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ROUTINE BLOOD TESTINGMany diagnostic and laboratory tests include the direction to perform routine blood testing and/or routine urine testing. The protocol for those tests is presented here and will be cross-referenced within the many tests requiring them.Before Explain the procedure to the patient. Tell the patient if fasting is necessary. (Fasting is most commonly required with glucose and lipid studies.) If fasting is required, instruct the patient not to consume any food or fluids. Only water is permitted. Fasting requirements usually vary from 8 to 12 hours. Instruct the patient to continue taking medications unless told otherwise by the healthcare provider.During• Collect the blood in a properly color-coded test tube (Table A, page xiv), which indicates the presence or absence of additives. Tube stopper colors may vary with different manufacturers. If uncertain, verify with the laboratory.After• Apply pressure or a pressure dressing to the venipuncture site.• Assess the site for bleeding. = Patient teachingROUTINE URINE TESTINGMany diagnostic and laboratory tests include the direction to perform routine blood testing and/or routine urine testing. The protocol for those tests is presented here and will be cross-referenced within the many tests requiring them.Before Explain the procedure to the patient. Inform the patient if food or fluid restrictions are needed.DuringRandom, fresh, or spot specimen:• Instruct the patient to urinate into an appropriate non-sterile container.24-hour specimen:1. Begin the 24-hour collection by discarding the first specimen.2. Collect all urine voided during the next 24 hours.3. Show the patient where to store the urine.4. Keep the urine on ice or refrigerated during the collection period. Foley bags are kept in a basin of ice. Some collec-tions require a preservative. Check with the laboratory.5. Post the hours for the urine collection in a prominent place to prevent accidentally discarding a specimen.6. Instruct the patient to void before defecating so that urine is not contaminated by stool.7. Remind the patient not to put toilet paper in the urine collection container.8. Collect the last specimen as close as possible to the end of the 24-hour period. Add this urine to the collection.After• Transport the specimen promptly to the laboratory. = Patient teachingMOSBY’SDIAGNOSTIC AND LABORATORY TEST REFERENCETwelfth Edit ionKathleen Deska Pagana, PhD, RNProfessor Emeritus Department of Nursing Lycoming College Williamsport, Pennsylvania http://www.KathleenPagana.com President, Pagana Keynotes & PresentationsTimothy J. Pagana, MD, FACSMedical Director The Kathryn Candor Lundy Breast Health Center Susquehanna Health System Williamsport, PennsylvaniaTheresa Noel Pagana, MD, FAAEMEmergency Medicine Physician Virtua Voorhees Hospital Voorhees, New Jerseyhttp://www.KathleenPagana.com3251 Riverport LaneSt. Louis, Missouri 63043MOSBY’S DIAGNOSTIC AND LABORATORY TEST REFERENCE, ISBN: 978-0-323-22576-2TWELFTH EDITIONCopyright © 2015, 2013 by Mosby, an imprint of Elsevier Inc.Copyright © 2011, 2009, 2007, 2005, 2003, 2001, 1999, 1997, 1995, 1992 by Mosby, Inc., an affiliate of Elsevier Inc. All rights reserved. No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be noted herein).ISBN: 978-0-323-22576-2Content Strategist: Jamie RandallContent Development Manager: Jean Sims FornangoPublishing Services Manager: Hemamalini RajendrababuProject Manager: Manchu MohanDesigner: Karen Pauls/Renee DuenowPrinted in the United States of AmericaLast digit is the print number: 9 8 7 6 5 4 3 2 1NoticeKnowledge and best practice in this field are constantly changing. As new research and experience broaden our understanding, changes in research methods, professional practices, or medical treatment may become necessary.Practitioners and researchers must always rely on their own experience and knowledge in evaluating and using any information, methods, compounds, or experiments described herein. In using such information or methods they should be mindful of their own safety and the safety of others, including parties for whom they have a professional responsibility.With respect to any drug or pharmaceutical products identified, readers are advised to check the most current information provided (i) on procedures featured or (ii) by the manufacturer of each product to be administered, to verify the recommended dose or formula, the method and duration of administration, and contraindications. It is the responsibility of practitioners, relying on their own experience and knowledge of their patients, to make diagnoses, to determine dosages and the best treatment for each individual patient, and to take all appropriate safety precautions.To the fullest extent of the law, neither the Publisher nor the authors, contributors, or editors assume any liability for any injury and/or damage to persons or property as a matter of products liability, negligence or otherwise, or from any use or operation of any methods, products, instructions, or ideas contained in the material herein.http://www.elsevier.com/permissionsWith love and adoration, we dedicate this book to our grandchildren:Ella Marie GaulJocelyn Elizabeth GaulTimothy William GaulJustin Aquinas GaulJuliana Kathleen PericciLuke Michael PericciJohn Henry Bullen, VivreviewersCrystal Botkin, MPH, CNMT, PETAssistant Professor and Clinical Coordinator Nuclear Medicine Technology Program Doisy College of Health Sciences Saint Louis University St. Louis, MissouriNoelle C. Bowdler, MDClinical Professor of Obstetrics and Gynecology University of Iowa Hospitals and Clinics Iowa City, IowaEileen M. Burd, PhD, D(ABMM)Director, Clinical Microbiology Emory University Atlanta, GADisaya Chavalitdhamrong, MDDivision of Gastroenterology, Hepatology and Nutrition Department of Medicine University of Florida Gainesville, FloridaLaurence M. Demers, PhD, DSc, DABCC, FACBDistinguished Professor Emeritus, Pathology and Medicine M.S. Hershey Medical Center Pennsylvania State University Hershey, PennsylvaniaSandra C. Hollensead, MDEmerita Professor of Pathology and Laboratory Medicine School of Medicine University of Louisville Louisville, KentuckyFrederick L. Kiechle, MD, PhDMedical Director, Clinical Pathology Pathology Consultants of South Broward Memorial Healthcare System Hollywood, Floridareviewers vChuany Mark Lu, MD, PhDProfessor of Laboratory Medicine University of California Chief, Hematology and Hematopathology/Laboratory Medicine Service Veterans Affairs Medical Center San Francisco, CaliforniaAlexander J. McAdam, MD, PhDAssociate Professor of Pathology Harvard Medical School Boston, MassachusettsRavinder Jit Singh, PhDDirector of Endocrine Laboratory Mayo Clinic Rochester, Minnesotavi prefaceThe 12th edition of Mosby’s Diagnostic and Laboratory Test Reference provides the user with an up-to-date, essential refer-ence that allows easy access to clinically relevant laboratory and diagnostic tests. A unique feature of this handbook is its consis-tent format, which allows for quick reference without sacrificing the depth of detail necessary for a thorough understanding of diagnostic and laboratory testing.deficiency, or hormonal hypertension due to increased mineralocorticoids. adrenal steroid precursors 19AA milder, non-classic form of CAH is characterized by premature puberty, acne, hirsutism, menstrual irregularity, and infertility.These same precursors can occur in adults due to adrenal or gonadal tumors. Patients with polycystic ovary syndrome (Stein-Leventhal syndrome) have particularly elevated levels of ADs. DHEA S levels are particularly high in patients with adrenal carcinoma.In patients suspected of CAH, testing for a panel of steroids involved in the cortisol biosynthesis pathway may be performed to establish the specific enzyme deficiency. In most cases, basal concentrations within the normal reference interval rule out CAH. The ratio of the precursor to the final pathway product (with and without ACTH stimulation) may be used to diagnose which enzyme is deficient.Interfering factors• A radioactive scan performed 1 week before the test may invalidate the test results if radioimmunoassay is performed. Drugs that may increase levels of ADs include clomiphene, corticotropin, and metyrapone. Drugs that may decrease levels of ADs include steroids.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: serum separator or red Tell the female patient that the specimen should be collected 1 week before or after the menstrual period.• Indicate the date of the last menstrual period (if applicable) on the laboratory form.Abnormal findings Increased levels Decreased levelsAdrenal tumor Gonadal failureCongenital adrenal hyperplasiaEctopic ACTH-producing tumorsCushing syndrome (some cases)Primary or secondary adrenal insufficiencyStein-Leventhal syndrome Ovarian sex cord tumor notes20 age-related macular degeneration risk analysisage-related macular degeneration risk analysis (ARMD risk analysis, Y402H, and A69S)Type of test BloodNormal findings No mutation notedTest explanation and related physiologyAge-related macular degeneration (ARMD) is recognized as a leading cause of blindness in the United States. Blurred or distorted vision and difficulty adjusting to dim light are com-mon symptoms. ARMD, both wet and dry types, is considered a multifactorial disorder because it is thought to develop due to interplay between environmental (smoking) and genetic (gen-der, ethnicity) risk and protective (antioxidants) factors. At least two genetic variants (Y402H and A69S) have been found to be associated with an increased risk for ARMD. The Y402H and the A69S genetic variants are common polymorphisms in ARMD. An individual with two copies of the Y402H variant in the gene CFH and two copies of the A69S variant in the gene LOC387715 has an approximately sixtyfold increased risk for ARMD. This is significant, given how common ARMD is in the general population.This information can be clinically useful when making medi-cal management decisions (for example, the use of inflammatory markers) and emphasizing to patients the benefits of smoking cessation and dietary modification. In some cases, genotype information may also assist with clinical diagnosis.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: lavender or yellow Tell the patient that results may not be available for a few weeks.Abnormal findingsIncreased risk of ARMDnotesalanine aminotransferase 21Aalanine aminotransferase (ALT, formerly Serum glutamic-pyruvic transaminase [SGPT])Type of test BloodNormal findingsAdult/child: 4-36 units/L at 37 ° C, or 4-36 units/L (SI units)Elderly: may be slightly higher than adultInfant: may be twice as high as adultTest explanation and related physiologyALT is found predominantly in the liver; lesser quantities are found in the kidneys, heart, and skeletal muscles. Injury or dis-ease affecting the liver parenchyma causes a release of this hepa-tocellular enzyme into the bloodstream, thus elevating serum ALT levels. Generally, most ALT elevations are caused by liver disease. Therefore, this enzyme is not only sensitive but also very specific in indicating hepatocellular disease. In hepatocellular disease other than viral hepatitis, the ALT/AST ratio (DeRitis ratio) is less than 1. In viral hepatitis, the ratio is greater than 1. This is helpful in the diagnosis of viral hepatitis.Interfering factors• Previous IM injections may cause elevated levels. Drugs that may cause increased ALT levels include acetamino-phen, allopurinol, aminosalicylic acid (PAS), ampicillin, aza-thioprine, carbamazepine, cephalosporins, chlordiazepoxide, chlorpropamide, clofibrate, cloxacillin, codeine, dicumarol, indomethacin, isoniazid (INH), methotrexate, methyldopa, nafcillin, nalidixic acid, nitrofurantoin, oral contraceptives, oxacillin, phenothiazines, phenylbutazone, phenytoin, pro-cainamide, propoxyphene, propranolol, quinidine, salicylates, tetracyclines, and verapamil.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: red• Patients with liver dysfunction often have prolonged clotting times.22 alanine aminotransferaseAbnormal findings Increased levelsHepatitisHepatic necrosisHepatic ischemiaCirrhosisCholestasisHepatic tumorHepatotoxic drugsObstructive jaundiceSevere burnsTrauma to striated muscleMyositisPancreatitisMyocardial infarctionInfectious mononucleosisShocknotesaldolase 23AaldolaseType of test BloodNormal findingsAdult: 3-8.2 Sibley-Lehninger units/dL or 22-59 mU/L at 37 ° C (SI units)Child: approximately two times the adult valuesNewborn: approximately four times the adult valuesTest explanation and related physiologySerum aldolase is very similar to the enzymes aspartate amino- transferase AST (SGOT) (see p. 129) and CPK (see p. 308). Aldolase is an enzyme used in glycolysis (breakdown of glucose). As with AST and creatine phosphokinase, aldolase exists through-out the body in most tissues. This test is most useful for indi-cating muscular or hepatic cellular injury or disease. The serum aldolase level is very high in patients with muscular dystrophies, dermatomyositis, and polymyositis. Levels also are increased in patients with gangrenous processes, muscular trauma, and mus-cular infectious diseases (e.g., trichinosis). Elevated levels are also noted in chronic hepatitis, obstructive jaundice, and cirrhosis.Neurologic diseases causing weakness can be differentiated from muscular causes of weakness with this test. Normal values are seen in patients with such neurologic diseases as poliomyeli-tis, myasthenia gravis, and multiple sclerosis. Elevated aldolase levels are seen in the primary muscular disorders.Interfering factors• Previous IM injections may cause elevated levels.• Strenuous exercise can cause a transient spike in aldolase. Drugs that may cause increased aldolase levels include hepato-toxic agents. Drugs that may cause decreased aldolase levels include phenothiazines.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: verify with lab• Blood tube commonly used: red24 aldolaseAbnormal findings Increased levels Decreased levelsHepatocellular diseases (e.g., hepatitis)Late muscular dystrophyMuscular diseases (e.g., muscular dystrophy, dermatomyositis, and polymyositis)Hereditary fructose intoleranceMuscle-wasting diseaseMuscular trauma (e.g., severe crush injuries)Muscular infections (e.g., trichinosis) Gangrenous processes (e.g., gangrene of the bowel) Myocardial infarction notesaldosterone 25AaldosteroneType of test Blood; urine (24-hour)Normal findingsBloodSupine: 3-10 ng/dL or 0.08-0.30 nmol/L (SI units)Upright:Female: 5-30 ng/dL or 0.14-0.80 nmol/L (SI units)Male: 6-22 ng/dL or 0.17-0.61 nmol/L(SI units)Child/adolescent:Newborn: 5-60 ng/dL1 week-1 year: 1-160 ng/dL 5-7 years: 5-50 ng/dL1-3 years: 5-60 ng/dL 7-11 years: 5-70 ng/dL3-5 years: 5-80 ng/dL 11-15 years: 5-50 ng/dLUrine (24-hour)2-26 mcg/24 hr or 6-72 nmol/24 hr (SI units)Test explanation and related physiologyThis test is used to diagnose hyperaldosteronism. Production of aldosterone, a hormone produced by the adrenal cortex, is regulated primarily by the renin-angiotensin system. Secondarily, aldosterone is stimulated by ACTH, low serum sodium levels, and high serum potassium levels. Aldosterone in turn stimu-lates the renal tubules to absorb sodium (water follows) and to secrete potassium into the urine. In this way, aldosterone regu-lates serum sodium and potassium levels. Because water follows sodium transport, aldosterone also partially regulates water absorption (and plasma volume).Increased aldosterone levels are associated with primary al -dosteronism, in which a tumor (usually an adenoma) of the adrenal cortex (Conn syndrome) or bilateral adrenal nodular hyperplasia causes increased production of aldosterone. Patients with primary aldosteronism characteristically have hypertension, weakness, polyuria, and hypokalemia.Increased aldosterone levels also occur with secondary al dosteronism caused by nonadrenal conditions. These include the following:• Renal vascular stenosis or occlusion• Hyponatremia (from diuretic or laxative abuse) or low salt intake• Hypovolemia• Pregnancy or use of estrogens26 aldosterone• Malignant hypertension• Potassium loading• Edematous states (e.g., congestive heart failure, cirrhosis, nephrotic syndrome)The aldosterone assay can be done on a 24-hour urine speci-men or a plasma blood sample. The advantage of the 24-hour urine sample is that short-term fluctuations are eliminated. Plasma values are more convenient to sample, but they are affected by the short-term fluctuations.Primary aldosteronism can be diagnosed by demonstrating very little to no rise in serum renin levels after an aldosterone stimulation test (using salt restriction as the stimulant). This is because aldosterone is already maximally secreted by the patho-logic adrenal gland. Failure to suppress aldosterone with saline infusion (1.5 to 2 L of NSS infused between 8 am and 10 am, called an aldosterone suppression test) is further evidence of pri-mary aldosteronism. Aldosterone can also be measured in blood obtained from adrenal venous sampling.Interfering factors• Strenuous exercise and stress can stimulate adrenocortical secretions and increase aldosterone levels.• Excessive licorice ingestion can cause decreased levels because it produces an aldosterone-like effect.• Values are influenced by posture, position, diet, diurnal varia-tion, and pregnancy.• If the test is performed using radioimmunoassay, recently administered radioactive medications will affect test results. Drugs that may cause increased levels include diazoxide, diuretics, hydralazine, laxatives, nitroprusside, potassium, and spironolactone. Drugs that may cause decreased levels include angiotensin-converting inhibitors (e.g., captopril), fludrocortisone, and propranolol, as well as licorice.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: serum separator Note that the patient is asked to be in the upright position (at least sitting) for at least 2 hours before the blood is drawn. Explain the procedure for collecting a 24-hour urine sample if urinary aldosterone is ordered. (See inside front cover for Routine Urine Testing.)aldosterone 27A Give the patient verbal and written instructions regarding dietary and medication restrictions. Instruct the patient to maintain a normal sodium diet (approximately 3 g/day) for at least 2 weeks before the blood or urine collection. Have the patient ask the physician whether drugs that alter sodium, potassium, and fluid balance (e.g., diuretics, antihy-pertensives, steroids, oral contraceptives) should be withheld. Test results will be more accurate if these are suspended at least 2 weeks before either the blood or the urine test. Inform the patient that renin inhibitors (e.g., propranolol) should not be taken 1 week before the test. Tell the patient to avoid licorice for at least 2 weeks before the test because of its aldosterone-like effect.During• Occasionally, for hospitalized patients, draw the sample with the patient in the supine position before he or she rises.• Obtain the specimen in the morning.• Note that sometimes a second specimen (upright sample) is collected 4 hours later, after the patient has been up and moving.After• Indicate on the laboratory slip if the patient was supine or standing during the venipuncture.• Handle the blood specimen gently. Rough handling may cause hemolysis and alter the test results.• Transport the specimen on ice to the laboratory.28 aldosteroneAbnormal findings Increased levels Decreased levelsPrimary aldosteronism Aldosterone deficiencyAldosterone-producing adrenal adenoma (Conn syndrome)Renin deficiencySteroid therapyAddison diseaseAdrenal cortical nodular hyperplasiaPatients on a high-sodium dietBartter syndromeSecondary aldosteronismHyponatremiaHyperkalemiaDiuretic ingestion resulting in hypovolemia and hyponatremiaHypernatremiaHypokalemiaToxemia of pregnancyAntihypertensive therapyLaxative abuse Stress Malignant hypertension Generalized edema Renal arterial stenosis Pregnancy Oral contraceptives Hypovolemia or hemorrhage Cushing syndrome notesalkaline phosphatase 29Aalkaline phosphatase (ALP)Type of test BloodNormal findingsAdult: 30-120 units/L or 0.5-2.0 μKat/LElderly: slightly higher than adultsChild/adolescent:Fasting: no• Blood tube commonly used: red• Note that overnight fasting may be required for isoenzymes.• Patients with liver dysfunction often have prolonged clotting times.Abnormal findings Increased levels Decreased levelsCirrhosis HypothyroidismIntrahepatic or extrahepatic biliary obstructionPrimary or metastatic liver tumorIntestinal ischemia or infarctionMetastatic tumor to the boneHealing fractureHyperparathyroidismPaget disease of boneMalnutritionMilk-alkali syndromePernicious anemiaHypophosphatemiaScurvy (vitamin C deficiency)Celiac diseaseExcess vitamin B ingestionHypophosphatasiaRheumatoid arthritis Sarcoidosis Osteomalacia Rickets notesallergy blood testing 31Aallergy blood testing (IgE antibody test, Radioallergosorbent test [RAST])Type of test BloodNormal findingsTotal IgE serumAdult: 0-100 international units/mLChild:0-23 months: 0-13 international units/mL2-5 years: 0-56 international units/mL6-10 years: 0-85 international units/mLTest explanation and related physiologyMeasurement of serum IgE is an effective method to diag-nose allergy and specifically identify the allergen (the substance to which the person is allergic). Serum IgE levels increase when allergic individuals are exposed to the allergen. Various classes of allergens can initiate the allergic response. They include animal dandruff, foods, pollens, dusts, molds, insect venoms, drugs, and agents in the occupational environment.Although skin testing (see p. 33) can also identify a specific allergen, measurement of serum levels of IgE is helpful when a skin test result is questionable, when the allergen is not available in a form for dermal injection, or when the allergen may incite an anaphylactic reaction if injected. IgE is particularly helpful in cases in which skin testing is difficult (e.g., in infants or in patients with dermatographism or widespread dermatitis), and it is not always necessary to remove the patient from antihistamines, ACE inhibitors, antidepressants, or beta-blockers. The decision con-cerning which method to use to diagnose an allergy and to iden-tify the allergen depends on the elapsed time between exposure to an allergen and testing, class of allergen, the age of the patient, the possibility of anaphylaxis, and the affected target organ (such as skin, lungs, or intestine). In general, allergy skin testing is the preferred method in comparison with various in vitro tests for assessing the presence of specific IgE antibodies because it is more sensitive and specific, simpler to use, and less expensive.IgE levels, similar to provocative skin testing, are used not only to diagnose allergy but also to identify the allergen so that an immunotherapeutic regimen can be developed. Increased lev-els of total IgE can be diagnostic of allergic disease in general. Specific IgE blood allergy testing, however, is an in vitro test for specific IgE directed to a specific allergen. Since the development 32 allergy blood testingof liquid allergen preparations, the use of in vitro blood allergy testing has increased considerably. It is more accurate and safer than skin testing. There are many methods of measuring IgE. One of the older methods is the radioallergosorbent test (RAST). Immunoassay for specific IgE has replaced RAST testing.Allergy testing of IgG antibodies can also be performed and may provide a more accurate correlation between allergen and allergic symptoms. Similar to IgE antibody testing, IgG antibody testing is often performed in “panels.” For example, there are meat panels that might include IgE or IgG testing for chicken, duck, goose, and turkey. Testing a fruit panel might include IgE or IgG antibody testing for apples, bananas, peaches, and pears. Testing in panels diminishes the cost of testing. Specific allergen antibody testing can follow panel testing.Contraindications• Patients with multiple allergies; no information will be obtained regarding identification of the specific allergen.Interfering factors• Concurrent diseases associated with elevated IgG levels will cause false-negative results.