Late-onset congenital adrenal hyperplasia
Ovarian stromal hyperplasia
Osteoporosis in females
Decreased androstenedione values are found in the following conditions:
Sickle cell anemia
Adrenal and ovarian failure
CLINICAL ALERT>1000 ng/dL or >34.9 mmol/L (suggests virilizing tumor)
Interventions
Pretest Patient Care
Explain purpose of test and blood-drawing procedure. Obtain pertinent history of signs and symptoms (e.g., excessive hair growth and infertility).
Ensure that the patient is fasting and that blood is drawn at peak production (7:00 a.m. or 0700 hours). Lowest levels are at 4:00 p.m. or 1600 hours.
Collect specimen 1 week before menstrual period in women.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal activities.
Review test results; report and record findings. Modify the nursing care plan as needed. Counsel appropriately for ovarian and adrenal dysfunction.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
• Aldosterone
Aldosterone is a mineralocorticoid hormone produced in the adrenal zona glomerulosa under complex control by the renin-angiotensin system. Its action is on the renal distal tubule, where it increases resorption of sodium and water at the expense of increased potassium excretion.
This test is useful in detecting primary or secondary aldosteronism (also called hyperaldosteronism). Patients with primary aldosteronism characteristically have hypertension, muscular pains and cramps, weakness, tetany, paralysis, and polyuria. This test is also used to evaluate causes of hypertension or low blood potassium levels and to check for adrenal tumors.
NOTE
A random aldosterone test is of no diagnostic value unless a plasma renin activity is performed at the same time.
Normal Findings
In Upright Position
Adults: 7 to 30 ng/dL or 0.19 to 0.83 nmol/L
Adolescents: 4 to 48 ng/dL or 0.11 to 1.33 nmol/L
Children: 5 to 80 mg/dL or 0.14 to 2.22 nmol/L
In Supine Position
Adults: 3 to 16 ng/dL or 0.08 to 0.44 nmol/L
Adolescents: 2 to 22 ng/dL or 0.06 to 0.61 nmol/L
Children: 3 to 35 mg/dL or 0.08 to 0.97 nmol/L
Low-sodium diet: values 3 to 5 times higher
Procedure
Take plasma with the patient in an upright position for 2 hours and with normal salt intake.
Obtain a 5-mL venous blood specimen in a heparinized or EDTA Vacutainer tube. Serum, EDTA, or heparinized blood may be used. The cells must be separated from plasma immediately. Blood should be drawn with the patient sitting. Observe standard precautions. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered.
Specify patient position (upright or supine) and record the site and time of the venipuncture. Circadian rhythm exists in normal subjects, with levels of aldosterone peaking in the morning. Specify if the blood has been drawn from the adrenal vein (values are much higher: 200 to 800 ng/dL or 5.5 to 22.6 nmol/L).
A 24-hour urine specimen with boric acid preservative may also be ordered. Refrigerate immediately following collection.
Have the patient follow a normal sodium diet 2 to 4 weeks before the test.
Clinical Implications
Elevated levels of aldosterone (primary aldosteronism) occur in the following conditions:
Aldosterone-producing adenoma (Conn’s disease)
Adrenocortical hyperplasia (pseudoprimary aldosteronism)
Indeterminate hyperaldosteronism
Glucocorticoid remediable hyperaldosteronism
Secondary aldosteronism, in which aldosterone output is elevated because of external stimuli or greater activity in the renin-angiotensin system, occurs in the following conditions:
Renovascular hypertension
Salt depletion
Potassium loading
Laxative abuse
Cardiac failure
Cirrhosis of liver with ascites
Nephrotic syndrome
Bartter’s syndrome
Diuretic abuse
Hypovolemia and hemorrhage
After 10 days of starvation
Toxemia of pregnancy
Decreased aldosterone levels are found in the following conditions:
Aldosterone deficiency
Primary adrenal insufficiency (e.g., Addison’s disease). Aldosterone is usually not affected in secondary adrenal insufficiency (hypopituitarism with decreased pituitary ACTH production) because the renin-angiotensin system is still intact.
Syndrome of renin deficiency (very rare)
Low aldosterone levels associated with hypertension are found in Turner’s syndrome, diabetes mellitus, and alcohol intoxication.
Interfering Factors
Values are increased by upright posture.
Recently administered radioactive medications affect test outcomes.
Heparin therapy causes levels to fall. See Appendix E for drugs that increase or decrease levels.
Thermal stress, late pregnancy, and starvation cause levels to rise.
Aldosterone levels decrease with age.
Many drugs—diuretics, antihypertensives, progestogens, estrogens—and licorice should be terminated 2 to 4 weeks before test.
CLINICAL ALERT
The simultaneous measurement of aldosterone and renin is helpful in differentiating primary from secondary hyperaldosteronism. Renin levels are high in secondary aldosteronism and low in primary aldosteronism.
Potassium deficiencies should be corrected before testing for aldosterone.
Interventions
Pretest Patient Care
Explain test purpose and procedures. Assess for history of diuretic or laxative abuse. If 24-hour urine specimen is required, follow protocols in Chapter 3.
Discontinue diuretic agents, progestational agents, estrogens, and black licorice for 2 weeks before the test.
Ensure that the patient’s diet for 2 weeks before the test is normal (other than the previously listed restrictions) and includes 3 g/day (135 mEq/L/day) of sodium. Check with your laboratory for special protocols.
Follow guidelines in Chapter 1 for safe, effective, informed pretest care.
Posttest Patient Care
Have the patient resume normal activities and diet.
Review test results and monitor appropriately for aldosteronism and aldosterone deficiency. Report and record findings. Modify the nursing care plan as needed.
Follow guidelines in Chapter 1 for safe, effective, informed posttest care.
• Antidiuretic Hormone (ADH); Arginine Vasopressin Hormone
Antidiuretic hormone (ADH) is secreted by the posterior pituitary gland. Its major physiologic function is regulation of body water. In the dehydrated (hyperosmolar) state, ADH release results in decreased urine excretion and conservation of water. ADH increases blood pressure.
When ADH activity is present, small volumes of concentrated urine are excreted. When ADH is absent, large amounts of diluted urine are produced. Higher secretion occurs at night, with erect posture, and with pain, stress, or exercise. Measurement of the level of ADH is useful in the differential diagnosis of polyuric and hyponatremic states. ADH testing aids in diagnosis of urine concentration disorders, especially diabetes insipidus, SIADH, psychogenic water intoxication, and syndromes of ectopic ADH production.
Normal Findings
<2.5 pg/mL or <2.3 pmol/L
Procedure
Draw venous blood samples, 5 mL, into prechilled tubes and put on ice. Plasma with EDTA anticoagulant is needed. Observe standard precautions. Label the specimen with the patient’s name, date and time of collection, and test(s) ordered. Place the specimen in a biohazard bag.
Ensure that the patient is in a sitting position and calm during blood collection.
Clinical Implications
Increased secretion of ADH is associated with the following conditions:
SIADH (with respect to plasma osmolality)
Ectopic ADH production (systemic neoplasm)
Nephrogenic diabetes insipidus
Acute intermittent porphyria
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