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: serum separator Inform the patient that the suspected allergen will be mixed with the patient’s blood specimen in the laboratory. The patient will not experience any allergic reaction by this method of testing.• Determine if the patient has recently been treated with a cor-ticosteroid for allergies.Abnormal findingsAllergy-related diseasesAsthmaDermatitisFood allergyDrug allergyOccupational allergyAllergic rhinitisAngioedemanotesallergy skin testing 33Aallergy skin testingType of test SkinNormal findingsless reliable.Contraindications• Patients with a history of prior anaphylaxisPotential complications• AnaphylaxisInterfering factors• False-positive results may occur with dermographism.• False-positive results may occur if the patient has a reaction to the diluent used to preserve the extract.• False-negative results may be caused by poor-quality aller-gen extracts, diseases that attenuate the immune response, or improper technique.• Infants and the elderly may have decreased skin reactivity. Drugs that may decrease the immune response of skin testing include ACE inhibitors, beta-blockers, corticosteroids, nifed-ipine, and theophylline.Procedure and patient careBefore Explain the procedure to the patient.• Observe skin testing precautions:1. Be sure that a physician is immediately available.2. Evaluate the patient for dermographism.3. Have medications and equipment available to handle anaphylaxis.4. Proceed with caution in patients with current allergic symptoms.5. Render great detail to the injection technique.6. Avoid bleeding due to injection.allergy skin testing 35A7. Avoid spreading of allergen solutions during the test.8. Record the skin reaction at the proper time.• Obtain a history to evaluate the risk of anaphylaxis.• Identify any immunosuppressive medications the patient may be taking.• Evaluate the patient for dermographism by rubbing the skin with a pencil eraser and looking for a wheal at the site of irritation.• Draw up 0.05 mL of 1:1000 aqueous epinephrine into a syringe before testing in the event of an exaggerated allergic reaction.• A negative prick-puncture test should be performed prior to an intradermal test.DuringPrick-puncture method• A drop of the allergen solution is placed onto the volar surface of the forearm or back.• A 25-gauge needle is passed through the droplet and inserted into the epidermal space at an angle with the bevel facing up.• The skin is lifted up and the fluid is allowed to seep in. Excess fluid is wiped off after about a minute.Intradermal method• With a 25-gauge needle, the allergen solution is injected into the dermis by creating a skin wheal. In this method, the bevel of the needle faces downward. A volume of between 0.01 and 0.05 mL is injected.• In general, the allergen solution is diluted 100- to 1000-fold before injection.Patch method• Clean the skin area (usually the back or arm).• Apply the patches to the skin (as many as 20-30 can be applied).• Instruct the patient to wear the patches for 48 hours. Tell the patient to avoid bathing or activities that cause heavy sweating.• Tell the patient the patches will be removed at the doctor’s office. Irritated skin at a patch site may indicate an allergy.After• Evaluate the patient for an exaggerated allergic response.• In the event of a systemic reaction, a tourniquet should be placed above the testing site and epinephrine should be administered subcutaneously.36 allergy skin testing• With a pen, circle the area of testing and mark the allergen used.• Read the skin test at the appropriate time.• Skin tests are read when the reaction is mature, after about 15 to 20 minutes. Both the largest and smallest diameters of the wheal are determined. The measurements are averaged.• The flare is measured in the same manner.• Observe the patient for 20 to 30 minutes prior to discharge.Abnormal findingsAllergy-related diseasesAsthmaDermatitisFood allergyDrug allergyOccupational allergyAllergic rhinitisAngioedemanotesAalpha1-antitrypsin 37alpha1-antitrypsin (A1AT, AAT, Alpha1-antitrypsin phenotyping)Type of test BloodNormal findings 85-213 mg/dL or 0.85-2.13 g/L (SI units)Test explanation and related physiologySerum alpha1-antitrypsin (AAT) determinations should be obtained when an individual has a family history of emphysema because a familial tendency to have a deficiency of this antien-zyme exists. Deficient or absent serum levels of this enzyme are found in some patients with early onset of emphysema. These people usually develop severe, disabling emphysema. A similar deficiency is seen in children with cirrhosis and other liver dis-eases. AAT is also an acute-phase reactant that is elevated in the face of inflammation, infection, or malignancy. It is not specific as to the source of the inflammatory process.Deficiencies of AAT can be genetic or acquired. Acquired deficiencies of AAT can occur in patients with protein deficiency syndromes (e.g., malnutrition, liver disease, nephrotic syndrome, and neonatal respiratory distress syndrome). People with AAT deficiency develop severe panacinar emphysema, although it is usually more severe in the lower third of the lungs in the third or fourth decade of life.Routine serum protein electrophoresis (see p. 760) is a good screening test for AAT deficiency because AAT accounts for about 90% of the protein in the alpha1-globulin region.Inherited AAT deficiency is associated with symptoms earlier in life than acquired AAT deficiency. Inherited AAT is also com-monly associated with liver and biliary disease. Individuals of the heterozygous state have diminished or low normal serum levels of AAT. Approximately 5% to 14% of the adult population is in the heterozygous state and is considered to be at increased risk for the development of emphysema. Homozygous individuals have severe pulmonary and liver disease very early in life. AAT phenotyping is particularly helpful when blood AAT levels are suggestive but not definitive.Interfering factors• Serum levels of AAT increase during pregnancy. Drugs that may cause increased levels include oral contraceptives.38 alpha1-antitrypsinProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no (Verify with lab).• Blood tube commonly used: red If the results show the patient is at risk for developing emphy-sema, begin patient teaching. Include such factors as avoid-ance of smoking, infection, and inhaled irritants; proper nutrition; adequate hydration; and education about the dis-ease process of emphysema.Abnormal findings Increased levels Decreased levelsAcute inflammatory disordersEarly onset of emphysema (in adults)Chronic inflammatory disordersNeonatal respiratory distress syndromeStress Cirrhosis (in children)Infection Low serum proteinsThyroid infections (e.g., nephrotic syndrome, malnutrition, end-stage cancer, protein-losing enteropathy)notesalpha-fetoprotein 39Aalpha-fetoprotein (AFP, a1-Fetoprotein)Type of test BloodNormal findingsAdult:after correction for age of gestation, maternal weight, race, and presence of diabetes are found in mothers carrying a fetus with trisomy 21 (Down syn-drome). See maternal screen testing (p. 628) and nuchal translu-cency (p. 697) for other pregnancy screening tests.AFP is also used as a tumor marker. Increased serum levels of AFP are found in as many as 90% of patients with hepato-mas. The higher the AFP level, the greater the tumor burden. A decrease in AFP is seen if the patient is responding to antineo-plastic therapy. Other neoplastic conditions (e.g., nonseminoma-tous germ cell tumors and teratomas of the testes; yolk sac and germ cell tumors of the ovaries; and to a lesser extent Hodgkin disease, lymphoma, and renal cell carcinoma) are also associated 40 alpha-fetoproteinwith elevated AFP levels. With improved methods of detection, AFP can also be detected in the serum of patients with cancer of the stomach, colon, breast, or lung. Elevated AFP levels can also occur in patients with noncancerous conditions, such as cirrhosis or chronic active hepatitis.Interfering factors• Fetal blood contamination, which may occur during amnio-centesis, can cause increased AFP levels.• Recent administration of radioisotopes can affect values.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: red• If AFP is to be performed on amniotic fluid, follow the Procedure and Patient Care for amniocentesis (see p. 52).• Include the gestational age on the laboratory slip.Abnormal findings Increased maternal AFP levels Decreased maternal serum AFP levelsNeural tube defects (e.g., anencephaly, encephalocele, spina bifida, myelomeningocele)Trisomy 21 (Down syndrome)Fetal wastageAbdominal wall defects (e.g., gastroschisis or omphalocele) Multiple pregnancy Threatened abortion Fetal distress or congenital anomalies Fetal death alpha-fetoprotein 41A Increased nonmaternal AFP levelsPrimary hepatocellular cancer (hepatoma)Germ cell or yolk sac cancer of the ovaryEmbryonal cell or germ cell tumor of the testesOther cancers (e.g., stomach, colon, lung, breast, or lymphoma)Liver cell necrosis (e.g., cirrhosis or hepatitis)notes42 aluminumaluminumType of test BloodNormal findingsAll ages: 0-6 ng/mLDialysis patients of all ages: 10 ng/mL in a patient with an aluminum-based implant suggest significant prosthesis wear. Chromium and other metals can be detected using similar labo-ratory techniques.Interfering factors• Special evacuated blood collection tubes are required for alu-minum testing.• Most of the common evacuated blood collection devices have rubber stoppers that are comprised of aluminum-silicate. Simple puncture of the rubber stopper for blood collection is sufficient to contaminate the specimen with aluminum.• Gadolinium- or iodine-containing contrast media that have been administered within 96 hours can alter test results for heavy metals, including aluminum.aluminum 43AProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: royal blue or tan• If the blood sample is sent to a central diagnostic laboratory, results will be available in 7 to 10 days.Abnormal findings Increased levelsAluminum toxicitynotes44 amino acid profilesamino acid profiles (Amino acid screen)Type of test Blood; urineNormal findingsNormal values vary for different amino acids.Test explanation and related physiologyAmino acids are “building blocks” of proteins, hormones, nucleic acids, and pigments. They can act as neurotransmitters, enzymes, and coenzymes. There are eight essential amino acids that must be provided to the body by the diet. The body can make the others. The essential amino acids must be transported across the gut and renal tubular lining cells. The metabolism of the essential amino acids is critical to the production of other amino acids, proteins, carbohydrates, and lipids. Amino acid lev-els can thereby be affected by defects in renal tubule or gastroin-testinal (GI) transport of amino acids.When there is a defect in the metabolism or transport of any one of these amino acids, excesses of their precursors or deficien-cies of their “end product” amino acid are evident in the blood and/or urine. There are more than 90 diseases described that are associated with abnormal amino acid function.Clinical manifestations of these diseases may be precluded if diagnosis is early, and appropriate dietary replacement of miss-ing amino acids is provided. Usually, urine testing for specific amino acids is used to screen for some of these errors in amino acid metabolism and transport. Blood testing is very accurate. Federal law now requires hospitals to test all newborns for inborn errors in metabolism including amino acids. Testing is required for errors in amino acid metabolism such as phenylketonuria (PKU), maple syrup urine disease (MSUD), and homocystinuria (see newborn metabolic screening, p. 657). Testing for more rare disorders may include testing for tyrosinemia and argininosuc-cinic aciduria.A few drops of blood are obtained from the heel of a new-born to fill a few circles on filter paper (Guthrie card) labeled with names of infant, parent, hospital, and primary physician. The sample is usually obtained on the second or third day of life, after protein-containing feedings (i.e., breast milk or formula) have started.After a presumptive diagnosis is made, amino acid levels can be determined by chromatographic methods on blood or amniotic fluid. The genetic defects for many of these diseases are becoming amino acid profiles 45Amore defined, allowing for even earlier diagnosis to be made in utero. Common examples of amino acid diseases include PKU, cystinosis, and cystic fibrosis.Interfering factors• The circadian rhythm affects amino acid levels. Levels are usu-ally lowest in the morning and highest by midday.• Pregnancy is associated with reduced levels of some amino acids. Drugs that may increase amino acids include bismuth, hepa-rin, steroids, and sulfonamides. Drugs that may decrease some amino acid levels include estro-gens and oral contraceptives.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes• Blood tube commonly used: redBefore• Obtain a history of the patient’s symptoms.• Obtain a pedigree highlighting family members with amino acid disorders. A 12-hour fast is generally required before blood collection. Occasionally, a particular protein or carbohydrate load is ordered to stimulate production of a particular amino acid metabolite.During• Usually a 24-hour random urine specimen is required. See inside front cover for Routine Urine Testing.• Screening is done on a spot urine using the first voidedspeci-men in the morning.After• Generally, genetic counseling is provided before testing. However, acute anxiety by the patient or parents often requires emotional support immediately after obtaining a specimen.46 amino acid profilesAbnormal findings Increased blood levels Decreased blood levelsSpecific aminoacidopathies (e.g., PKU, maple syrup disease)Hartnup diseaseNephritisNephrotic syndromesSpecific aminoacidemias (e.g., glutaric aciduria) Increased urine levels Specific aminoacidurias (e.g., cystinuria, homocystinuria) notesammonia level 47Aammonia levelType of test BloodNormal findingsAdult: 10-80 mcg/dL or 6-47 μmol/L (SI units)Child: 40-80 mcg/dLNewborn: 90-150 mcg/dLTest explanation and related physiologyAmmonia is used to support the diagnosis of severe liver dis-eases (fulminant hepatitis or cirrhosis). Ammonia levels are also used in the diagnosis and follow-up of hepatic encephalopathy.Ammonia is a by-product of protein catabolism. Most of the ammonia is made by bacteria acting on proteins present in the gut. By way of the portal vein, ammonia goes to the liver where it is normally converted into urea and then secreted by the kid-neys. With severe hepatocellular dysfunction, ammonia cannot be catabolized. Furthermore, when portal blood flow to the liver is altered (e.g., in portal hypertension), ammonia cannot reach the liver to be catabolized. Ammonia levels in the blood rise. Plasma ammonia levels do not correlate well with the degree of hepatic encephalopathy. Inherited deficiencies of urea cycle enzymes, inherited metabolic disorders of organic acids, and the dibasic amino acids lysine and ornithine are a major cause of high ammonia levels in infants and adults. Finally, impaired renal function diminishes excretion of ammonia, and blood levels rise. High levels of ammonia are often associated with encephalopathy and coma.Interfering factors• Hemolysis increases ammonia levels because the RBCs con-tain about three times the ammonia content of plasma.• Muscular exertion can increase ammonia.• Cigarette smoking can produce significant increases in ammo-nia levels.• Ammonia levels may be falsely increased if the tourniquet is too tight for a long period. Drugs that may cause increased ammonia levels include acet-azolamide, alcohol, ammonium chloride, barbiturates, diuret-ics (e.g., loop, thiazide), narcotics, and parenteral nutrition. Drugs that may cause decreased levels include broad-spectrum antibiotics (e.g., neomycin), lactobacillus, lactulose, levodopa, and potassium salts.48 ammonia levelProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: green• Note that some institutions require that the specimen be sent to the laboratory in an iced container.• Avoid hemolysis and send the specimen promptly to the laboratory.• Many patients with liver disease have prolonged clotting times.Abnormal findings Increased levels Decreased levelsPrimary hepatocellular diseaseReye syndromeAsparagine intoxicationEssential or malignant hypertensionHyperornithinemiaPortal hypertension Severe heart failure with congestive hepatomegaly Hemolytic disease of the newborn (erythroblastosis fetalis) Gastrointestinal bleeding with mild liver disease Gastrointestinal obstruction with mild liver disease Hepatic encephalopathy and hepatic coma Genetic metabolic disorder of the urea cycle notesamniocentesis 49Aamniocentesis (Amniotic fluid analysis)Type of test Fluid analysisNormal findingsWeeks’ gestation Amniotic fluid volume (mL)15 45025 75030-35 1500Full term > 1500Amniotic fluid appearance: clear; pale to straw yellowL/S ratio: ≥2:1Bilirubin: 30,000Alpha-fetoprotein: dependent on gestational age and lab techniqueFetal lung maturity (FLM):Mature: 290 mPOLTest explanation and related physiologyAmniocentesis is performed on pregnant women to gather information about the fetus. The following can be evaluated by studying the amniotic fluid:• Fetal maturity status, especially pulmonary maturity (when early delivery is preferred). Fetal maturity is determined by analysis of the amniotic fluid in the following manner:a. Lecithin/sphingomyelin (L/S) ratio. The L/S ratio is a measure of fetal lung maturity, which is determined by measuring the phospholipids in amniotic fluid. Lecithin is the major constituent of surfactant, an important sub-stance required for alveolar ventilation. If surfactant is insufficient, the alveoli collapse during expiration. This may result in respiratory distress syndrome (RDS), which is a major cause of death in immature babies. In immature fetal lungs, the sphingomyelin concentration in amniotic fluid is higher than the lecithin concentration. At 35 weeks of gestation, the concentration of lecithin rapidly increases, whereas sphingomyelin concentration decreases. An L/S 50 amniocentesisratio of 2:1 (3:1 in mothers with diabetes) or greater is a highly reliable indication that the fetal lungs and there-fore the fetus are mature. In such a case, the infant would be unlikely to develop RDS after birth. As the L/S ratio decreases, the risk of RDS increases.Lecithin concentrations can be measured directly, but offer no additional accuracy beyond the L/S ratio. As an alternative to measuring the L/S ratio, the fetal lung maturity (FLM) test is based on fluorescence depolariza-tion. This test determines the ratio of surfactant to albu-min to evaluate pulmonary maturity.b. Phosphatidylglycerol (PG). This is a minor component (about 10%) of lung surfactant phospholipids and there-fore, alone, is less accurate in measuring pulmonary matu-rity. However, because PG is almost entirely synthesized by mature lung alveolar cells, it is a good indicator of lung maturity. In healthy, pregnant women, PG appears in amniotic fluid after 35 weeks of gestation, and levels grad-ually increase until term. The simultaneous determination of the L/S ratio and the presence of PG is an excellent method of assessing fetal maturity based on pulmonary surfactant.c. Lamellar body count. This test to determine fetal maturity is also based on the presence of surfactant. These lamellar bodies represent the storage form of pulmonary surfactant. Lamellar body results are calculated in units of particle density per microliter of amniotic fluid. Some researchers have recommended cutoffs of 30,000/μl and 10,000/μl to predict low and high risks for RDS, respectively. If the count is greater than 30,000, there is a 100% chance that the infant’s lungs are mature enough to not experience RDS. If the lamellar body count is less than 10,000, the probability of RDS is high (67%). Values between 10,000 and 30,000/μl represent intermediate risk for RDS.d. Measurement of surfactant activity. Surfactant activity is a semi-quantitative group of tests performed by determining the development and stability of foam when amniotic fluid is shaken in a solution of alcohol. This testing may be called the tap test, the shake test, or the foam stability index test. If a ring of bubbles forms on the surface of the solution, fetal lung maturity is indicated. If no bubbles are present, varying levels of respiratory distress syndrome are indicated.e. Measurement of optical density of amniotic fluid. The mea-surement of amniotic fluid at 650 nm can be measured by amniocentesis 51Aabsorbance. A denser fluid will be associated with greater lung maturity. This testing method is often used as a rapid screening test for fetal lung maturity.• Sex of the fetus. Sons of mothers who are known to be carri-ers of X-linked recessive traits would have a 50:50 chanceof inheritance.• Genetic and chromosomal aberrations. Genetic and chromo-somal studies performed on cells aspirated within the amniotic fluid can indicate the gender of the fetus (important in sex-linked diseases such as hemophilia) or the existence of many genetic and chromosomal aberrations (e.g., trisomy 21). See Laboratory Genetics, p. 566.• Fetal status affected by Rh isoimmunization. Mothers with Rh isoimmunization may have a series of amniocentesis pro-cedures during the second half of pregnancy to assess the level of bilirubin pigment in the amniotic fluid. The quan-tity of bilirubin is used to assess the severity of hemolysis in Rh-sensitized pregnancy. Amniocentesis is usually initiated at 24 to 25 weeks when hemolysis is suspected.• Hereditary metabolic disorders, such as cystic fibrosis.• Anatomic abnormalities, such as neural tube closure defects (myelomeningocele, anencephaly, spina bifida). Increased levels of alpha-fetoprotein (AFP) in the amniotic fluid may indicate a neural crest abnormality (see p. 39). Decreased AFP may be associated with increased risk of trisomy 21.• Fetal distress, detected by meconium staining of the amniotic fluid. This is caused by relaxation of the anal sphincter. In this case, the normally colorless or pale, straw-colored amniotic fluid may be tinged with green. Other color changes may also indicate fetal distress. There are, however, more accurate and safer methods of determining fetal stress such as the fetal bio-physical profile (see page 423).• Assessment of amniotic fluid for infection. Amniocentesis is used to obtain fluid for bacterial culture and sensitivity when infection is suspected. This is especially helpful if premature membrane rupture is suspected. Amniotic fluid can also be obtained if viral infections that may affect the fetus are sus-pected during pregnancy.• Assessment for rupture of membranes. Through amniocente-sis, a dye can be injected into the amniotic fluid. If this same dye is found in vaginal fluid, rupture of the amniotic mem-brane is documented. This is sometimes referred to as the amnio-dye test. There are, however, more practical tests of vag-inal fluid to determine membrane rupture. Most commonly, 52 amniocentesisthe pH of the vaginal fluid is determining using a nitrazine test strip. If the test strip turns dark or blue, amniotic fluid is present in the vagina, and membrane rupture is documented.The timing of the amniocentesis varies according to the clinical circumstances. With advanced maternal age and if chro-mosomal or genetic aberrations are suspected, the test should be done early enough (at 14 to 16 weeks of gestation; at least 150 mL of fluid exists at this time) to allow a safe abortion. If information on fetal maturity is sought, performing the study during or after the 35th week of gestation is best.Contraindications• Patients with abruptio placentae• Patients with placenta previa• Patients with a history of premature labor (before 34 weeks of gestation unless the patient is receiving antilabor medication)• Patients with an incompetent cervix or cervical insufficiency• Patients with anhydramnios• Patients with suspected premature laborPotential complications• Miscarriage• Fetal injury• Leak of amniotic fluid• Infection (amnionitis)• Abortion• Premature labor• Maternal hemorrhage• Maternal Rh isoimmunization• Amniotic fluid embolism• Abruptio placentae• Inadvertent damage to the bladder or intestinesInterfering factors• Fetal blood contamination can cause false AFP elevations.• Hemolysis of the specimen can alter results.• Contamination of the specimen with meconium or blood may give inaccurate L/S ratios.Procedure and patient careBefore Explain the procedure to the patient. Allay any fears, and allow the patient to verbalize her concerns.• Obtain an informed consent from the patient and her spouse.amniocentesis 53A Tell the patient that no food or fluid is restricted.• Evaluate the mother’s blood pressure and the fetal heart rate.• Follow instructions regarding emptying the bladder, which depend on gestational age. Before 20 weeks of gestation, the bladder may be kept full to support the uterus. After 20 weeks, the bladder may be emptied to minimize the chance of puncture.• Note that the placenta is localized before the study by ultrasound to permit selection of a site that will avoid placental puncture.During• Place the patient in the supine position.• Note the following procedural steps:1. The skin overlying the chosen site is prepared and usually anesthetized locally.2. A needle with a stylet is inserted through the midabdomi-nal wall and is directed at an angle toward the middle of the uterine cavity (Figure 2).3. The stylet is then removed and a sterile plastic syringe attached.90 FIGURE 2 Amniocentesis. Ultrasound scanning is usually used to determine the placental site and to locate a pocket of amniotic fluid. The needle is then inserted. Three levels of resistance are felt as the needle penetrates the skin, fascia, and uterine wall. When the needle is placed within the uterine cavity, amniotic fluid is withdrawn.54 amniocentesis4. After 5 to 10 mL of amniotic fluid is withdrawn, the needle is removed.5. The specimen is placed in a light-resistant container to pre-vent breakdown of bilirubin.6. The site is covered with an adhesive bandage.7. If the amniotic fluid is bloody, the physician must deter-mine whether the blood is maternal or fetal in origin. The Kleinhauer-Boetke stain will stain fetal cells pink. Meconium in the fluid is usually associated with a compro-mised fetus.8. Amniotic fluid volume is calculated.• Note that this procedure is performed by a physician and takes approximately 20 to 30 minutes. Tell the patient that the discomfort associated with amniocen-tesis is usually described as a mild uterine cramping that occurs when the needle contacts the uterus. Some women may complain of a pulling sensation as the amniotic fluid is withdrawn.• Remember that many women are extremely anxious during this procedure.After• Place amniotic fluid in a sterile, siliconized glass container and transport it to a special chemistry laboratory for analysis. Sometimes the specimen may be sent by airmail to another commercial laboratory. Inform the patient that the results of this study are usually not available for more than 1 week.• For women who have Rh-negative blood, administer RhoGAM because of the risk of isoimmunization from the fetal blood.• Assess the fetal heart rate after the test to detect any ill effects related to the procedure. Compare this value with the prepro-cedure baseline value. If the patient felt dizzy or nauseated during the procedure, instruct her to lie on her left side for several minutes before leaving the examining room.• Observe the puncture site for bleeding or other drainage. Instruct the patient to call her physician if she has any amni-otic fluid loss, bleeding, temperature elevation, abdominal pain, abdominal cramping, fetal hyperactivity, or unusual fetal lethargy.amniocentesis 55AAbnormal findingsHemolytic disease of the newbornRh isoimmunizationNeural tube closure defects (e.g., myelomeningocele, anencephaly, spina bifida)Abdominal wall closure defects (e.g., gastroschisis, omphalocele)Sacrococcygeal teratomaMeconium stainingImmature fetal lungsHereditary metabolic disorders (e.g., cystic fibrosis, Tay-Sachs disease, galactosemia)Genetic or chromosomal aberrations (e.g., sickle cell anemia, thalassemia, trisomy 21 [Down syndrome])Sex-linked disorders (e.g., hemophilia)PolyhydramniosOligohydramniosnotes56 amylaseamylaseType of test Blood; urineNormal findingsBloodAdult: 60-120 Somogyi units/dL or 30-220 units/L (SI units) Values may be slightly increased during normal pregnancy and in the elderly.Newborn: 6-65 units/LUrine (24-hour)Up to 5000 Somogyi units/24 hr or 6.5-48.1 units/hr (SI units)Possible critical values Blood: More than three times the upper limit of normal (depending on the method)Test explanation and related physiologySerum amylase is an easily and rapidly performed test that is commonly used to diagnose and monitor the treatment of pancreatitis. Amylase is normally secreted from the pancreatic acinar cell into the pancreatic duct and then into the duodenum. Once in the intestine, it aids the catabolism of carbohydrates to their component simple sugars. Damage to acinar cells (as occurs in pancreatitis) or obstruction of the pancreatic duct flow (as a result of pancreatic carcinoma) causes an outpouring of this enzyme into the intrapancreatic lymph system and the free peritoneum. Blood vessels draining the free peritoneum and absorbing the lymph pick up the excess amylase. An abnormal rise in the serum level of amylase occurs within 12 hours of the onset of disease. Because amylase is rapidly cleared by the kid-neys, serum levels return to normal 48 to 72 hours after the initial insult. Persistent pancreatitis, duct obstruction, or pancre-atic duct leak will cause persistent elevated amylase levels.Although serum amylase is a sensitive test for pancreatic dis-orders, it is not specific. Other nonpancreatic diseases can cause elevated amylase levels in the serum. For example, in a bowel perforation, intraluminal amylase leaks into the free peritoneum and is picked up by the peritoneal blood vessels. Also, a penetrat-ing peptic ulcer into the pancreas will cause elevated amylase lev-els. Duodenal obstruction can be associated with less significant elevations in amylase. Because salivary glands contain amylase, elevations can be expected in patients with parotiditis (mumps). Amylase isoenzyme testing can differentiate pancreatic from sali-vary hyperamylasemia.amylase 57AUrine amylase levels rise after the blood levels. Several days after the onset of the disease process, serum amylase levels may be normal, but urine amylase levels are significantly elevated. Urine amylase is particularly useful in detecting pancreatitis late in the disease course.As with serum amylase, urine amylase is sensitive but not spe-cific for pancreatic disorders. A comparison of the renal clearance ratio of amylase with creatinine provides more specific diagnostic information than either the urine amylase level or the serum amy-lase level alone. When the amylase/creatinine clearance ratio is 5% or more, the diagnosis of pancreatitis can be made with certainty.Interfering factors• Serum lipemia may falsely decrease amylase levels. IV dextrose solutions can cause a false-negative result. Drugs that may cause increased serum amylase levels include aminosalicylic acid, aspirin, azathioprine, corticosteroids, dexa-methasone, ethyl alcohol, glucocorticoids, iodine- containing contrast media, loop diuretics, methyldopa, narcotic analgesics, oral contraceptives, and prednisone. Drugs that may cause decreased levels include citrates, glucose, and oxalates.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: red• See inside front cover for Routine Urine Testing.Abnormal findings Increased levelsAcute or chronic relapsing pancreatitisPenetrating or perforated peptic ulcerNecrotic or perforated bowelAcute cholecystitisParotiditis (mumps)Ectopic pregnancyPulmonary infarctionDiabetic ketoacidosisDuodenal obstructionOsteogenic sarcomaCryoglobulinemiaRheumatoid diseasesnotes58 amyloid beta protein precursor, solubleamyloid beta protein precursor, soluble (sBPP)Type of test Cerebrospinal fluid (CSF) analysisNormal findings >450 units/LTest explanation and related physiologyThis test is used to help diagnose Alzheimer disease and other forms of senile dementia. Amyloid protein is a 42-amino-acid peptide that is broken off of a larger amyloid precursor protein (beta APP). These beta amyloid proteins have been shown to be neurotrophic and neuroprotective. Beta amyloid is deposited on the brain in the form of plaques in patients with Alzheimer disease. As a result of this deposition, levels of beta amyloid are decreased in the cerebrospinal fluid of patients with Alzheimer disease and other forms of dementia. Ongoing research has also focused on using CSF levels of tau protein as another biochemi-cal marker for Alzheimer disease.Recently, PET scanning with amyloid imaging has shown prom-ise for the diagnosis of Alzheimer disease. Pittsburgh Agent B (PIB) appears to reliably detect brain amyloid due to the accumulation of A beta 42 within plaques. Studies so far have revealed high levels of amyloid retention in the brain at prodromal stages of Alzheimer disease and the possibility of discriminating Alzheimer disease from other dementia disorders by scanning with PIB. Because amy-loid accumulation is one of the earliest signs of Alzheimer disease, early diagnosis may be facilitated by identifying amyloid early in the disease progression, perhaps before symptoms emerge.Procedure and patient careBefore Explain the procedure to the patient.• Refer to the instructions for a lumbar puncture and CSF examination (see p. 596).During• Collect a CSF specimen as per the lumbar puncture discussion.After• Follow the postprocedure guidelines after a lumbar puncture.Abnormal findings Decreased levelsAlzheimer diseasenotesangiotensin 59AangiotensinType of test bloodNormal findingsAngiotensin I: ≤25 pg/mLAngiotensin II: 10-60 pg/mLTest explanation and related physiologyRenin (page 800) is an enzyme that is released by the jux-taglomerular apparatus of the kidneys. Its release is stimulated by hypokalemia, hyponatremia, decreased renal blood perfusion, or hypovolemia. Renin stimulates the release of angiotensino-gen. Angiotensin-converting enzyme (ACE) (page 60) metab-olizes angiotensinogen to angiotensin I and subsequently to angiotensin II and III. Angiotensin then stimulates the release of catecholamines, antidiuretic hormone, ACTH, oxytocin, and aldosterone. Angiotensin is also a vasoconstrictor. Angiotensin is used to identify renovascular sources of hypertension. It can be measured as angiotensin I or as angiotensin II. The test is per-formed by direct radioimmunoassay.Interfering factors: See renin, page 807.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: lavender Instruct the patient to maintain a normal diet with a restricted amount of sodium (~3 g/day) for 3 days before the test. Instruct the patient to check with a health care provider about discontinuing any medications that may interrupt renin activity.• Record the patient’s position, dietary status, and time of day on the laboratory slip.• Place the tube of blood on ice and immediately send it to the laboratory.Abnormal findings Increased levelsEssential hypertensionMalignant hypertensionRenovascular hypertension Decreased levelsPrimary hyperaldosteronismSteroid therapyCongenital adrenal hyperplasianotes60 angiotensin-converting enzymeangiotensin-converting enzyme (ACE, Serum angiotensin-converting enzyme [SACE])Type of test BloodNormal findings 8-53 U/LTest explanation and related physiologyACE is used to detect and monitor the clinical course of sarcoidosis (a granulomatous disease that affects many organs, especially the lungs). It is also used to differentiate sarcoidosis from other granulomatous diseases, and to differentiate between active and dormant sarcoid disease.Elevated ACE levels are found in a high percentage of patients with sarcoidosis. This test is used primarily in patients with sar-coidosis to evaluate the severity of disease and the response to therapy. Levels are especially high with active pulmonary sar-coidosis and can be normalwith inactive (dormant) sarcoid-osis. Elevated ACE levels also occur in conditions other than sarcoidosis, including Gaucher disease (a rare familial lysosomal disorder of fat metabolism), leprosy, alcoholic cirrhosis, active histoplasmosis, tuberculosis, Hodgkin disease, myeloma, sclero-derma, pulmonary embolism, and idiopathic pulmonary fibrosis. ACE is elevated in the CSF of patients with neurosarcoidosis.Interfering factors• Patients younger than 20 years of age normally have very high ACE levels.• Hemolysis or hyperlipidemia may falsely decrease ACE levels. Drugs that may cause decreased ACE levels include ACE inhibitor antihypertensives and steroids.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: red• Note on the laboratory slip if the patient is taking steroids.angiotensin-converting enzyme 61AAbnormal findings Increased levelsSarcoidosisGaucher diseaseTuberculosisLeprosyAlcoholic cirrhosisActive histoplasmosisHodgkin diseaseMyelomaIdiopathic pulmonary fibrosisDiabetes mellitusPrimary biliary cirrhosisAmyloidosisHyperthyroidismSclerodermaPulmonary embolismnotes62 anion gapanion gap (AG, R factor)Type of test BloodNormal findings16 ± 4 mEq/L (if potassium is used in the calculation)12 ± 4 mEq/L (if potassium is not used in the calculation)Test explanation and related physiologyThe anion gap (AG) is the difference between the cations and the anions in the extracellular space that is routinely calculated in the laboratory (i.e., AG = [sodium + potassium] – [chloride + bicar-bonate]). In some laboratories, the potassium is not measured because the level of potassium in acid/base abnormalities varies. The normal value of the AG is adjusted downward if potassium is eliminated from the equation. The AG, although not real physi-ologically, is created by the small amounts of anions in the blood (e.g., lactate, phosphates, sulfates, organic anions, and proteins) that are not measured.This calculation is most often helpful in identifying the cause of metabolic acidosis. As such acids as lactic acid or ketoacids accumu-late in the bloodstream, bicarbonate neutralizes them to maintain a normal pH within the blood. Mathematically, when bicarbonate decreases, the AG increases. In general, most metabolic acidotic states (excluding some types of renal tubular acidosis) are associ-ated with an increased AG. The higher the gap is above normal, the more likely that the metabolic acidotic state is associated with the AG. Proteins can have a significant effect on AG. As albumin (usually negatively charged) increases, AG will increase.A decreased AG is very rare but can occur when there is an increase in unmeasured (calcium or magnesium) cations. A reduction in anionic proteins (nephrotic syndrome) will also decrease AG. For example, a 1 g/dL drop in serum protein is associated with a 2.5 mEq/L drop in AG. Because the anion pro-teins are lost, the HCO3 increases to maintain electrical neutral-ity. An increase in cationic proteins (some immunoglobulins) will also decrease AG. Except for hypoproteinemia, conditions that cause a reduced or negative AG are relatively rare compared with those associated with an elevated AG.Interfering factors• Hyperlipidemia may cause undermeasurement of sodium and falsely decrease AG.anion gap 63A• Normal values of AG vary according to different normal values for electrolytes, depending on laboratory methods of measurement. Drugs that increase AG are many. Examples include carbonic anhydrase inhibitors (e.g., acetazolamide), ethanol, metha-nol, and salicylate. Drugs that decrease AG are also many. Examples include acet-azolamide, lithium, spironolactone, and sulindac.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: red or green• If the patient is receiving an IV infusion, obtain the blood from the opposite arm.• The sodium, potassium, chloride, and bicarbonate levels are determined by an automated multichannel analyzer. The AG is then calculated as indicated in the test explanation section.Abnormal findings Increased levels Decreased levelsLactic acidosis Excess alkali ingestionDiabetic ketoacidosis Multiple myelomaAlcoholic ketoacidosisStarvationChronic vomiting or gastric suctionRenal failure HyperaldosteronismRenal tubular acidosis HypoproteinemiaIncreased gastrointestinal losses of bicarbonate (e.g., diarrhea or fistulae)Lithium toxicityBromide (cough syrup) toxicityHypoaldosteronism notes64 anticardiolipin antibodiesanticardiolipin antibodies (aCL antibodies, ACA, Antiphospholipid antibodies, Lupus anticoagulant)Type of test BloodNormal findingsNegative:titer and severity of CREST syndrome.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: redAbnormal findingsPositive resultsCREST syndromenotesantichromatin antibody test 67Aantichromatin antibody test (Antinucleosome antibody [anti-NCS], Antihistone antibody test [anti-HST, AHA])Type of test BloodNormal findingsAntinucleosome antibodiesNo antibodies present in 2.5 unitsTest explanation and related physiologyThere are several chromatin antinuclear antibodies associated with autoimmune diseases. Nucleosome (NCS) represents the main autoantigen-immunogen in systemic lupus erythematosus (SLE), and these specific antibodies are an important marker of the disease activity. Antinucleosome (anti-NCS; antichromatin) antibodies play a key role in the pathogenesis of SLE. Nearly all patients with SLE have anti-NCS antibodies. Anti-NCS is also an antinuclear antibody (see p. 86). Anti-NCS has a sensitivity of 100% and specificity of 97% for SLE diagnosis. Anti-NCS anti-bodies show the highest correlation with disease activity. Anti-NCS antibodies also show strong association with renal damage (glomerulonephritis and proteinuria) associated with SLE. Anti-NCS autoantibodies are more prevalent than anti-DNA in SLE patients.Histone antibodies are present in 20% to 55% of idiopathic SLE and 80% to 95% of drug-induced lupus erythematosus. They occur in less than 20% of other types of connective tissue diseases. This antibody is particularly helpful in identifying patients with drug-induced lupus erythematosus from drugs such as procain-amide, quinidine, penicillamine, hydralazine, methyldopa, iso-niazid, and acebutolol. There are several subtypes of antihistone antibodies (AHAs). In drug-induced lupus erythematosus, a spe-cific AHA (anti-[(H2A-H2B)-DNA] IgG) is produced, while in most of the other associated diseases (rheumatoid arthritis, juve-nile rheumatoid arthritis, primary biliary cirrhosis, autoimmune hepatitis, and dermatomyositis/polymyositis), the AHAs are of other varying specificities.68 antichromatin antibody testProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: red or goldAbnormal findings Increased levelsSystemic lupus erythematosusDrug-induced lupus erythematosusOther autoimmune diseasesnotesanti–cyclic citrullinated peptide antibody 69Aanti–cyclic citrullinated peptide antibody (Cyclic citrullinated peptide antibody, CCP IgG anti-CCP)Type of test BloodNormal findings 100Urine specific gravityAll tests begin on a new page and are listed in alphabetical order by their complete names. The alphabetical format is a strong feature of the book; it allows the user to locate tests quickly without first having to place them in an appropriate category or body system. The User’s Guide to Test Preparation and Procedures section outlines the responsi-bilities of health care providers to ensure that the tests are accu-rately and safely performed. Use of this guide should eliminate the need for test repetition resulting from problems with patient preparation, test procedures, or collection techniques. Every fea-ture of this book is designed to provide pertinent information in a sequence that best simulates priorities in the clinical setting.The following information is provided, wherever applicable, for effective diagnostic and laboratory testing:Name of test. Tests are listed by their complete names. A complete list of abbreviations and alternate test names follows each main entry.Type of test. This section identifies whether the test is, for example, an x-ray procedure, ultrasound, nuclear scan, blood test, urine test, sputum test, or microscopic examination of tis-sue. This section helps the reader identify the source of the labo-ratory specimen or location of the diagnostic procedure.Normal findings. Where applicable, normal values are listed for the infant, child, adult, and elderly person. Also, where appro-priate, values are separated into male and female. It is important to realize that normal ranges of laboratory tests vary from institu-tion to institution. This variability is even more obvious among the various laboratory textbooks. For this reason, we have delib-erately chosen not to add a table of normal values as an appendix, and we encourage the user to check the normal values at the institution where the test is performed. This should be relatively easy because laboratory reports include normal values. Results are given in both conventional units and the International System of Units (SI units) where possible.PB preface preface viiPossible critical values. These values give an indication of results that are well outside the normal range. These results require health care provider notification and usually result in some type of intervention. The Joint Commission is looking at the timely and reliable communication of critical laboratory val-ues as one of its patient safety goals.Test explanation and related physiology. This section pro-vides a concise yet comprehensive description of each test. It includes fundamental information about the test itself, specific indications for the test, how the test is performed, what disease or disorder the various results may show, how it will affect the patient or client, and relevant pathophysiology that will enhance understanding of the test.Contraindications. These data are crucial because they alert health care providers to patients to whom the test should not be administered. Patients highlighted in this section frequently include those who are pregnant, are allergic to iodinated or con-trast dyes, or have bleeding disorders.Potential complications. This section alerts the user to potential problems that necessitate astute assessments and interventions. For example, if a potential complication is renal failure, the implication may be to hydrate the patient before the test and force fluids after the test. A typical potential com-plication for many x-ray procedures is allergy to iodinated dye. Patient symptoms and appropriate interventions are described in detail.Interfering factors. This section contains pertinent informa-tion because many factors can invalidate the test or make the test results unreliable. An important feature is the inclusion of drugs that can interfere with test results. Drugs that increase or decrease test values are always listed at the end of this section for consistency and quick access. A drug symbol ( ) is used to emphasize these drug interferences.Procedure and patient care. This section emphasizes the role of nurses and other health care providers in diagnostic and laboratory testing by addressing psychosocial and physiologic interventions. Patient teaching priorities are noted with a spe-cial icon ( ) to highlight information to be communicated to patients. For quick access to essential information, this section is divided into before, during, and after time sequences.Before. This section addresses the need to explain the pro-cedure and to allay patient concerns or anxieties. If patient consent is usually required, this is listed as a bulleted item. viii preface preface ixOther important features include requirements such as fasting, obtaining baseline values, and performing bowel preparations.During. This section gives specific directions for clinical specimen studies (e.g., urine and blood studies). Diagnostic procedures and their variations are described in a numbered, usually step-by-step format. Important information, such as who performs the test, where the study is performed, patient sensation, and duration of the procedure, is bulleted for emphasis. The duration of the procedure is very helpful for patient teaching because it indicates the time generally allot-ted for each study.After. This section includes vital information that the nurse or other health care provider should heed or convey after the test. Examples include such factors as maintaining bed rest, comparing pulses with baseline values, encouraging fluid intake, and observing the patient for signs and symptoms of sepsis.Abnormal findings. As the name implies, this section lists the abnormal findings for each study. Diseases or conditions that may be indicated by increased ( ) or decreased ( ) values are listed where appropriate.Notes. This blank space at the end of the tests facilitates indi-vidualizing the studies according to the institution at which the test is performed. Variations in any area of the test (e.g., patient preparation, test procedure, normal values, postprocedural care) can be noted here.This logical format emphasizes clinically relevant information. The clarity of this format allows for quick understanding of con-tent essential to both students and health care providers. Color has been used to help locate tests and to highlight critical infor-mation (e.g., possible critical values). Color is also used in the illustrations to enhance the reader’s understanding of many diag-nostic procedures (e.g., bronchoscopy, fetoscopy, ERCP, peri-cardiocentesis, TEE). Many tables are used to simplify complex material on such topics as bioterrorism infectious agents, blood collection tubes, hepatitis testing, and protein electrophoresis. Extensive cross-referencing exists throughout the book, which facilitates understanding and helps the user tie together or locate related studies, such as hemoglobin and hematocrit.New to this edition are standard guidelines for routine blood and urine testing located on the inside front cover for easy access. A list of abbreviations for test names is included on the book’s endpapers. Appendix A includes a list of studies according to body viii preface preface ixsystem. This list may familiarize the user with other related studies the patient or client may need or the user may want to review. This should be especially useful for students and health care pro-viders working in specialized areas. Appendix B provides a list of studies according to test type. This list may help the user read and learn about similarly performed tests and procedures (e.g., barium enema and barium swallow). Appendix C provides a list of blood tests used for disease and organ panels. Appendix D pro-vides a list of symbols and units of measurement. Finally, a compre-hensive index includes the names of all tests, their synonyms and abbreviations, and any other relevant terms found(see below).The water load test (ADH suppression test) is used to differen-tiate SIADH from other causes of hyponatremia or edematous states. Usually this test is done concomitant with measurements of urine and serum osmolality. Patients with SIADH will excrete none or very little of the water load. Furthermore, their urine osmolality will never be 100. Patients with other hyponatremia, edematous states, or chronic renal diseases will excrete up to 80% of the water load and will develop midrange osmolality results.Interfering factors• Patients with dehydration, hypovolemia, and stress may have increased ADH levels.• Patients with overhydration, decreased serum osmolality, and hypervolemia may have decreased ADH levels.• Use of a glass syringe or collection tube causes degradation of ADH. Drugs that increase ADH levels and may cause SIADH include acetaminophen, barbiturates, carbamazepine, cholinergic agents, cyclophosphamide, some diuretics (e.g., thiazides), estrogen, narcotics, nicotine, oral hypoglycemic agents (particularly sulfo-nylureas), and tricyclic or SSRI antidepressants. Drugs that decrease ADH levels include alcohol, beta-adrenergic agents, morphine antagonists, and phenytoin.72 antidiuretic hormoneProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes• Blood tube commonly used: red• Evaluate the patient for high levels of physical or emotional stress.• Collect a venous blood sample in a plastic red-top tube with the patient in the sitting or recumbent position.• The water load test necessitates a baseline serum sodium prior to water administration. Urine is later collected for specific gravity and osmolality. Blood is collected for osmolality.Abnormal findings Increased levels Decreased levelsSyndrome of inappropriate antidiuretic hormone (SIADH)Nephrogenic diabetes insipidus caused by primary renal diseasesPostoperative days 1 to 3Neurogenic (or central) diabetes insipidusSurgical ablation of the pituitary glandHypervolemiaDecreased serum osmolalitySevere physical stress (e.g., trauma, pain, prolonged mechanical ventilation) Hypovolemia Dehydration Acute porphyria notesAanti-DNA antibody test 73anti-DNA antibody test (Anti–deoxyribonucleic acid antibodies, Antibody to double-stranded DNA, Anti–double-stranded DNA, Anti–ds-DNA, DNA antibody, Native double-stranded DNA)Type of test BloodNormal findingsNegative: 100 unitsTest explanation and related physiologyThis test is used to detect the presence of circulating glomeru-lar basement membrane (GBM) antibodies commonly present in autoimmune-induced nephritis (Goodpasture syndrome).Goodpasture syndrome is an autoimmune disease characterized by the presence of antibodies circulating against antigens in the basement membrane of the renal glomerular and the pulmonary alveoli. These immune complexes activate the complement system and thereby cause tissue injury. Patients with this problem usu-ally display a triad of glomerulonephritis (hematuria), pulmonary hemorrhage (hemoptysis), and antibodies to basement membrane antigens. About 60% to 75% of patients with immune-induced glomerular nephritis have these pulmonary complications.Lung or renal biopsies are required to obtain tissue on which to demonstrate these antibodieswith immunohistochemical techniques. Serum assays are faster and more reliable methods for diagnosing Goodpasture syndrome, especially in patients in whom a renal or lung biopsy may be difficult or contraindicated. Furthermore, serum levels can be used in monitoring response to therapy (plasmapheresis or immunosuppression).Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes• Blood tube commonly used: red If a lung biopsy (see p. 604) or renal biopsy (see p. 792) will be used to collect the specimen, explain these procedures to the patient.78 anti–glomerular basement membrane antibodiesAbnormal findingsPositiveGoodpasture syndromeAutoimmune glomerulonephritisLupus nephritisnotesanti-glycan antibodies 79Aanti-glycan antibodies (Crohn disease prognostic panel, Multiple sclerosis antibody panel)Type of test BloodNormal findings NegativeTest explanation and related physiologyAnti-glycan antibodies are immunologically directed to sugar-containing components on the surface of cells (particularly erythrocytes). Antibodies to glycans can be instigated by bac-terial, fungal, and parasite infections. The use of glycan arrays for systematic screening of patients with multiple sclerosis (MS) and inflammatory bowel disease (particularly Crohn disease) has been helpful in differentiating these diseases. Furthermore, these antibodies are used to determine treatment and prognosis.Utilizing enzyme-linked immunosorbent assays, these antibod-ies can be identified and quantified. Anti-Saccharomyces cerevisiae antibody (ASCA), anti-laminaribioside carbohydrate antibody (ALCA), anti-mannobioside carbohydrate antibody (AMCA), and anti-chitobioside carbohydrate antibody (ACCA) are used to eval-uate Crohn disease and differentiate Crohn colitis from ulcerative colitis. When all are positive, Crohn disease is much more likely than ulcerative colitis.Other anti-glycan antibodies are specific for MS patients.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: lavender, pink, or greenAbnormal findings Increased levelsCrohn diseaseMultiple sclerosisnotes80 anti-liver/kidney microsomal type 1 antibodiesanti-liver/kidney microsomal type 1 antibodies (Anti-LKM-1 antibodies)Type of test BloodNormal findings≤20 units (negative)20.1-24.9 units (equivocal)≥25 units (positive)Test explanation and related physiologyAutoimmune liver disease (e.g., autoimmune hepatitis and pri-mary biliary cirrhosis) is characterized by the presence of autoan-tibodies, including smooth muscle antibodies (SMA) (page 93), antimitochondrial antibodies (AMA) (page 82), and anti-liver/kidney microsomal antibodies type 1 (anti-LKM-1). Subtypes of autoimmune hepatitis (AIH) are based on autoantibody reactivity patterns. For example, the presence of smooth muscle antibodies (SMAs) is consistent with the diagnosis of chronic autoimmune hepatitis. The presence of anti-liver/kidney microsomal type 1 antibodies with or without SMAs is consistent with autoimmune hepatitis type 2. The presence of antimitochondrial antibodies is consistent with primary biliary cirrhosis.Anti-LKM-1 antibodies serve as a serologic marker for AIH type 2 and typically occur in the absence of SMAs and antinuclear antibodies. Children often have other autoantibodies (e.g., pari-etal cell antibodies and thyroid microsomal antibodies). These antibodies react with a short linear sequence of the recombinant antigen cytochrome monooxygenase P450 2D6. Patients with AIH type 2 more often tend to be young and female and have a severe form of disease that responds well to immunosuppressive therapy.Patients with chronic hepatitis resulting from hepatitis C can also have elevated anti-LKM-1 antibodies. The diagnosis of autoimmune liver disease cannot be made on antibody testing alone. In many instances, autoimmune liver disease panel testing, including the antibodies discussed in the preceding paragraph, is performed. Testing is performed by semi-quantitative enzyme-linked immunosorbent assay/semi-quantitative indirect fluores-cent antibody.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: noanti-liver/kidney microsomal type 1 antibodies 81A• Blood tube commonly used: serum separator Explain the importance of performing the test in the morning.• Blood may be sent to a reference laboratory. Results are avail-able in about 1 week.Abnormal findings Increased levelsAutoimmune hepatitisnotes82 antimitochondrial antibodyantimitochondrial antibody (AMA)Type of test BloodNormal findings No antimitochondrial antibodies (AMAs) at titers >1:5 orof WG and other systemic vasculitis syndromes.When ANCAs are detected with indirect immunofluorescence microscopy, two major patterns of staining are present: cyto-plasmic ANCA (c-ANCA) and perinuclear ANCA (p-ANCA). Specific immunochemical assays demonstrate that c-ANCA con-sists mainly of antibodies to proteinase 3 (PR3), and p-ANCA consists of antibodies to myeloperoxidase (MPO). Using the antigen-specific immunochemical assay to characterize ANCA (rather than the pattern of immunofluorescence microscopy) is more specific and more clinically relevant; therefore, the terms proteinase 3-ANCA (PR3-ANCA) and myeloperoxidase-ANCA (MPO-ANCA) are used.The PR3 autoantigen is highly specific (95% to 99%) for WG. When the disease is limited to the respiratory tract, the PR3 is positive in about 65% of patients. Nearly all patients with WG limited to the kidney do not have positive PR3. When WG is inactive, the percentage of positive PR3 drops to about 30%.The MPO autoantigen is found in 50% of patients with WG centered in the kidney. It also occurs in patients with non-WG glomerulonephritis, such as microscopic polyangiitis (MPA). P-ANCA antibodies can also differentiate various forms of inflam-matory bowel disease. See also anti-glycan antibodies, page 79. P-ANCA antibodies are found in 50% to 70% of ulcerative colitis (UC) patients, but in only 20% of Crohn disease (CD) patients.antineutrophil cytoplasmic antibody 85AProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: verify with labAbnormal findings Increased levelsWegener granulomatosisMicroscopic polyarteritisIdiopathic crescentic glomerulonephritisUlcerative colitisPrimary sclerosing cholangitisAutoimmune hepatitisChurg-Strauss vasculitisActive viral hepatitisCrohn diseasenotes86 antinuclear antibodyantinuclear antibody (ANA)Type of test BloodNormal findings Negative at 1:40 dilutionTest explanation and related physiologyANA is a group of antinuclear antibodies used to diagnose sys-temic lupus erythematosus (SLE) and other autoimmune (rheu-matic) diseases (Box 1). Some of the antibodies in this group are specific for SLE, and others are specific for other autoimmune dis-eases. ANA can be tested as a specific antibody or as a group with nonspecific antigens (Box 2). The former is more specific, but testing ANA with less specific antigens may be an excellent pre-liminary test for those suspected of having autoimmune diseases.Because almost all patients with SLE develop autoantibod-ies, a negative ANA test excludes the diagnosis. Positive results occur in approximately 95% of patients with this disease; how-ever, many other rheumatic diseases (see Box 1) are also associ-ated with ANA.ANA tests are performed using different assays (indirect immu-nofluorescence microscopy or enzyme-linked immunosorbent assay [ELISA]), and results are reported as a titer with a particular type of immunofluorescence pattern (when positive). Low-level titers are considered negative, while increased titers are positive and indicate an elevated concentration of antinuclear antibodies.ANA shows up on indirect immunofluorescence as fluores-cent patterns in cells that are fixed to a slide and are evaluated BOX 1 Diseases associated with antinuclear antibodiesSystemic lupus erythematosusSjögren syndromeSclerodermaRaynaud diseaseRheumatoid arthritisDermatomyositisMixed connective tissue diseaseAutoimmune hepatitisAutoimmune thyroiditisJuvenile rheumatoid arthritisPrimary biliary cirrhosisPolymyositisantinuclear antibody 87Aunder a UV microscope. Different patterns are associated with a variety of autoimmune disorders. When combined with a more specific subtype of ANA (Box 2), the pattern can increase speci-ficity of the ANA subtypes for the various autoimmune diseases (Figure 3). An example of a positive result might be: “Positive at 1:320 dilution with a homogeneous pattern.”As the disease becomes less active because of therapy, the ANA titers can be expected to fall (Table 1). In this text, the more commonly used ANA subtypes are separately discussed. About 95% of SLE patients have a positive ANA test result. If a TABLE 1 Autoimmune disease and positive ANAsAutoimmune disease Positive antibodiesSLE ANA, SLE prep, ds-DNA, ss-DNA, anti-DNP, SS-ADrug-induced SLE ANASjögren syndrome RF, ANA, SS-A, SS-BScleroderma ANA, Scl-70, RNA, ds-DNARaynaud disease ACA, Scl-70Mixed connective tissue diseaseANA, RNP, RF, ss-DNARheumatoid arthritis RF, ANA, RANA, RAPPrimary biliary cirrhosis AMAThyroiditis Antimicrosomal, antithyroglobulinChronic active hepatitis ASMABOX 2 Antinuclear antibodiesAnti-RNA antibodiesAnti-ENA antibodiesAntinuclear Smith (SM) antibodiesAntinuclear RNP antibodiesAntihistidyl antibodiesAntichromatin antibodiesAntinucleosome antibodiesAntihistone antibodiesAnti-DNA antibodiesAnti–ds-DNA antibodiesAnti–ss-DNA antibodiesAnti–SS-A (Ro)Anti–SS-B (La)88 antinuclear antibodypatient also has symptoms of SLE (e.g., arthritis, rash, autoim-mune thrombocytopenia), then he or she probably has SLE.Interfering factors Drugs that may cause a false-positive ANA test include acet-azolamide, aminosalicylic acid, chlorprothixene, chlorothia-zides, griseofulvin, hydralazine, penicillin, phenylbutazone, phenytoin sodium, procainamide, streptomycin, sulfon-amides, and tetracyclines. Drugs that may cause a false-negative test include steroids.Homogeneous pattern (diffuse)Associated with: SLE Mixed connective tissue diseaseOutline pattern (peripheral)Associated with: SLESpeckled patternAssociated with: SLESclerodermaSjögren syndromePolymyositis Rheumatoid arthritisMixed connective tissue diseaseNucleolar patternAssociated with: Scleroderma PolymyositisCell membraneNucleusFIGURE 3 Patterns of immunofluorescent staining of antinuclear antibodies and the diseases with which they are associated.antinuclear antibody 89AProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: redAbnormal findings Increased levelsSystemic lupus erythematosusRheumatoid arthritisChronic hepatitisPeriarteritis (polyarteritis) nodosaDermatomyositisSclerodermaInfectious mononucleosisRaynaud diseaseSjögren syndromeOther immune diseasesLeukemiaMyasthenia gravisCirrhosisnotes90 antiparietal cell antibodyantiparietal cell antibody (APCA)Type of test BloodNormal findings NegativeTest explanation and related physiologyParietal cells exist in the proximal stomach and produce hydrochloric acid and intrinsic factor. Intrinsic factor is neces-sary for the absorption of vitamin B12 (see p. 986). Antiparietal cell antibodies (APCAs) are found in nearly 90% of patients with pernicious anemia. Nearly 60% of these patients also have antiin-trinsic factor antibodies. It is thought that these antibodies con-tribute to the destruction of the gastric mucosa in these patients. APCA is also found in patients with atrophic gastritis, gastric ulcers, and gastric cancer.APCA is present in other autoimmune-mediated diseases, such as thyroiditis, myxedema, juvenile diabetes, Addison dis-ease, and iron-deficiency anemia. Nearly 10% to 15% of the nor-mal population has APCA. As one ages, the incidence of having APCA increases (especially in relatives of patients with pernicious anemia).APCA can cross-react with other antibodies, especially anti-cellular and antithyroid antibodies. Titer levels greater than 1:240 are considered positive.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: redAbnormal findings Increased levelsPernicious anemiaAtrophic gastritisHashimoto thyroiditisMyxedemaInsulin-dependent diabetes mellitusAddison diseasenotesantiscleroderma antibody91Aantiscleroderma antibody (Scl-70 antibody, Scleroderma antibody, RNA polymerase III antibody)Type of test BloodNormal findings NegativeTest explanation and related physiologyThis antibody is diagnostic for scleroderma (progressive sys-temic sclerosis [PSS]) and is present in 45% of patients with that disease. Scl-70 antibody is an antinuclear antibody (see p. 86). PSS is a multisystem disorder characterized by inflammation with subsequent fibrosis of the small blood vessels in skin and visceral organs, including the heart, lungs, kidneys, and gastrointestinal tract. A collagen-like substance is also deposited into the tissue of these organs. In general, the higher the titer of Scl-70 antibody, the more likely that PSS exists and the more active the disease is. As the disease becomes less active because of therapy, the Scl-70 antibody titers can be expected to fall.The absence of this antibody does not exclude the diagnosis of PSS. The antibody is rather specific for PSS but is occasion-ally seen in other autoimmune diseases (e.g., systemic lupus ery-thematosus, mixed connective tissue disease, Sjögren syndrome, polymyositis, and rheumatoid arthritis).RNA polymerase III antibodies are found in 11% to 23% of patients with PSS. PSS patients who are positive for RNA poly-merase III antibodies form a distinct serologic subgroup and usually do not have any of the other antibodies typically found in PSS patients, such as anticentromere (p. 66) or anti-Sc170. PSS patients with anti-RNA polymerase III have an increased risk of the diffuse cutaneous form of scleroderma, with a high likelihood of skin involvement and hypertensive renal disease. A positive result supports a possible diagnosis of PSS. This autoantibody is strongly associated with diffuse cutaneous scleroderma and with an increased risk of acute renal crisis. A negative result indicates no detectable IgG antibodies to RNA polymerase III, but does not rule out the possibility of PSS (11% to 33% sensitivity).Interfering factors Drugs that may cause increased levels include aminosalicylic acid, isoniazid, methyldopa, penicillin, propylthiouracil, streptomycin, and tetracycline.92 antiscleroderma antibodyProcedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: redAbnormal findingsPositive resultsSclerodermaCREST syndromenotesanti–smooth muscle antibody 93Aanti–smooth muscle antibody (ASMA)Type of test BloodNormal findings No anti–smooth muscle antibodies (ASMAs) at titers >1:20Test explanation and related physiologyThe ASMA is used primarily to aid in the diagnosis of auto-immune chronic active hepatitis (CAH), which has also been referred to as lupoid CAH. ASMA is an anticytoplasmic antibody directed against actin, a cytoskeletal protein. Normally the serum does not contain ASMA at a titer greater than 1:20. ASMA is the most commonly recognized autoantibody in the setting of CAH. It appears in 70% to 80% of patients with CAH. Some types of CAH do not have positive ASMA antibodies.ASMA is not specific for CAH and can be positive in patients with viral infections, malignancy, multiple sclerosis, primary biliary cirrhosis, and Mycoplasma infections. Usually the titer of ASMA is low in these diseases. With CAH, the titer is usually higher than 1:160. The titers are not helpful in prognosis, nor do they indicate disease response to therapy.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: redAbnormal findings Increased levelsChronic active hepatitisMononucleosis hepatitisPrimary biliary cirrhosisViral hepatitisMultiple sclerosisMalignancyIntrinsic asthmanotes94 antispermatozoal antibodyantispermatozoal antibody (Sperm agglutination and inhibition, Sperm antibodies, Antisperm antibodies, Infertility screen)Type of test Fluid analysis; bloodNormal findingsof the lacrimal and salivary exocrine glands, leading to mucosal and conjunctival dryness. This disease can occur by itself (primary) or in association with other autoimmune diseases, such as sys-temic lupus erythematosus (SLE), rheumatoid arthritis (RA), and scleroderma. In the latter case, it is referred to as secondary Sjögren syndrome.Anti–SS-A antibodies may be found in approximately 60% to 70% of patients with primary Sjögren syndrome. Anti–SS-B antibodies may be found in approximately half of patients with primary Sjögren syndrome. When anti–SS-A and anti–SS-B anti-bodies are both positive, Sjögren syndrome can be diagnosed. These antibodies are only occasionally found when secondary Sjögren syndrome is associated with RA. In fact, anti–SS-B is found only in primary Sjögren syndrome. However, anti–SS-C is positive in about 75% of patients with RA or patients with RA and secondary Sjögren syndrome. Therefore, these antibodies are also useful in differentiating primary from secondary Sjögren syndrome.Anti–SS-A can also be found in 25% of patients with SLE. This is particularly useful in ANA-negative cases of SLE because these antibodies are present in the majority of such patients. Anti–SS-B is rarely found in SLE, however. In general, the higher the titer Aanti–SS-A (Ro), anti–SS-B (La), and anti–SS-C antibodies 97of anti-SS antibodies, the more likely that Sjögren syndrome exists and the more active the disease is. As Sjögren syndrome becomes less active with therapy, the anti-SS antibody titers can be expected to fall.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: redAbnormal findingsPositiveSjögren syndromeRheumatoid arthritisANA-negative systemic lupus erythematosusNeonatal lupusnotes98 antithrombin activity and antigen assayantithrombin activity and antigen assay (Antithrombin III [AT-III] activity/assay, Functional antithrombin III assay, Heparin cofactor, Immunologic antithrombin III, Serine protease inhibitor)Type of test BloodNormal findingsAntithrombin activity:Newborn: 35% to 40%>6 months to adult: 80% to 130%Antithrombin antigen assay:Plasma: >50% of control valueSerum: 15% to 34% lower than plasma valueImmunologic: 17-30 mg/dLFunctional: 80% to 120%Values vary according to laboratory methods.Test explanation and related physiologyAT-III is an alpha2 globulin produced in the liver. It inhib-its the serine proteases involved in coagulation (II, X, IX, XI, XII). In normal homeostasis, coagulation results from a bal-ance between AT-III and thrombin. A deficiency of AT-III increases coagulation or the tendency toward thrombosis. A hereditary deficiency of AT-III is characterized by a predis-position toward thrombus formation. This is passed on as an autosomal dominant abnormality. Individuals with hereditary AT-III deficiency typically develop thromboembolic events in their early twenties. These thrombotic events are usually venous.Acquired AT-III deficiency may be seen in patients with cir-rhosis, liver failure, advanced carcinoma, nephrotic syndrome, disseminated intravascular coagulation (DIC), protein-losing enteropathies, and acute thrombosis. AT-III is also decreased as much as 30% in pregnant women and women who take estro-gens. Antithrombin activity testing is ordered, along with other tests for hypercoagulable disorders (e.g., protein C and protein S, and lupus anticoagulant), when a patient has been experienc-ing recurrent venous thrombosis. Antithrombin should be mea-sured after a blood clot has been treated and resolved as both the presence of the clot and the therapy used to treat it will affect antithrombin results.antithrombin activity and antigen assay 99AAT-III provides most of the anticoagulant effect of heparin. Heparin increases antithrombin activity by 1000-fold. Patients who are deficient in AT-III may be heparin resistant and require unusually high doses for an anticoagulation effect. In general, patients respond to heparin if more than 60% of normal AT-III levels exist.There are two tests for AT-III. The first is a functional assay and measures AT-III activity. The second quantifies the AT-III antigen. The antithrombin activity test is performed before the antigen test to evaluate whether the total amount of functional antithrombin activity is normal. Antithrombin activity is the primary (screening) antithrombin assay. If antithrombin activity is normal, AT-III is not the cause of the hypercoagulable state. If antithrombin activity is abnormal, antithrombin antigen should be quantified.Asymptomatic individuals with an antithrombin deficiency should receive prophylactic anticoagulation to increase their antithrombin levels before any medical/surgical interventions in which inactivity increases the risk of thrombosis. Increased levels of AT-III are not usually considered a problem and may occur in patients with acute hepatitis, obstructive jaundice, vitamin K deficiency, and kidney transplantation.Antithrombin studies are also used as an adjunct in the diag-nosis and management of carbohydrate-deficient glycoprotein syndromes (CDGSs) because defective glycosylation of this AT-III in individuals with CDGSs will cause hypercoagulation. Deficient AT-III may also contribute to recurrent miscarriages.Antithrombin activity testing is also used to monitor treat-ment of antithrombin deficiency disorders by infusion of anti-thrombin concentrates.Interfering factors Drugs that may cause increased levels include anabolic ster-oids, androgens, oral contraceptives (containing progeste-rone), and sodium warfarin. Drugs that may cause decreased levels include fibrinolytics, heparin, L-asparaginase, and oral contraceptives (containing estrogen).Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: light blue or red• Patients receiving heparin therapy may develop a hematoma at the venipuncture site.100 antithrombin activity and antigen assayTest results and clinical significance Increased levels Decreased levelsKidney transplantAcute hepatitisDisseminated intravascular coagulation (DIC)Obstructive jaundiceVitamin K deficiencyHypercoagulation states (e.g., deep vein thrombosis)Hepatic disorders (especially cirrhosis)Nephrotic syndrome Protein-wasting diseases (malignancy) Hereditary familial deficiency of AT-IIInotesantithyroglobulin antibody 101Aantithyroglobulin antibody (Thyroid autoantibody, Thyroid antithyroglobulin antibody, Thyroglobulin antibody)Type of test BloodNormal findingsno• Blood tube commonly used: redAbnormal findings Increased levelsHashimoto thyroiditisRheumatoid arthritisRheumatoid-collagen diseasePernicious anemiaThyrotoxicosisHypothyroidismThyroid carcinomaMyxedemaAutoimmune hemolytic anemianotes102 antithyroid peroxidase antibodyantithyroid peroxidase antibody (Anti-TPO, TPO-Ab, Antithyroid microsomal antibody, Thyroid autoantibody)Type of test BloodNormal findings Titerfetal hemoglobin stool test, Stool for swallowed blood)Type of test StoolNormal findingsNo fetal blood present.Maternal blood may be present.Test explanation and related physiologyBlood in the stool of a newborn must be rapidly evaluated. Furthermore, some serious diseases present as rectal bleeding in the newborn. Much more commonly, however, newborns may simply be defecating maternal blood that was swallowed during birth or breastfeeding.The Apt test is performed on the stool specimen to differenti-ate maternal from fetal blood in the stool. Fetal hemoglobin is resistant to denaturation; adult hemoglobin (hemoglobin A) is not. This test can be performed on stool, a stool-stained diaper, amniotic fluid, or vomitus.Procedure and patient careBefore Explain the procedure to the newborn’s parents.• Assess the vital signs of the newborn with possible intestinal bleeding.During• Obtain an adequate stool or vomitus specimen.• In the laboratory, 1% NaOH is added to the specimen. Vomitus (and sometimes stool) is diluted and centrifuged first. Maternal blood turns brown; newborn blood stays red or pink.After• If maternal blood is present, reassure the parents and examine the mother for nipple erosion and/or cracking.• If newborn blood is present, begin close observation and sup-port during further diagnostic procedures.Abnormal findingsActive gastrointestinal bleedingNecrotizing enterocolitisnotesarterial blood gases 109Aarterial blood gases (ABGs, blood gases)Type of test BloodNormal findingspHAdult/child: 7.35-7.45Newborn: 7.32-7.492 months-2 years: 7.34-7.46pH (venous): 7.31-7.41Pco2Adult/child: 35-45 mm HgChild 7.55Pco2: 60HCO3: 40Po2: 7.4) and acidity (pHO2 con-tent decreases with the same diseases that diminish Po2.Base excess/deficitThis number is calculated by the blood gas machine by using the pH, Pco2, and hematocrit. It represents the amount of buff-ering anions in the blood. HCO3 is the largest of these. Others include hemoglobin, proteins, and phosphates. Base excess is a way to take all these anions into account when determining acid/base treatment based on the metabolic component. Negative base excess (deficit) indicates a metabolic acidosis (e.g., lactic acido-sis). A positive base excess indicates metabolic alkalosis or com-pensation to prolonged respiratory acidosis.Alveolar (A) to arterial (a) O2 difference (A-a gradient)This is a calculated number that indicates the difference between alveolar (A) O2 and arterial (a) O2. The normal value is less than 10 mm Hg (torr). If the A-a gradient is abnormally high, there is either a problem in diffusing O2 across the alveo-lar membrane (thickened edematous alveoli) or unoxygenated blood is mixing with the oxygenated blood.Contraindications• Patients with a negative Allen test• Patients with arteriovenous fistula proximal to the site of pro-posed access• Patients with severe coagulopathyPotential complications• Occlusion of the artery used for access• Penetration of other important structures anatomically juxta-posed to the artery (e.g., nerve)114 arterial blood gasesInterfering factors• O2 saturation can be falsely increased with the inhalation of carbon monoxide. Respiration can be inhibited by sedatives or narcotics.Procedure and patient careBefore Explain the procedure to the patient. Tell the patient that an arterial puncture is associated with more discomfort than a venous puncture.• Notify the laboratory before drawing ABGs so that the nec-essary equipment can be calibrated before the blood sample arrives.• Perform the Allen test to assess collateral circulation.• To perform the Allen test, make the patient’s hand blanch by obliterating both the radial and the ulnar pulses, and then release the pressure over the ulnar artery only. If flow through the ulnar artery is good, flushing will be seen immediately. The Allen test is then positive, and the radial artery can be used for puncture.• If the Allen test is negative (no flushing), repeat it on the other arm.• If both arms give a negative result, choose another artery for puncture.During• Note that arterial blood can be obtained from any area of the body where strong pulses are palpable, usually from the radial, brachial, or femoral artery.• Cleanse the arterial site.• Use a small gauge needle to collect the arterial blood in an air-free heparinized syringe.• After drawing blood, remove the needle and apply pressure to the arterial site for 3 to 5 minutes.• Expel any air bubbles in the syringe.• Cap the syringe and gently rotate to mix the blood and heparin.• Note that an arterial puncture is performed by laboratory technicians, respiratory-inhalation therapists, nurses, or phy-sicians in approximately 10 minutes.After• Place the arterial blood on ice and immediately take it to the chemistry laboratory for analysis.arterial blood gases 115A• Apply pressure or a pressure dressing to the arterial puncture site for 3 to 5 minutes to avoid hematoma formation.• Assess the puncture site for bleeding. Remember that an artery rather than a vein has been stuck.Abnormal findings Increased pH (alkalosis) Decreased pH (acidosis)Metabolic alkalosis Metabolic acidosisHypokalemia KetoacidosisHypochloremia Lactic acidosisChronic and high-volume gastric suctionSevere diarrheaRenal failureChronic vomiting Aldosteronism Mercurial diuretics Respiratory alkalosis Respiratory acidosisChronic heart failure Respiratory failureCystic fibrosis Carbon monoxide poisoning Pulmonary emboli Shock Acute and severe pulmonary diseases Anxiety neuroses Pain Pregnancy Increased Pco2 Decreased Pco2Chronic obstructive pulmonary disease (COPD) (bronchitis, emphysema)HypoxemiaPulmonary emboliAnxietyOversedation PainHead trauma PregnancyOveroxygenation in a patient with COPD Pickwickian syndrome 116 arterial blood gases Increased HCO3 Decreased HCO3Chronic vomitingChronic and high-volume gastric suctionAldosteronismChronic and severe diarrheaChronic use of loop diureticsUse of mercurial diuretics StarvationChronic obstructive pulmonary diseaseDiabetic ketoacidosisAcute renal failure Increased Po2, increased O2 content Decreased Po2, decreased O2 contentPolycythemia AnemiasIncreased inspired O2 Mucus plugHyperventilation Bronchospasm Atelectasis Pneumothorax Pulmonary edema Adult respiratory distress syndrome Restrictive lung disease Atrial or ventricular cardiac septal defects Emboli Inadequate O2 in inspired air (suffocation) Severe hypoventilation (e.g., oversedation, neurologic somnolence)notesarteriography 117Aarteriography (Angiography)Type of test X-ray with contrast dyeNormal findings Normal arterial vasculatureTest explanation and related physiologyWith the injection of radiopaque contrast material into arter-ies, blood vessels can be visualized to determine arterial anatomy or vascular disease. With a catheter usually placed through the femoral artery and into the desired artery, radiopaque contrast is rapidly injected while x-ray images are obtained. Blood flow dynamics, arterial occlusive disease, or vascular anomalies are eas-ily seen. With the use of digital subtraction angiography (DSA), bony structures can be obliterated from the picture. Coronary arteriography is described under cardiac catheterization (see p. 214).Renal angiography permits evaluation of renal artery blood flow dynamics. Arteriosclerotic narrowing (stenosis) of the renal artery is best demonstrated with this study. The angiographic location of the stenotic area is helpful if considering surgical repair of stenting.Lower extremity arteriography allows for accurate identifica-tion and location of occlusions within the abdominal aorta and lower extremity arteries. Total or near-total occlusion of the flow of dye is seen in arteriosclerotic vascular occlusive disease. Emboli are seen as total occlusions of the artery. Arterial traumas, such as lacerations or intimal tears (laceration of the inner arterial lin-ing), likewise appear as total or near-total obstruction of the flow of dye. Unusual arterial disorders, such as Buerger disease and fibromuscular dysplasia, have the classic arterial beading, which is pathognomonic.Arterial vascular balloon dilation and stenting can be per-formed if a short-segment arterial stenosis is identified. In these instances, the wire is placed through the angiocatheter into the area of narrowing. A balloon catheter is inserted over the wire. The dilating balloon is inflated, and the arteriosclerotic plaque is gently and persistently dilated, and can then be stented.With angiography, there is always a concern that the arterial puncture site may not seal, leading to a pseudoaneurysm. More recently, vascular closure products have been used to quickly seal femoral artery punctures following catheterization procedures. This allows for early ambulation and hospital discharge. The injection of these materials on the vascular entrance site creates a 118 arteriographymechanical seal by sandwiching the arteriotomy between a bio-absorbable anchor and a collagen sponge, which dissolve within 60 to 90 days.ContraindicationsThe following represent relative contraindications. If the information/therapy is necessary to obtain through arteri-ography, appropriate steps can be taken to reduce risks in these patients. As in all diagnostic testing, the risks must be weighed against the benefits.• Patients with allergies to shellfish or iodinated dye• Patients who are uncooperativeor agitated• Patients who are pregnant, unless the benefits outweigh the risks• Patients with renal disorders, because iodinated contrast is nephrotoxic• Patients with a bleeding propensity• Patients with unstable cardiac disorders• Patients who are dehydrated, because they are especially sus-ceptible to dye-induced renal failurePotential complications• Allergic reaction to iodinated dye• Hemorrhage from the arterial puncture site• Arterial embolism from dislodgment of an arteriosclerotic plaque• Soft tissue infection around the puncture site• Renal failure, especially in elderly patients who are chronically dehydrated or have a mild degree of renal failure• Dissection of the intimal lining of the artery causing complete or partial arterial occlusion• Pseudoaneurysm development as a result of failure of the puncture site to seal• Lactic acidosis may occur in patients who are taking metfor-min. The metformin should not be taken the day of the test to prevent this complication.Procedure and patient careBefore Explain the procedure to the patient. Allay any fears and allow the patient to verbalize concerns.• Obtain written and informed consent for this procedure. Inform the patient that a warm flush may be felt when the dye is injected.• Assess the possibility of allergies to iodinated dye.arteriography 119A• Determine if the patient has been taking anticoagulants.• Keep the patient NPO for 2 to 8 hours before testing.• Mark the site of the patient’s peripheral pulses with a pen before arterial catheterization. This will permit assessment of the peripheral pulses after the procedure.• If the patient does not have peripheral pulses before arteriog-raphy, document that fact so that arterial occlusion will not be suspected on the postangiogram assessment.• Ensure that the appropriate renal function studies are normal.• If the patient has diminished renal function, provide IV hydra-tion to minimize further renal damage. Instruct the patient to void before the study because the iodinated dye can act as an osmotic diuretic. Inform the patient that bladder distention may cause some discomfort during the study.During• Note the following preprocedure steps:1. The patient may be sedated before being taken to the angiography room, which is usually within the radiology department.2. The patient is placed on the x-ray table in the supine position.3. If the femoral artery is to be used, the groin is shaved, prepared as per protocol, and draped in a sterile manner.4. The femoral artery is cannulated, and a wire is threaded up that artery and into or near the opening of the desired artery to be examined.5. A catheter is then placed over the wire. The wire and cath-eter are placed under fluoroscopic visualization. Because the catheter and wire have curled tips at their ends, they can be manipulated directly into the artery to be studied. The wire is removed.6. Through the catheter, iodinated contrast material is injected by the use of an automated injector at a preset, controlled rate. This occurs over several seconds.7. Cinefluoroscopy is used to visualize the injection in real time.• Note that this procedure is usually performed by an angiogra-pher (radiologist) in approximately 1 hour. During the dye injection, remind the patient that an intense, burning flush may be felt throughout the body but lasts only a few seconds. Tell the patient that the most significant discomfort is the groin puncture that was necessary for arterial access.120 arteriography Remind the patient of the discomfort of lying on a hard x-ray table for a long period.After• After x-ray studies are completed, remove the catheter and apply a pressure dressing to the puncture site.• Monitor the patient’s vital signs for indications of hemorrhage.• Assess the peripheral arterial pulse in the extremity used for vascular access and compare it with the preprocedure baseline.• Observe the arterial puncture site frequently for signs of bleeding or hematoma.• Maintain pressure at the puncture site with a 1- to 2-lb sand-bag or an IV bag.• Keep the patient on bed rest for up to 8 hours after the pro-cedure to allow for complete sealing of the arterial puncture site. If a vascular closure product is used, the patient may ambulate within 2 hours.• Note and compare the color and temperature of the extremity with that of the uninvolved extremity.• Notify the physician if the patient has severe, continuous pain. Instruct the patient to drink fluids to prevent dehydration caused by the diuretic action of the dye.• Evaluate the patient for delayed allergic reaction to the dye. Instruct the patient to report any signs of numbness, tingling, pain, or loss of function in the involved extremity.Abnormal findingsArteriography of the peripheral vascular systemArteriosclerotic occlusionEmbolus occlusionPrimary arterial diseases (e.g., fibromuscular dysplasia, Buerger disease)AneurysmKidney arteriographyAtherosclerotic narrowing of the renal arteryFibrodysplasia of the renal arteryRenal vascular causes of hypertensionnotesarthrocentesis with synovial fluid analysis 121Aarthrocentesis with synovial fluid analysisType of test Fluid analysisNormal findingsAppearance Clear, straw colored, no bloodRBC NoneWBC 0-150/mm3WBC differential Neutrophils 7%Lymphocytes 24%Monocytes 48%Macrophages 10%Glucose Equal to fasting blood glucoseProtein 1-3 dLLDHfalls with increasing severity of inflam-mation. Although lowest in septic arthritis (the synovial fluid glucose value may bein the tests.Many new studies, such as galectin-3, nicotine and metabo-lites, pepsinogen, and thromboelastography, have been added. All other studies have been revised and updated. Outdated stud-ies have been eliminated.We sincerely thank our editors for their enthusiasm and con-tinued support. We are most grateful to the many nurses and other health care providers who made the first eleven editions of this book so successful. Thank you so much. This success vali-dated the need for a user-friendly and quick-reference approach to laboratory and diagnostic testing.We invite additional comments from current users of this book so that we may continue to provide useful, relevant diag-nostic and laboratory test information to users of future editions.Kathleen D. PaganaTimothy J. PaganaTheresa N. PaganaxcontentsList of figures, xiUser’s guide to test preparation and procedures, xiiDiagnostic and laboratory tests, 1Tests presented in alphabetical orderAppendices Appendix A: List of tests by body system, 1003 Appendix B: List of tests by type, 1015 Appendix C: Disease and organ panels, 1026 Appendix D: Symbols and units of measurement, 1030Bibliography, 1032Index, 1036list of figuresFigure 1 Ultrasound of the abdomen, 2Figure 2 Amniocentesis, 53Figure 3 Immunofluorescent staining of antinuclear antibodies, 88Figure 4 Arthroscopy, 125Figure 5 Bilirubin metabolism and excretion, 143Figure 6 Bone marrow aspiration, 169Figure 7 Bronchoscopy, 194Figure 8 Cardiac catheterization, 216Figure 9 Chorionic villus sampling, 255Figure 10 Hemostasis and fibrinolysis, 264Figure 11 Colposcopy, 274Figure 12 Cardiac enzymes after myocardial infarction, 309Figure 13 Cystoscopic examination of the male bladder, 326Figure 14 Ureteral catheterization through the cystoscope, 327Figure 15 Disseminated intravascular coagulation, 346Figure 16 Ductoscopy, 354Figure 17 ECG planes of reference, 360Figure 18 Electrocardiography, 361Figure 19 Endoscopic retrograde cholangiopancreatography, 386Figure 20 Esophageal function studies, 400Figure 21 Fetoscopy, 437Figure 22 Glucose tolerance test, 480Figure 23 Hematocrit, 498Figure 24 Holter monitoring, 525Figure 25 Hysteroscopy, 549Figure 26 Laparoscopy, 578Figure 27 Liver biopsy, 591Figure 28 Lumbar puncture, 602Figure 29 Transbronchial needle biopsy, 605Figure 30 Stereotactic breast biopsy, 625Figure 31 Oximetry, 674Figure 32 Papanicolaou (Pap) smear, 683Figure 33 Paracentesis, 685Figure 34 Pericardiocentesis, 702Figure 35 Rectal ultrasonography, 754Figure 36 Lung volumes and capacities, 774Figure 37 Renal biopsy, 793Figure 38 Renovascular hypertension, 801Figure 39 Rectal culture of the female, 831Figure 40 Urethral culture of the male, 832Figure 41 Thoracentesis, 884Figure 42 Fibrin clot formation, 894Figure 43 Transesophageal echocardiography, 922xixiiuser’s guide to test preparation and proceduresHealth care economics demands that laboratory and diagnos-tic testing be performed accurately and in the least amount of time possible. Tests should not have to be repeated because of improper patient preparation, test procedure, or specimen collec-tion technique. The following guidelines delineate the responsi-bilities of health care providers to ensure safety of test procedures and accuracy of test results. Guidelines are described for the fol-lowing major types of tests: blood, urine, stool, x-ray, nuclear scanning, ultrasound, and endoscopy.Blood testsOverviewBlood studies are used to assess a multitude of body processes and disorders. Common studies include enzymes, serum lipids, electrolyte levels, red and white blood cell counts, clotting factors, hormone levels, and levels of breakdown products (e.g., blood urea nitrogen).Multiphasic screening machines can perform many blood tests simultaneously using a very small blood sample. The advantages of using these machines are that results are available quickly and the cost is lower when compared with individually performing each test.Appendix C provides a list of current disease and organ pan-els. For example, the basic metabolic panel and the comprehen-sive metabolic panel have replaced the Chem-7 and Chem-12 panels. These changes are the result of federal guidelines that have standardized the nomenclature for chemistry panels.Guidelines• Observe universal precautions when collecting a blood specimen.• Check whether fasting is required. Many studies, such as fasting blood sugar and cholesterol levels, require fasting for a designated period of time. Water is permitted.• If ordered, withhold medications until the blood is drawn.• Record the time of day when the blood test is drawn. Some blood test results (e.g., those for cortisol) vary according to a diurnal pattern, and this must be considered when blood levels are interpreted.• In general, two or three blood tests can be done per tube of blood collected (e.g., two or three chemistry tests from one red-top tube of blood).user’s guide to test preparation and procedures xiiiuser’s guide to test preparation and procedures• Note the patient’s position for certain tests (e.g., renin, because levels are affected by body position).• Collect the blood in a properly color-coded test tube. Blood collection tubes have color-coded stoppers to indi-cate the presence or absence of different types of additives (preservatives and anticoagulants). A preservative prevents change in the specimen, and an anticoagulant inhibits clot formation or coagulation. Charts are available from the lab-oratory indicating the type of tube needed for each partic-ular blood test. A representative chart is shown in Table A, p. xiv.• Follow the recommended order of draw when collecting blood in tubes. Draw specimens into nonadditive (e.g., red-top) tubes before drawing them into tubes with addi-tives. This prevents contamination of the blood specimen with additives that may cause incorrect test results. Fill the tubes in the following order:1. Blood culture tubes (to maintain sterility)2. Nonadditive tubes (e.g., red-top)3. Coagulation tubes (e.g., blue-top)4. Heparin tubes (e.g., green-top)5. Ethylenediaminetetraacetic acid (EDTA) tubes (e.g., lavender-top)6. Oxalate/fluoride tubes (e.g., gray-top)• To obtain valid results, do not fasten the tourniquet for longer than 1 minute. Prolonged tourniquet application can cause stasis and hemoconcentration.• Collect the blood specimen from the arm without an intra-venous (IV) device, if possible. IV infusion can influence test results.• Do not use the arm bearing a dialysis arteriovenous fistula for venipuncture unless the physician specifically autho-rizes it.• Because of the risk of cellulitis, do not take specimens from the side on which a mastectomy or axillary lymph node dissection was performed.• Follow the unit guidelines for drawing blood from an indwelling venous catheter (e.g., a triple-lumen catheter). Guidelines will specify the amount of blood to be drawn from the catheter and discarded before blood is collected for laboratory studies. The guidelines will also indicate the amount and type of solution needed to flush the catheter after drawing the blood to prevent clotting.xiv user’s guide to test preparation and proceduresTABLE A Common blood collection tubesTop color Additive Purpose Test examplesRed Clot activator Allows blood sample to clotSeparates the serum for testingChemistryBilirubinBlood urea nitrogenRed/Black Clot activator & gel for serum separatorSerum separator tube for serum determinatives in chemistry and serologyChemistry, serologyRoyal Blue Heparin/ethylene-diaminetetraacetic acid (EDTA)Provides low levels of trace elements Trace metals, toxicologyTan Heparin/EDTA Contains no lead Lead determinativesPurple or lavenderEDTA Prevents blood from clotting HematologyCBCGray Oxalate/fluoride Prevents glycolysisand wrapped with an elastic bandage from the toes to the lower thigh to drain as much blood from the leg as possible.3. A tourniquet is placed on the patient’s leg. If the tourni-quet is not used, a fluid solution may be instilled into the patient’s knee immediately before insertion of the arthro-scope to distend the knee and help reduce bleeding.4. The foot of the table is lowered so that the patient’s knee is at a 45-degree angle.5. A small incision is made in the skin around the knee.6. The arthroscope (a lighted instrument) is inserted into the joint space to visualize the inside of the knee joint. In the past, the surgeon looked directly into the scope. More recently, a video camera has been attached to the scope in order for the image to be projected onto a TV monitor.7. Although the entire joint can be viewed from one punc-ture site, additional punctures for better visualization are often necessary.8. After the area is examined, biopsy or appropriate surgery can be performed.9. Before removal of the arthroscope, the joint is irrigated. Pressure is then applied to the knee to remove the irrigat-ing solution.10. After a few stitches are placed into the skin, a pressure dressing is applied over the incision site.• Note that this procedure is performed in the operating room by an orthopedic surgeon in approximately 15 to 30 minutes. Tell the patient receiving local anesthesia that there may be transient discomfort from the injection of the local anesthetic and from the pressure of the tourniquet on the leg. Inform the patient that a thumping sensation may be felt as the arthroscope is inserted into the joint and that the joint may be painful for several days.After• Assess the patient’s neurologic and circulatory status.• Assess vital signs and observe the patient for signs of infection, including fever, swelling, increased pain, and redness or drain-age at the incision site.128 arthroscopy Instruct the patient to elevate the knee when sitting and to avoid overbending the knee, so that swelling is minimized. Inform the patient that he or she can usually walk with the assistance of crutches; however, this depends on the extent of the procedure and the physician’s protocol. Tell the patient to minimize use of the joint for several days.• Examine the incision site for bleeding. Educate the patient to look for signs of bleeding into the joint (significant swelling, increasing pain, or joint weakness).• Apply ice to reduce pain and swelling, and instruct the patient to continue this at home. Educate the patient to look for signs of phlebitis. This is not uncommon in a person immobilized by joint pain. The involved leg may become swollen, painful, and edematous. Instruct the patient not to drive until it is approved by the physician. Inform the patient that the sutures will be removed in approx-imately 7 to 10 days.Abnormal findingsTorn cartilageTorn ligamentPatellar diseasePatellar fractureChondromalaciaOsteochondritis dissecansCyst (e.g., Baker)SynovitisRheumatoid arthritisDegenerative arthritisMeniscal diseaseOsteochondromatosisTrapped synoviumnotesaspartate aminotransferase 129Aaspartate aminotransferase (AST; Formerly called serum glutamic-oxaloacetic transaminase [SGOT])Type of test BloodNormal findingsAdult: 0-35 units/L or 0-0.58 μKat/L (SI units); females tend to have slightly lower values than malesElderly: values slightly higher than adult valuesChildren:0-5 days: 35-140 units/Levaluated by a BE, reflux of barium into the terminal ileum also allows adequate visualiza-tion of the distal part of the small intestine. Diseases that affect the terminal ileum, especially Crohn disease (regional enteritis), can be identified. Inflammatory bowel disease involving the colon can be detected with a BE. Fistulas involving the colon can be demonstrated by a BE.In many instances, air is insufflated into the colon after the instillation of barium. This provides an air contrast to the bar-ium. With air contrast, the colonic mucosa can be much more accurately visualized. This is called an air-contrast BE. It is used especially when small polyps are suspected. The accuracy of the regular BE in detecting small colonic tumors is approximately 60%; however, the accuracy of an air-contrast BE in detecting small colonic tumors exceeds 85%.Contraindications• Patients suspected of a perforation of the colon In these patients, diatrizoate (Gastrografin), a water-soluble contrast medium, is used.• Patients who are unable to cooperate This test requires the patient to hold the barium in the rectum and colon. This is especially difficult for elderly patients.• Patients with megacolon Barium may worsen the disease.barium enema 133BPotential complications• Colonic perforation, especially when the colon is weakened by inflammation, tumor, or infection• Barium fecal impactionInterfering factors• Barium within the abdomen from previous barium tests• Significant residual stool within the colon precludes adequate visualization of the entire bowel wall. Stool may be confused with polyps.• Spasm of the colon can mimic the radiographic signs of a cancer.Procedure and patient careBefore Explain the procedure to the patient. Encourage the patient to verbalize questions and fears.• Assist the patient with the bowel preparation, which varies among institutions. In elderly patients, this preparation can be exhausting and may even cause severe dehydration. A typi-cal preparation for most adults would include the following actions:Day before examination• Give the patient clear liquids for lunch and supper (no dairy products). Instruct the patient to drink one glass of water or clear fluid every hour for 8 to 10 hours.• Administer a cathartic (10 ounces of magnesium citrate) or X-Prep (extract of senna fruit) at 2 pm. In children, lesser vol-umes may be used.• Administer three 5-mg bisacodyl (Dulcolax) tablets at 7 pm.• A pediatric Fleet enema the night before testing and repeated 3 hours before testing may be adequate prep for an infant.• Keep the patient NPO after midnight the day of the test.Day of examination• Keep the patient NPO.• Administer a bisacodyl suppository at 6 am and/or a cleansing enema.• Note that pediatric patients will have individualized bowel preparations.• Note that special preparations will be ordered for patients with an ileostomy or colostomy.• Determine whether the bowel is adequately cleansed. When the fecal return is similar to clear water, preparation is 134 barium enema adequate; if large, solid fecal waste is still being evacuated, preparation is inadequate. Notify the radiologist, who may want to extend the bowel preparation. Suggest that the patient take reading material to the x-ray department to occupy the time while expelling the barium.During• Note the following procedural steps:1. The test begins with placement of a rectal balloon catheter.2. The balloon on the catheter is inflated tightly against the anal sphincter to hold the barium within the colon.3. The patient is asked to roll into the lateral, supine, and prone positions.4. The barium is dripped into the rectum by gravity. The colon of the young child is not able to tolerate the volume and pressure of instillation of barium that an adult’s can. Both volume and pressure should be reduced.5. The barium flow is monitored fluoroscopically.6. The colon is thoroughly examined as the barium flow pro-gresses through the large colon and into the terminal ileum.7. The barium is drained out.8. If an air-contrast BE has been ordered, air is insufflated into the large bowel.9. The patient is asked to expel the barium, and a postevacu-ation x-ray image is taken.• The standard procedure for administering the barium through a colostomy is to instill the contrast medium through an irrigation cone placed in the stoma. When the x-ray series is completed, the barium is allowed to be expelled from the stoma. A gentle stream of clean water for irrigation is helpful in expelling residual barium.• Note that this test is usually performed in the radiology department by a radiologist in approximately 45 minutes. Inform the patient that abdominal bloating and rectal pres-sure will occur during instillation of barium.After• Ensure that the patient defecates as much barium as possible. Suggest the use of soothing ointments on the anal area to minimize any anorectal pain that may result from the test preparation. Encourage ingestion of fluids to avoid dehydration caused by the cathartics. Encourage rest after the procedure. The cleansing regimen and BE procedure may be exhausting.barium enema 135BB Be aware of dehydration and electrolyte abnormalities. Instruct parents to hydrate the child well with electrolyte-containing fluids after the BE. Inform the patient that bowel movements will be white. When all the barium has been expelled, the stool will return to a normal color.• Note that laxatives may be ordered to facilitate evacuation of barium.Abnormal findingsMalignant tumorPolypsDiverticulaInflammatory bowel diseases (e.g., ulcerative colitis, Crohn disease)Colonic stenosis secondary to ischemia, infection, or previous surgeryPerforated colonColonic fistulaAppendicitisExtrinsic compression of the colon from extracolonic tumors (e.g., ovarian)Extrinsic compression of the colon from an abscessMalrotation of the gutColon volvulusIntussusceptionHernianotes136 barium swallowbarium swallowType of test X-ray with contrast dyeNormal findings Normal size, contour, filling, patency, and positioning of the esophagusTest explanation and related physiologyThis barium contrast study provides a more thorough exami-nation of the esophagus than most upper GI series (see p. 941). As in most barium contrast studies, defects in normal filling and narrowing of the barium column indicate tumor, strictures, or extrinsic compression from extraesophageal tumors or an abnor-mally enlarged heart and great vessels. Varices also can be seen as serpiginous, linear-filling defects. Such anatomic abnormalities as hiatal hernia, Schatzki rings, and diverticula (Zenker or epi-phrenic) can be seen as well.In patients with esophageal reflux, the radiologist may iden-tify reflux of the barium from the stomach back into the esopha-gus. Muscular abnormalities (e.g., achalasia, diffuse esophageal spasm) can be detected easily by a barium swallow. If perforations or rupture of the esophagus are suspected, it is best not to use barium; rather, water-soluble x-ray contrast should be used. If swallowing function is to be evaluated and there is a concern for the potential of aspiration during the test, barium should be used instead of Gastrografin, which can cause a chemical pneumonitis.Contraindications• Patients with evidence of bowel obstruction Barium may create a stonelike impaction.• Patients with a perforated viscus If barium were to leak, the degree and duration of infection would be much worse. Usually, when perforation is suspected, diatrizoate (Gastrografin), a water-soluble contrast medium, is used.• Patients who are unable to cooperate for the testPotential complications• Barium-induced fecal impactionInterfering factors• Food within the esophagus prevents adequate visualization.barium swallow 137BProcedure and patientcareBefore Explain the procedure to the patient. Instruct the patient not to take anything by mouth for at least 8 hours before testing. Usually the patient is kept NPO after midnight on the day of the test.• Assess the patient’s ability to swallow. If the patient tends to aspirate, inform the radiologist.• Accompany the hospitalized patient to the x-ray depart-ment if vital signs are not stable and the test still needs to be performed.During• Note the following procedural steps:1. The fasting patient is asked to swallow the contrast medium. Usually this is barium sulfate in a milkshake-like substance; however, if a perforated viscus is possible, Gastrografin is used.2. As the patient drinks the contrast through a straw, the x-ray table is tilted to the near-erect position.3. The patient is asked to roll into various positions so that the entire esophagus can be adequately visualized.4. With fluoroscopy, the radiologist follows the barium col-umn through the entire esophagus.• Note that this procedure is usually performed in the radiol-ogy department by a radiologist in approximately 15 to 20 minutes. Tell the patient that no discomfort is associated with this test.After Inform the patient of the need to evacuate all the barium. Cathartics are recommended. Initially stools are white but should return to a normal color with complete evacuation.138 barium swallowAbnormal findingsTotal or partial esophageal obstructionCancerScarred stricturesLower esophageal ringsPeptic esophageal ulcersVaricesPeptic or corrosive esophagitisAchalasiaEsophageal motility disorders (e.g., presbyesophagus, diffuse esophageal spasm)DiverticulaChalasiaExtrinsic compression from extraesophageal tumors, cardiomegaly, or aortic aneurysmnotesBBence Jones protein 139Bence Jones protein (Free kappa and lambda light chains)Type of test UrineNormal findingsKappa total light chain: 1000 ng/24 hoursTest explanation and related physiologyMeasurement of 11 beta-prostaglandin F(2) alpha in urine is useful in the evaluation of patients suspected of having sys-temic mastocytosis (systemic mast cell disease [SMCD]). SMCD is characterized by mast cell infiltration of extracutaneous organs (usually the bone marrow). Focal mast cell lesions in the bone marrow are found in approximately 90% of adult patients with SMCD.Prostaglandin D(2) (PGD[2]) is generated by human mast cells, activated alveolar macrophages, and platelets. Although the most definitive test for SMCD is bone marrow biopsy (p. 166), measurement of mast cell mediators like beta prosta-glandin in urine is advised for the initial evaluation of suspected cases. Elevated levels of 11 beta-prostaglandin F(2) alpha in urine are not specific for SMCD and may be found in patients with angioedema, diffuse urticaria, or myeloproliferative diseases in the absence of diffuse mast cell proliferation.Procedure and patient care• See inside front cover for Routine Urine Testing.Abnormal findings Increased levelsSystemic mast cell disease (SMCD)notes142 bilirubinbilirubinType of test BloodNormal findingsAdult/elderly/child:Total bilirubin: 0.3-1.0 mg/dL or 5.1-17 mmol/L (SI units)Indirect bilirubin: 0.2-0.8 mg/dL or 3.4-12.0 mmol/L (SI units)Direct bilirubin: 0.1-0.3 mg/dL or 1.7-5.1 mmol/L (SI units)Newborn:Total bilirubin: 1.0-12.0 mg/dL or 17.1-205 mmol/L (SI units)Possible critical valuesTotal bilirubinAdult: >12 mg/dLNewborn: >15 mg/dLTest explanation and related physiologyBile, which is formed in the liver, has many constituents, including bile salts, phospholipids, cholesterol, bicarbonate, water, and bilirubin. Bilirubin metabolism begins with the break-down of red blood cells (RBCs) in the reticuloendothelial sys-tem (Figure 5). Hemoglobin is released from RBCs and broken down to heme and globin molecules. Heme is then catabolized to form biliverdin, which is transformed into bilirubin. This form of bilirubin is called unconjugated (indirect) bilirubin. In the liver, indirect bilirubin is conjugated with a glucuronide, result-ing in conjugated (direct) bilirubin. The conjugated bilirubin is then excreted from the liver cells and into the intrahepatic cana-liculi, which eventually lead to the hepatic ducts, the common bile duct, and the bowel.Jaundice is the discoloration of body tissues caused by abnormally high blood levels of bilirubin. This yellow discol-oration is recognized when the total serum bilirubin exceeds 2.5 mg/dL.Physiologic jaundice of the newborn occurs if the newborn’s liver is immature and does not have enough conjugating enzymes. This results in a high circulating blood level of uncon-jugated bilirubin, which can pass throughthe blood-brain bar-rier and be deposited in the brain cells of the newborn. This can cause encephalopathy (kernicterus).bilirubin 143BWhen the jaundice is recognized either clinically or chemi-cally, it is important (for therapy) to differentiate whether it is predominantly caused by unconjugated or conjugated bilirubin. This in turn will help differentiate the etiology of the defect. In general, jaundice caused by hepatocellular dysfunction (e.g., hepatitis) results in elevated levels of unconjugated bilirubin. Jaundice resulting from extrahepatic obstruction of the bile ducts (e.g., gallstones or tumor blocking the bile ducts) results in elevated conjugated bilirubin levels; this type of jaundice usually can be resolved surgically or endoscopically.SpleenLiverIndirect bilirubin(unconjugated)Red blood cellHemoglobinGlobin HemeBiliverdinGlucuronideDirect bilirubin(conjugated)UrobilinogenUrobilinogenStool UrineBacteriaKidneyBile ductLysisFIGURE 5 Bilirubin metabolism and excretion. The spleen, liver, kidneys, and gastrointestinal tract contribute to this process.144 bilirubinThe total serum bilirubin level is the sum of the conju-gated (direct) and unconjugated (indirect) bilirubin. These are separated out when fractionation or differentiation of the total bilirubin to its direct and indirect parts is requested from the lab-oratory. Normally the unconjugated bilirubin makes up 70% to 85% of the total bilirubin. In patients with jaundice, when more than 50% of the bilirubin is conjugated, it is considered a conju-gated hyperbilirubinemia from gallstones, tumors, inflammation, scarring, or obstruction of the extrahepatic ducts. Unconjugated hyperbilirubinemia exists when less than 15% to 20% of the total bilirubin is conjugated. Diseases that typically cause this form of jaundice include accelerated erythrocyte (RBC) hemolysis or hepatitis.Interfering factors• Blood hemolysis and lipemia can produce erroneous results. Drugs that may cause increased levels of total bilirubin include allopurinol, anabolic steroids, antibiotics, antimalarials, ascor-bic acid, azathioprine, chlorpropamide, cholinergics, codeine, dextran, diuretics, epinephrine, meperidine, methotrexate, methyldopa, monoamine oxidase inhibitors, morphine, nico-tinic acid (large doses), oral contraceptives, phenothiazines, quinidine, rifampin, salicylates, steroids, sulfonamides, the-ophylline, and vitamin A. Drugs that may cause decreased levels of total bilirubin include barbiturates, caffeine, penicillin, and salicylates (large doses).Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: verify with lab• Blood tube commonly used: red• Note that fasting requirements vary among different labora-tories. Some require keeping the patient NPO after midnight the day of the test except for water.• Use a heel puncture for blood collection in infants.• Prevent hemolysis of blood during phlebotomy.• Do not shake the tube; inaccurate test results may occur.• Protect the blood sample from bright light. Prolonged expo-sure (longer than 1 hour) to sunlight or artificial light can reduce bilirubin content.bilirubin 145BAbnormal findings Increased levels of conjugated (direct) bilirubinGallstonesExtrahepatic duct obstruction (tumor, inflammation, gallstone, scarring, or surgical trauma)Extensive liver metastasisCholestasis from drugsDubin-Johnson syndromeRotor syndrome Increased levels of unconjugated (indirect) bilirubinHemolytic disease of the newbornHemolytic jaundiceLarge-volume blood transfusionResolution of a large hematomaHepatitisSepsisNeonatal hyperbilirubinemiaHemolytic anemiaCrigler-Najjar syndromeGilbert syndromePernicious anemiaCirrhosisTransfusion reactionSickle cell anemianotes146 bioterrorism infectious agents testingbioterrorism infectious agents testingType of test Various (e.g., blood, urine, stool, tissue culture, sputum, lymph node biopsy, skin)Normal findings Negative for evidence of infectious agentTest explanation and related physiologyThere are many infectious agents used in bioterrorism, and it would be difficult to discuss each possible agent. In this test, those agents to which humans are most likely to be exposed, either in war or a civilian terrorist attack, are discussed. Refer to Table 4 for specific information on each agent. All documented cases must be reported to the Department of Public Health.Botulism infectionThe botulinum toxin produced by Clostridium botulinum causes this disease. The GI tract usually absorbs this organism after eating undercooked meat or sauces exposed to room tem-perature for prolonged periods. The organism also can be inhaled by handling these items or by open wound contamination of soil that contains C. botulinum.Blurred vision, dysphagia, and muscle weakness progress-ing to flaccid paralysis are symptoms of the disease. Symptoms begin 6 to 12 hours after ingestion of the contaminated food or approximately 1 week after wound contamination.The test used to diagnose this disease involves the identifica-tion of the toxin in the blood, stool, or vomitus of the affected individual. The food itself can also be tested.Treatment involves the use of botulinum antitoxin, which can be obtained from the Centers for Disease Control and Prevention (CDC). However, this antitoxin presents a risk of serum sickness in nearly one fourth of the patients who receive it.AnthraxAnthrax is caused by Bacillus anthracis, which is a spore-forming gram-positive rod. Gastrointestinal anthrax is contracted by eating undercooked meat. Pulmonary anthrax results from inhalation of spores or tissues from infected animals. Once inhaled, it is always fatal without treatment. Cutaneous anthrax occurs after contact with contaminated meat, wool, hides, or leather from infected animals.The three forms of the disease are cutaneous, GI, and pulmo-nary. Symptoms include fever, malaise, and fatigue progressing to cutaneous lesions, or pulmonary failure. Symptoms occur about 2 to 6 days after exposure.bioterrorism infectious agents testing 147Bt0010TABLE 4 Bioterrorism infectious agents testingInfection/Infectious agent Site of entry Sources Specimen TestsBotulism/ Clostridium botulinumGI mucosal surfaces, lung, wound contaminationUndercooked meats, soil, dustBlood, stool, vomitus, foodBotulinum toxin, mouse bioassayAnthrax/ Bacillus anthracisLung, GI Undercooked meats, inhalation of spores from animal products, skinSputum, blood, stool, skin vesicle, food, sporesCulture, Gram stainYellow fever/ Hantavirus, Ebola virus, multiple other virusesSkin bite Rodent or mosquito bitesBlood, sputum, tissue Culture, serology for viral antigensPlague infections/ Yersinia pestisSkin bite Infected fleas Blood, sputum, lymph node aspirateCulture of organism (Continued)148 bioterrorism infectious agents testingBrucellosis/ Brucella abortus, canis, etc.GI, lung, wound Infected meat and milk productsBlood, sputum, food Culture of organismSmallpox/ Variola virusLungs Respiratory droplets, direct contact, contaminated clothingVesicle Viral culture or viral identification with electron microscopyTularemia/ Francisella tularensisSkin, GI tract, lungsIngestion of contaminated plants or waterBlood, sputum, stool Culture of organismTABLE 4 Bioterrorism infectious agents testing—cont'dbioterrorism infectious agents testing 149BCulturing the organism in sheep blood agar makes the diag-nosis. Appropriate specimens for culture would be stool, blood, sputum, and the cutaneous vesicle. Treatment for this disease is early institution of antibiotics and supportive care.Hemorrhagic fever (yellow fever)This disease complex has many causative viruses, including arenavirus, bunyavirus (includinghantavirus), filovirus (includ-ing Ebola), and flavivirus. Symptoms include fever, thrombocy-topenia, shock, multiorgan failure, lung edema, and jaundice. Symptoms develop 4 to 21 days after a mosquito or rodent bite (depending on the disease). This disease is contagious, and patients with suspicious symptoms should be quarantined.The diagnosis is determined by clinical evaluation. However, viral cultures with polymerase chain reaction identification, serol-ogy, and immunohistochemistry of tissue specimens are possible. There is no specific treatment other than aggressive medical ther-apy and support of organ failure.PlagueThis disease is caused by Yersinia pestis and has three forms: bubonic (enlarged lymph nodes), septicemic (blood-borne), and pneumonic (aerosol). Pneumonic is by far the deadliest form of the infection. Symptoms may include fever, chills, weakness, enlarged lymph nodes, or pneumonia and respiratory failure.The diagnosis is made by culture of the blood, sputum, or lymph node aspirate. This disease complex can be treated with antibiotics when started early in the course of the disease. The risk for bioterrorism is attack or spread by aerosol transmission.BrucellosisThis disease is caused by Brucella abortus, suis, melitensis, or canis. It is contracted by ingestion of contaminated milk prod-ucts, direct puncture of the skin (in butchers and farmers), or by inhalation. The illness is characterized by acute or insidious onset of fever, night sweats, undue fatigue, anorexia, weight loss, headache, and arthralgia. Brucella can be cultured from a blood, sputum, or food specimen. Serology testing is also possible. Diagnosis is confirmed by a fourfold or greater rise in Brucella agglutination titer between acute- and convalescent-phase serum specimens obtained 2 weeks or more apart and studied at the same laboratory. Demonstration by immunofluorescence of a Brucella organism in a clinical specimen is another method of diagnosis.SmallpoxSmallpox is a serious, contagious, and sometimes fatal infec-tious disease caused by the variola virus (a DNA virus). There 150 bioterrorism infectious agents testingis no specific treatment for smallpox disease, and the only pre-vention is vaccination. There are two clinical forms of smallpox. Variola major is the severe and most common form of smallpox, with a more extensive rash and higher fever. Variola minor is a less common presentation of smallpox and a much less severe disease. The disease was eradicated after a successful worldwide vaccination program. It is very easily spread and is therefore con-sidered a potential bioterrorism weapon.The first symptoms of smallpox include fever, malaise, head and body aches, and sometimes vomiting. Next a rash occurs in the mouth and then on the skin. This rash proceeds to become pustular. As the pustules dry up and scab, the patient is no longer contagious.Viral culture, serology, immunohistochemistry, or electron microscopy can make the diagnosis. The best specimen is the vesicular rash. There is no treatment for the disease, but vaccina-tion is available and is offered to all those at risk for bioterrorism.TularemiaThis disease is caused by a bacterium called Francisella tula-rensis. It is contracted by drinking contaminated water or eat-ing vegetation contaminated by infected animals. When it enters through the skin, tularemia can be recognized by the presence of a lesion and swollen glands. Ingestion of the organism may produce a throat infection, intestinal pain, diarrhea, and vomit-ing. Symptoms generally appear from 2 to 10 days—but usually 3 days—after exposure.Inhalation of the organism may produce fever only or com-bined with a pneumonia-like illness. Diagnosis is made by culture of the blood, sputum, or stool.Procedure and patient careBefore• Maintain strict adherence to all procedures to avoid violations in isolation or contamination.• Biohazard precautions are to be taken with each specimen.• Laboratory personnel must strictly adhere to all universal standard precautions.During• If an enema is used to obtain a botulinum stool specimen, use sterile water. Saline can negate results.• Send enough blood for adequate testing. Usually two red-top tubes are adequate. It is best to send it on ice.bioterrorism infectious agents testing 151B• If food is sent for testing, it should be sent in its original container.• For anthrax or smallpox testing of a cutaneous lesion, soak one or two culture swabs with fluid from a previously unopened lesion.After• Identify all potential sources of contamination.• Isolate individuals who are suspected of having a contagious disease.Abnormal findingsSee Table 4.notes152 bladder cancer markersbladder cancer markers (Bladder tumor antigen [BTA], Nuclear matrix protein 22 [NMP22])Type of test UrineNormal findingsBTA:Bladder cancerNon-bladder urologic cancer (ureters, renal pelvis, etc.)notes154 blood culture and sensitivityblood culture and sensitivityType of test BloodNormal findings NegativeTest explanation and related physiologyBlood cultures are obtained to detect the presence of bacteria in the blood. Bacteremia (the presence of bacteria in the blood) can be intermittent and transient, except in endocarditis or sup-purative thrombophlebitis. An episode of bacteremia is usually accompanied by chills and fever; thus, the blood culture should be drawn when the patient manifests these signs to increase the chances of growing bacteria on the cultures. It is important that at least two culture specimens be obtained from two different sites. If one produces bacteria and the other does not, it is safe to assume that the bacteria in the first culture may be a contaminant and not the infecting agent. When both cultures grow the infect-ing agent, bacteremia exists and is caused by the organism that is growing in the culture.If the patient is receiving antibiotics during the time that the cultures are drawn, the laboratory should be notified. Resin can be added to the culture medium to negate the antibiotic effect in inhibiting growth of the offending bacteria in the culture. If cultures are to be performed while the patient is on antibiotics, the blood culture specimen should be taken shortly before the next dose of the antibiotic is administered. All cultures preferably should be performed before antibiotic therapy is initiated.Culture specimens drawn through an IV catheter are fre-quently contaminated, and tests using them should not be per-formed unless catheter sepsis is suspected. In these situations, blood culture specimens drawn through the catheter help iden-tify the causative agent more accurately than a culture specimen from the catheter tip.Most organisms require approximately 24 hours to grow in the laboratory, and a preliminary report can be given at that time. Often, 48 to 72 hours are required for growth and identification of the organism. Anaerobic organisms may take longer to grow.Interfering factors• Contamination of the blood specimen, especially by skin bac-teria, may occur.blood culture and sensitivity 155BProcedure and patient careBefore Explain the procedure to the patient. Tell the patient that no fasting is required.During• Carefully prepare the venipuncture site with povidone-iodine (Betadine). Allow the skin to dry.• Clean the tops of the Vacutainer tubes or culture bottles with povidone-iodine and allow them to dry. Some labora-tories suggest cleaning with 70% alcohol after cleaning with povidone-iodine and air drying.• Collect approximately 10 to 15 mL of venous blood by veni-puncture from each site in a 20-mL syringe.• Discard the needle on the syringe and replace it with a second sterile needle before injecting the blood sample into the cul-ture bottle.• Inoculate the anaerobic bottle first if both anaerobic and aer-obic cultures are needed.• Mix gently after inoculation.• Label the specimen with the patient’s name, date, time, and tentative diagnosis.• Indicate on the laboratory slip any medications that may affect test results.After• Transport the culture bottles immediately to the laboratory (or at least within 30 minutes).• Notify the physician of any positive results so that appropriate antibiotic therapy can be initiated.Abnormal findingsBacteremianotes156 blood smearblood smear (Peripheral blood smear, Red blood cell [RBC] morphology, RBC smear)Type of test BloodNormal findingsNormal quantity of red and white blood cells (RBCs, WBCs) and plateletsNormal size, shape, and color of RBCsNormal WBC differential countNormal size and granulation of plateletsTest explanation and related physiologyExamination of the peripheral blood smear can provide a sig-nificant amount of information concerning drugs and diseases that affect erythrocytes (RBCs), leukocytes (WBCs), or platelets. Furthermore, other congenital and acquired diseases can be diag-nosed. When special stains are applied to the blood smear, leuke-mia, infection, infestation, and other diseases can be identified.When adequately prepared and examined microscopically by an experienced technologist or pathologist, a smear of peripheral blood is the most informative of all hematologic tests. All three hematologic cell lines—RBCs, platelets, and WBCs—can be examined. In the peripheral blood, five different types of WBCs can routinely be identified: neutrophils, eosinophils, basophils, lymphocytes, and monocytes. The first three are also referred to as granulocytes. Please see the discussion in bone marrow biopsy (p. 166) for more information concerning the various elements of blood.Microscopic examination of the RBCs can reveal variations in RBC size (anisocytosis), shape (poikilocytosis), color, or intracel-lular content (Box 3). Classification of RBCs according to these BOX 3 Microscopic examination of RBCsRBC size abnormalitiesMicrocytes (small RBCs)Iron deficiencyThalassemiaHemoglobinopathiesMacrocytes (larger size)Vitamin B12 or folic acid deficiencyblood smear 157BReticulocytosis secondary to increased erythropoiesis (RBC production)Occasional liver disorderRBC shape abnormalitiesSpherocytes (small and round)Hereditary spherocytosisAcquired immunohemolytic anemiaElliptocytes (crescent)Iron deficiencyHereditary elliptocytosisCodocytes or target cells (thin cells with less hemoglobin)HemoglobinopathiesThalassemiaEchinocytes (Burr cells)UremiaLiver diseaseRBC color abnormalitiesHypochromic (pale)Iron deficiencyThalassemiaHyperchromasia (more colored)Concentrated hemoglobin, usually caused by dehydrationRBC intracellular structureNucleated (normoblasts) (Mature RBCs are round with a small central pallor without any intracellular structures. They do not have a nucleus. Immature RBCs (reticulocytes) do contain intracellular RNA. Immature nucleated cells are not normally found in the peripheral blood and indicate increased RBC synthesis.)AnemiaChronic hypoxemiaNormal for an infantMarrow-occupying neoplasm or fibrotic tissueBasophilic stippling (refers to bodies enclosed or included in the cytoplasm of the RBCs)Lead poisoningReticulocytosisHowell-Jolly bodies (small, round remnants of nuclear material remaining within the RBC)After a surgical splenectomyHemolytic anemiaMegaloblastic anemiaFunctional asplenia (after splenic infarction)BOX 3 Microscopic examination of RBCs—cont'd158 blood smearvariables is most helpful in identifying the causes of anemia and the presence of other diseases.The WBCs are examined for total quantity, differential count, and degree of maturity. An increased number of immature WBCs may indicate leukemia or infection. A decreased WBC count indicates a failure of marrow to produce WBCs (due to drugs, chronic disease, neoplasia, or fibrosis), peripheral destruction, or sequestration.Platelet examinationFinally, an experienced laboratory technologist also can esti-mate platelet number. Platelets are small cell fragments that do not contain a nucleus. The contents of the granules in a platelet are released to promote clotting.Procedure and patient careBefore Explain the procedure to the patient. Tell the patient that no fasting is required.During• Collect a drop of blood from a finger stick or heel stick and place it on a slide.• If necessary, perform a venipuncture and collect the blood in a lavender-top tube.• Note that a blood smear is first studied with an automated cytometer programmed to recognize abnormal blood cell shapes and other variations. An evaluation smear is performed by a technologist. Low counts may be hand counted to ensure accuracy. The most accurate smear requires review by a pathologist.After• Apply pressure to thevenipuncture site.Abnormal findingsSee Box 3 in the Test explanation and related physiology section.notesblood typing 159Bblood typing (Blood group microarray testing)Type of test BloodNormal findings CompatibilityTest explanation and related physiologyWith blood typing, ABO and Rh antigens can be detected in the blood of prospective blood donors and potential blood recipients. This test is also used to determine the blood type of expectant mothers and newborns. A description of the ABO sys-tem, Rh factors, and blood crossmatching is reviewed here.ABO systemHuman blood is grouped according to the presence or absence of A or B antigens. The surface membranes of group A red blood cells (RBCs) contain A antigens; group B RBCs con-tain B antigens on their surface; group AB RBCs have both A and B antigens; and group O RBCs have neither A nor B antigens. In general, a person’s serum does not contain anti-bodies to match the surface antigen on their RBCs. That is, persons with group A antigens (type A blood) will not have anti-A antibodies; however, they will have anti-B antibodies. The converse is true for persons with group B antigens. Group O blood will have both anti-A and anti-B antibodies (Table 5). These antibodies against A and B blood group antigens are formed in the first 3 months of life after exposure to similar antigens on the surface of naturally occurring bacteria in the intestine.TABLE 5 Blood typingBlood type (ABO, Rh)Antigens presentAntibodies possibly presentPercent of general populationO, +O, –*A, +A, –B, +B, –AB, +†AB, –RhNoneA, RhAB, RhBA, B, RhA, BA, BA, B, RhBB, RhAA, RhNoneRh35 735 7 8 2 4 2* Universal donor; † Universal recipient160 blood typingBlood transfusions are actually transplantations of tissue (blood) from one person to another. It is important that the recipient not have antibodies to the donor’s RBCs. If this were to occur, there could be a hypersensitivity reaction, which can vary from mild fever to anaphylaxis with severe intravascular hemo-lysis. If donor ABO antibodies are present against the recipient antigens, usually only minimal reactions occur.Persons with group O blood are considered universal donors because they do not have antigens on their RBCs. People with group AB blood are considered universal recipients because they have no antibodies to react to the transfused blood. Group O blood is usually transfused in emergent situations in which rapid, life-threatening blood loss occurs and immediate transfusion is required. The chance of a transfusion reaction is least when type O is used. Women of childbearing potential should receive group O negative blood, and men generally receive group O positive blood when emergency transfusion prior to type-specific or crossmatched blood is required.ABO typing is not required for autotransfusions (blood donated by a patient several weeks prior to a major operation and then transfused post-operatively). However, in most hospitals, ABO typing is performed on those patients in the event that fur-ther blood transfusion of banked blood is required.Rh factorsThe presence or absence of Rh antigens on the RBC’s surface determines the classification of Rh positive or Rh negative. After ABO compatibility, Rh factor is the next most important antigen affecting the success of a blood transfusion. The major Rh fac-tor is Rho(D). There are several minor Rh factors. If Rho(D) is absent, the minor Rh antigens are tested. If negative, the patient is considered Rh negative (Rh–).Rh– persons may develop antibodies to Rh antigens if exposed to Rh-positive (Rh+) blood by transfusions or fetal–maternal blood mixing. All women who are pregnant should have a blood typing and Rh factor determination. If the mother’s blood is Rh–, the father’s blood should also be typed. If his blood is Rh+, the wom-an’s blood should be examined for the presence of Rh antibodies (by the indirect Coombs test; see page 299). Hemolytic disease of the newborn can be prevented by Rh typing during pregnancy. If the mother is Rh–, she should be advised that she is a candidate for RhoGAM (Rh immunoglobulin that “neutralizes” the Rh anti-gen) after the delivery. RhoGAM can reduce the chance of fetal hemolytic problems during subsequent pregnancies.blood typing 161BOther blood typing systemsThere are nine different gene codes for blood groups assayed. Most are minor and not clinically significant. However in cer-tain clinical circumstances, these minor blood group antigens and acquired antigens can become significant. This may occur with frequent blood transfusions or in patients with leukemia or lymphoma. Multiplex PCR microarray analysis provides identifi-cation of the many variants involving these blood group systems and is particularly helpful in the described patients.Blood crossmatchingAlthough typing for the major ABO and Rh antigens is no guarantee that a reaction will not occur, it does greatly reduce the possibility of such a reaction. Many potential minor antigens are not routinely detected during blood typing. If allowed to go unrecognized, these minor antigens also can initiate a blood transfusion reaction. Therefore, blood is not only typed but also crossmatched to identify a mismatch of blood caused by minor antigens. Crossmatching always includes an indirect Coombs test. Only blood products containing RBCs need to be cross-matched. Plasma products do not need to be crossmatched but should be ABO compatible because other cells (WBCs and plate-lets) have ABO antigens.Homologous (donor and recipient are different people) and directed (recipient chooses the donor) blood for donation must be rigorously tested before transfusion. Autologous (recipient and donor is the same person) blood for transfusions, however, is not subject to that same testing.Finally, one must be aware of graft-versus-host disease (GVHD) in which donor lymphocytes included in the blood transfusion may engraft and multiply in the recipient.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes• Blood tube commonly used: red. Verify with lab.Abnormal findingsSee Test explanation and related physiology section (p. 159).notes162 bone densitometrybone densitometry (Bone mineral content [BMC], Bone mineral density [BMD], DEXA scan)Type of test X-rayNormal findingsNormal: –1)Osteopenia: 1-2.5 standard deviations below normal (–1 to –2.5)Osteoporosis: >2.5 standard deviations below normal (cellous and cortical) bone. However, specific bone sites can be evaluated if they are particularly symptomatic.Dual-energy x-ray absorptiometry (DEXA) is the method most commonly used. Because DEXA uses two photons, more energy is produced so that bones (spine and hip [femoral neck]) surrounded by a lot of soft tissue can be more easily penetrated. The source of the photon is placed on one side of the bone to be studied. The gamma detector is placed on the other side. Increased bone density is associated with increased bone photon absorption and, therefore, less photon recognition at the site of the gamma detector.bone densitometry 163BSeveral other methods are available to measure BMD. Quantitative computed tomography (QCT) uses CT technology to measure central bones, especially the spine. Ultrasound absorp-tion (quantitative ultrasound) can be used to measure peripheral bones (heel [calcaneus], patella, or midtibia).BMD is usually reported in terms of standard deviation (SD) from mean values. T scores compare the patient’s results to a group of young healthy adults. Z scores compare the patient’s results to a group of age-matched controls. The World Health Organization has defined low bone mass as a BMD value greater than 1 SD below peak bone mass levels in young women, and osteoporosis as a value greater than 2.5 SD below that same measurement scale. Positive T scores indicate a normal BMD. Negative T scores indicate reduced BMD.Based on the BMD of the femoral neck, and upon other clini-cal criteria, the risk of a major osteoporotic fracture and the risk of a hip fracture can be calculated (see www.shef.ac.uk/FRAX/index.htm). This is called Fracture Risk Assessment. Furthermore, the identification of vertebral fracture is important in the diagno-sis of osteoporosis because the presence of one or more of these fractures is a strong indicator of a patient’s future fracture risk at the spine, hip, and other sites. Vertebral Fracture Assessment (VFA) can be performed utilizing the images generated by the DEXA scan. Images of the lower thoracic and lumbar spine are examined. If a vertebral fracture is identified, bone mineral strengthening medications are recommended despite T score. Presence of a vertebral fracture indicates a substantial risk for a subsequent vertebral or nonvertebral fracture independent of the bone mineral density or other osteoporosis risk factors. VFA is commonly recommended on postmenopausal women with reduced BMD and the following:• Age >70• Height loss >1.6 inches• Prior vertebral fracture• Chronic disease with increased risk for vertebral fracture (e.g., COPD, rheumatoid arthritis, Crohn disease)• Women with osteoporosis• Postmenopausal women chronically receiving glucocorticoid therapyBMD testing is an important part of routine screening test-ing for postmenopausal women. In general, BMD is recom-mended every 2 years to screen for osteoporosis. Women and men with known osteoporotic fractures, hyperparathyroidism, http://www.shef.ac.uk/FRAX/index.htmhttp://www.shef.ac.uk/FRAX/index.htm164 bone densitometryor administration of long-term steroid therapy may benefit from annual BMD testing.Interfering factors• Barium may falsely increase the density of the lumbar spine. BMD measurements should not be performed for about 10 days after barium studies.• Calcified abdominal aortic aneurysm may falsely increase BMD of the spine.• Internal fixation devices of the hip or radius will falsely increase BMD of those bones.• Overlying metal jewelry or other objects may falsely increase BMD.• Previous fractures or severe arthritis changes of the bone can falsely increase BMD.• Metallic clips placed in the vertebrae of patients who have had previous abdominal surgery can falsely increase BMD.• Prior bone scans can falsely decrease BMD because the pho-tons generated from the bone (as a result of the previously administered bone scan radionuclide) will be detected by the scintillator detector.Procedure and patient careBefore Explain the procedure to the patient. Tell the patient that no fasting or sedation is required. Instruct the patient to remove all metallic objects (e.g., belt buckles, zippers, coins, keys) that might be in the scanning path.During• Note the following procedural steps:1. The patient lies supine on an imaging table, with his or her legs supported and placed on a padded box to flatten the pelvis and lumbar spine.2. Under the table, a photon generator is slowly and succes-sively passed under the lumbar spine.3. A scintillator (gamma or x-ray) detector/camera is passed over the patient in a manner parallel to that of the genera-tor. An image of the lumbar spine and hip bone is obtained by the scintillator camera and projected onto a computer monitor.4. Next, the appropriate foot is applied to a brace that inter-nally rotates the nondominant hip, and the procedure is bone densitometry 165Brepeated over the hip. A similar procedure is performed for radius evaluation.5. When the radius is examined, the nondominant arm is pre-ferred unless there is a history of fracture to that bone.• Note that the data are interpreted and reported by a radiolo-gist or a physician trained in nuclear medicine.• Note that BMD studies take about 15 minutes to perform and are free of any discomfort. Only minimal radiation is used for this procedure.• Note that there are numerous types of bone densitometry machines. Peripheral units that quickly scan the finger, heel, or forearm are often used to identify patients at risk for osteo-porosis. Abnormal results are followed up with the more comprehensive table procedure previously described.After• On the computer screen, a small window of the lumbar spine, femoral neck, or distal radius is drawn. The computer calcu-lates the amount of photons not absorbed by the bone. This is the BMC. BMD is computed as follows:BMDBMC g/cmSurface area of the bone2=( )Abnormal findingsLow bone massOsteoporosisnotes166 bone marrow biopsybone marrow biopsy (Bone marrow examination, Bone marrow aspiration)Type of test Microscopic examination of tissueNormal findingsActive erythroid cell line, myeloid and lymphoid cell lines, and megakaryocyte (platelet) production. See range of cell types below.Cell type Range (%)Neutrophilic series 49.2-65.0Myeloblasts 0.2-1.5Promyelocytes 2.1-4.1Myelocytes 8.2-15.7Eosinophilic series 1.2-5.3Myelocytes 0.2-1.3Metamyelocytes 0.4-2.2Bands 0.2-2.4Segmented 0-1.3Basophilic and mast cells 0-0.2Erythrocyte series 18.4-33.8Pronormoblasts 0.2-1.3Basophilic 0.5-2.4Polychromatophilic 17.9-29.2Orthochromatic 0.4-4.6Monocytes 0-0.8Lymphocytes 11.1-23.2Plasma cells 0.4-3.9Megakaryocytes 0-0.4Reticulum cells 0-0.9Monocyte to erythrocyte (M/E) ratio 1.5-3.3Normal iron content is demonstrated by staining with Prussian blue.Test explanation and related physiologyBone marrow examination is an important part of the evalu-ation of patients with hematologic diseases. Indications for bone marrow examination include the following:• To evaluate anemias, leukopenia, or thrombocytopenia• To diagnose leukemia, myelodysplastic syndromes, myelo-proliferative neoplasms, and plasma cell dyscrasia• To document abnormal iron storesbone marrow biopsy 167B• To document bone marrow infiltrative diseases (e.g., neoplasm, infection, or fibrosis)• To stage lymphomas or other cancersThe bone marrow is located in the central fatty core of can-cellous bone (particularly sternum, rib, and pelvis). There, the blood-forming cells produce blood cells and release them into the circulation.By examining a bone marrow specimen, a hematologist can fully evaluate hematopoiesis. Examination of bone mar-row reveals the number, size, and shape of the RBCs, WBCs, and megakaryocytes (platelet precursors) as these cells evolve through theirvarious stages of development in the bone marrow. Samples of bone marrow can be obtained by aspiration, bone marrow biopsy, or surgical removal. An aspiration is obtained for cell morphology, immunophenotyping, cytogenetics, or micro-biology cultures. Microscopic examination of the marrow biopsy includes estimation of cellularity, identification of disordered hematopoiesis, and determination of the presence of infiltrative diseases (fibrosis or neoplasms, both primary and metastatic). Estimation of iron storage is performed on bone marrow aspi-rates or non-decalcified clot sections.For the estimation of cellularity, the specimen is examined and the relative quantity of each cell type is determined. Leukemias or leukemoid drug reactions are suspected when increased numbers of leukocyte precursors are present. Physiologic marrow leukemoid compensation is also seen with infection. Decreased numbers of marrow leukocyte precursors occur in patients with myelofibrosis, metastatic neoplasia, or agranulocytosis/aplastic anemia; in elderly patients; and following radiation therapy or chemotherapy. Some drugs or infections can diminish leukocyte production.Increased numbers of marrow RBC precursors occur with polycythemia vera or as physiologic compensation to blood loss (hemorrhage or hemolysis). Decreased numbers of marrow RBC precursors occur with erythroid hypoplasia following chemother-apy, infection (parvovirus), aplastic anemia, radiation therapy, administration of other toxic drugs, iron administration, or mar-row replacement by fibrotic tissue or neoplasms.Increased numbers of platelet precursors (megakaryocytes) can be the result of compensation to platelet loss from a recent hemorrhage. They are also seen in some forms of acute and chronic myeloid leukemias. This increase also may be com-pensatory in patients with platelet sequestration (secondary hypersplenism associated with portal hypertension) or platelet 168 bone marrow biopsydestruction (idiopathic thrombocytopenic purpura). Platelet counts decrease, and the marrow compensates by increasing production. Decreased numbers of megakaryocytes occur in patients who have had radiation therapy, chemotherapy, or other drug therapy and in patients with neoplastic or fibrotic mar-row infiltrative diseases. Patients with aplastic anemia also have decreased numbers of megakaryocytes.Increased numbers of lymphocyte precursors occur in chronic, viral, or mycoplasmal infections (e.g., mononucleosis), lympho-cytic leukemia, and lymphoma. Plasma cells and lymphocytes are increased in patients with plasma cell dyscrasia, lymphomas, hypersensitivity states, autoimmune disease, chronic infections, and other chronic inflammatory diseases.Estimation of cellularity also can be expressed as a ratio of myeloid (WBC) to erythroid (RBC) cells (M/E ratio). The nor-mal M/E ratio is approximately 3:1. The M/E ratio is greater than normal in those diseases in which leukocyte precursors are increased or erythroid precursors are decreased. The M/E ratio is below normal when either leukocyte precursors are decreased or erythroid precursors are increased.Drug-induced myelofibrosis or myelofibrosis associated with hematologic, myeloproliferative, or other neoplasms can be detected by examination of the bone marrow using reticulin or collagen stains. Using special stains, iron stores can be estimated with a marrow aspirate or decalcified clot sections (biopsies are decalcified leading to artificial decrease in iron staining).Bone marrow aspiration and biopsy are performed by a phy-sician or mid-level health care provider. The duration of these procedures is approximately 20 minutes. The patient may have some apprehension when pressure is applied to puncture the outer table of the bone during biopsy-specimen removal or aspi-ration. The patient probably will feel pain during lidocaine infil-tration and pressure when the syringe plunger is withdrawn for aspiration.Contraindications• Patients with acute coagulation disorders, because of the risk of excessive bleeding• Patients who cannot cooperate or remain still during the procedurePotential complications• Hemorrhage, especially if the patient has a coagulopathy• Infection, especially if the patient is leukopenicbone marrow biopsy 169BProcedure and patient careBefore Explain the procedure to the patient.• Obtain a written informed consent for this procedure.• Encourage the patient to verbalize fears because many patients are anxious concerning this study. Conscious sedation may be required.• Assess the results of the coagulation studies. Report any evi-dence of coagulopathy to the physician. Platelets should be >20,000 and INR should bephoton it receives from the gamma ray. When these light patterns are arranged in a spatial order, a realistic image of the bones is apparent.The degree of radionuclide uptake is related to the metabo-lism of the bone. Normally a uniform concentration should be seen throughout the bones of the body. There is symmetrical distribution of activity throughout the skeletal system in healthy adults. Urinary bladder activity, faint renal activity, and minimal soft tissue activity are also normally present. An increased uptake of radionuclide is abnormal and may represent tumor, arthritis, fracture, degenerative bone and joint changes, osteomyelitis, bone necrosis, osteodystrophy, and Paget disease. These areas of concentrated radionuclide uptake are often called hot spots and are detectable months before an ordinary x-ray image can reveal the pathology. Hot spots occur because new bone growth is usually stimulated around areas of pathology. If pathology exists and there is no new bone formation around the lesion, the scan will not pick up the abnormality. Increased uptake of radionu-clide is also seen in the normal physiologic active epiphyses of children.The major reason a bone scan is performed is to detect meta-static cancer to the bone. All malignancies capable of metastasis may reach the bone, especially those of the prostate, breast, lung, kidney, urinary bladder, and thyroid gland. Bone scans are also useful in staging primary bone tumors, such as osteogenic sarco-mas and Ewing sarcoma. Bone scans may be serially repeated to monitor tumor response to antineoplastic therapy.Bone scans also provide valuable information in the evalua-tion of patients with trauma or unexplained pain. Bone scanning is much more sensitive than routine x-ray images in detecting small and difficult-to-find fractures, especially in the spine, ribs, face, and small bones of the extremities. Bone scans are used to 172 bone scandetermine the age of a fracture as well. If a fracture line is seen on a plain x-ray image and the uptake around that fracture is not increased on a bone scan, the injury is said to be an old fracture, exceeding several months in age.Although the bone scan is extremely sensitive, unfortunately it is not very specific. Fractures, infections, tumors, and arthritic changes all appear similar in this scan. A three-phase bone scan may be performed if inflammation (arthritis) or infection (osteo-myelitis, septic arthritis) is suspected. In a three-phase bone scan, imaging is performed at three different times after injection of the radionuclide. Early uptake of the radionuclide would indi-cate infection or inflammation rather than neoplasm. Uptake of the radionuclide on delayed imaging that is not present on early imaging would indicate neoplasm.When the metastatic process is diffuse, virtually all of the radionuclide is concentrated in the skeleton, with little or no activity in the soft tissues or urinary tract. The resulting pat-tern, which is characterized by excellent bone detail, is fre-quently referred to as a superscan. A superscan may also be associated with metabolic bone diseases (e.g., Paget disease, renal osteodystrophy, or osteomalacia). Unlike in metastatic disease, however, the uptake in metabolic bone disease is more uniform in appearance and extends into the distal appendicular skeleton.Contraindications• Patients who are pregnant, unless the benefits outweigh the risk of fetal damage• Patients who are lactatingProcedure and patient careBefore Explain the procedure to the patient. Assure patients they will not be exposed to large amounts of radioactivity because only tracer doses of the isotope are used. Tell the patient that no fasting or sedation is required. Inform the patient that the injection of the radionuclide may cause slight discomfort, nausea, or vomiting.During• Note the following procedural steps:1. The patient receives an IV injection of radionuclide, usually 99mTc-MDP (technetium-99 m-methylene diphosphonate) or 99mTc-HDP 99 m (hydroxymethane diphosphonate), into a peripheral vein in the arm.bone scan 173B2. The patient is encouraged to drink several glasses of water between the time of radionuclide injection and the scan-ning. This facilitates renal clearance of the circulating tracer not picked up by the bone. The waiting period before scanning is approximately 2 to 3 hours.3. The patient is instructed to urinate.4. The patient is situated in the supine position on the scan-ning table in nuclear medicine.5. A radionuclide detector is placed over the patient’s body and records the radiation emitted by the skeleton.6. This information is translated into a two- or three- dimensional view of the skeleton.7. The patient may be repositioned in the prone and lateral positions during the test.• Note that this scan is performed by a nuclear medicine tech-nician in 30 to 60 minutes. It is interpreted by a physician trained in nuclear medicine imaging. Inform patients in significant pain that lying on the hard scan-ning table can be uncomfortable.After• Because only tracer doses of radionuclide are used, no radia-tion precautions need to be taken. Assure the patient that the radioactive substance is usually excreted from the body within 6 to 24 hours. Encourage the patient to drink fluids to aid in the excretion of the radioactive substance.Abnormal findingsPrimary or metastatic tumor of the boneFractureDegenerative arthritisRheumatoid arthritisOsteomyelitisBone necrosisRenal osteodystrophyPaget disease of bonenotes174 bone turnover markersbone turnover markers (BTMs, N-telopeptide [NTx], Bone collagen equivalents (BCEs), Osteocalcin [bone G1 a protein, BGP, osteocalc], Pyridinium [PYD] crosslinks, Bone-specific alkaline phosphatase [BSAP], Amino-terminal propeptide of type I procollagen [P1NP], C-telopeptide [CTx])Type of test Blood; urineNormal findings (Results vary greatly with age)N-telopeptideUrine (nm BCE*/mm creatinine)Male: 21-83Female, premenopausal: 17-94Female, postmenopausal: 26-124Serum (nm BCE*)Male: 5.4-24.2Female: 6.2-19.0(*BCE = bone collagen equivalents)C-telopeptideUrine (ng/mL)Adults: 1.03 ± 0.41Children: 8.00 ± 3.37Serum (pg/mL)Female, premenopausal: 40-465Female, postmenopausal: 104-1008Male: 60-700Amino-terminal propeptide of type I procollagen, serum (mg/L)Male: 22-105Female, premenopausal: 19-101Female, postmenopausal: 16-96Osteocalcin, serum (ng/mL)Adult (>22 years)Male: 5.8-14.0Female: 3.1-14.4Pyridium, urine (nm/mm)Male: 10.3-33.6Female: 15.3-33.6Bone-specific alkaline phosphatase, serum (mg/L)Male: 6.5-20.1Female, premenopausal: 4.5-16.9Female, postmenopausal: 7.0-22.4bone turnover markers 175BTest explanation and related physiologyWith the increased use of bone density scans (see p. 162), osteoporosis can now be diagnosed and treated more easily. This has prompted an interest in biochemical markers of bone metabolism. Bone is continuously turned over: bone resorption by osteoclasts and bone formation by osteoblasts. Osteoporosis is a common disease of postmenopausal women and is associated with increased bone resorption and decreased bone formation. The result is thin and weak bones that are prone to fracture. The same process is now becoming increasingly recognized in elderly men as well. Early diagnosis allows therapeutic intervention to prevent bone fracture.Bone mineral density studies (p. 162) are valuable tools in the identification of osteoporosis; however, they cannot recognize small changes in bone metabolism. Although bone density studies can be used to monitor the effectiveness of therapy, it takes years to detect measurable changes in bone density. Bone turnover markers (BTMs), however, can identify significant improvement in a few months after instituting successful therapy. Furthermore, the cost of bone densityChemistryGlucoseGreen Heparin Prevents blood from clotting when plasma needs to be testedChemistryAmmoniaBlue (Light) Sodium citrate Prevents blood from clotting when plasma needs to be testedProthrombin timePartial thromboplastin timeBlack Sodium citrate Binds calcium to prevent blood clottingWestergren erythrocyte sedimentation rate (ESR)Yellow Citrate dextrose Preserves red cells Blood cultures, blood banking studiesuser’s guide to test preparation and procedures xvuser’s guide to test preparation and procedures• Do not shake the blood specimen. Hemolysis may result from vigorous shaking and can invalidate test results. Use gentle inversions.• Collect blood cultures before the initiation of antibiotic therapy. Blood cultures are often drawn when the patient manifests a fever. Often two or three cultures are taken at 30-minute intervals from different venipuncture sites.• Skin punctures can be used for blood tests on capillary blood. Common puncture sites include the fingertips, earlobes, and heel surfaces. Fingertips are often used for small children, and the heel is the most commonly used site for infants.• Ensure that the blood tubes are correctly labeled and delivered to the laboratory.• After the specimen is drawn, apply pressure or a pres-sure dressing to the venipuncture site. Assess the site for bleeding.• If the patient fasted before the blood test, reinstitute the appropriate diet.Urine testsOverviewUrine tests are easy to obtain and provide valuable information about many body system functions (e.g., kidney function, glu-cose metabolism, and various hormone levels). The ability of the patient to collect specimens appropriately should be assessed to determine the need for assistance.Guidelines• Observe universal precautions in collecting a urine specimen.• Use the first morning specimen for routine urinalysis because it is more concentrated. To collect a first morn-ing specimen, have the patient void before going to bed and collect the first urine specimen immediately upon rising.• Random urine specimens can be collected at any time. They are usually obtained during daytime hours and with-out any prior patient preparation.• If a culture and sensitivity (C&S) study is required or if the specimen is likely to be contaminated by vaginal discharge or bleeding, collect a clean-catch or midstream specimen. This requires meticulous cleansing of the urinary meatus with an antiseptic preparation to reduce contamination of the specimen by external organisms. Then the cleansing agent must be completely removed because it may contaminate xvi user’s guide to test preparation and proceduresthe specimen. Obtain the midstream collection by doing the following:1. Have the patient begin to urinate in a bedpan, urinal, or toilet and then stop urinating. (This washes the urine out of the distal urethra.)2. Correctly position a sterile urine container, and have the patient void 3 to 4 ounces of urine into it.3. Cap the container.4. Allow the patient to finish voiding.• One-time composite urine specimens are collected over a period that may range anywhere from 2 to 24 hours. To collect a timed specimen, instruct the patient to void and discard the first specimen. This is noted as the start time of the test. Instruct the patient to save all subsequent urine in a special container for the designated period. Remind the patient to void before defecating so that urine is not contaminated by feces. Also, instruct the patient not to put toilet paper in the collection container. A preservative is usually used in the collection container. At the end of the specified time period, have the patient void and then add this urine to the specimen container, thus completing the collection process.• Collection containers for 24-hour urine specimens should hold 3 to 4 L of urine and have tight-fitting lids. They should be labeled with the patient’s name, the starting col-lection date and time, the ending collection date and time, the name of the test, the preservative, and storage require-ments during collection.• Many urine collections require preservatives to maintain their stability during the collection period. Some specimens are best preserved by being kept on ice or refrigerated.• Urinary catheterization may be needed for patients who are unable to void. This procedure is not preferred because of patient discomfort and the risk of patient infection.• For patients with an indwelling urinary catheter, obtain a specimen by aseptically inserting a needleless syringe into the catheter at a drainage port distal to the sleeve leading to the balloon. Aspirate urine and then place it in a sterile urine container. The urine that accumulates in the plastic reservoir bag should never be used for a urine test.• Urine specimens from infants and young children are usu-ally collected in a disposable pouch called a U bag. This bag has an adhesive backing around the opening to attach to the child’s perineum. After the bag is in place, check the user’s guide to test preparation and procedures xviiuser’s guide to test preparation and procedureschild every 15 minutes to see if an adequate specimen has been collected. Remove the specimen as soon as possible after the collection, and then label it and transport it to the laboratory.Stool testsOverviewThe examination of feces provides important information that aids in the differential diagnosis of various gastrointestinal dis-orders. Fecal studies may also be used for microbiologic studies, chemical determinations, and parasitic examinations.Guidelines• Observe universal precautions in collecting a stool specimen.• Collect stool specimens in a clean container with a fitted lid.• Do not mix urine and toilet paper with the stool specimen. Both can contaminate the specimen and alter the results.• Fecal analysis for occult blood, white blood cells, or quali-tative fecal fat requires only a small amount of a randomly collected specimen.• Quantitative tests for daily fecal excretion of a particular substance require a minimum of a 3-day fecal collection. This collection is necessary because the daily excre-tion of feces does not correlate well with the amount of food ingested by the patient in the same 24-hour period. Refrigerate specimens or keep them on ice during the col-lection period. Collect stool in a 1-gallon container.• A small amount of fecal blood that is not visually apparent is termed occult blood. Chemical tests using commercially prepared slides are routinely used to detect fecal blood. Numerous commercial slide tests use guaiac as the indica-tor. These guaiac tests are routinely done on nursing units and in medical offices.• Consider various factors (e.g., other diagnostic tests and medications) in planning the stool collection. For exam-ple, if the patient is scheduled for x-ray studies with barium sulfate, collect the stool specimen first. Various medica-tions (e.g., tetracyclines and antidiarrheal preparations) affect the detection of intestinal parasites.• Some fecal collections require dietary restrictions before the collection (e.g., tests for occult blood).• Correctly label and deliver stool specimens to the labora-tory within 30 minutes after collection. If you are unable to deliver the specimen within 30 minutes, it may be refrigerated for up to 2 hours.xviii user’s guide to test preparation and proceduresX-ray studiesOverviewBecause of the ability of x-rays to penetrate tissues, x-ray stud-ies provide a valuable picture of body structures. X-ray studies can be as simple as a routine chest x-ray image or as complex as dye-enhanced cardiac catheterization. With the concern about radiation exposure, it is important to realize that the patient may question if the proposed benefits outweigh the risks involved.Guidelines• Assess the patient for any similar or recentstudies limits the feasibility of performing this test as frequently as may be required to monitor treatment.Because the levels of BTMs vary according to the time of day and bone volume, these studies are not widely used or helpful in screening for detection of osteoporosis. Their use is in determin-ing the effect of treatment by comparing BTMs with pretreatment levels. Levels will decline with the use of antiresorption drugs (e.g., estrogen, bisphosphonates, calcitonin, raloxifene). BTMs have been shown to be accurately predictive of early improvement in bone mineral density and antifracture treatment efficacy. BTMs are also useful in documenting treatment compliance.N- and C-telopeptides (NTx and CTx) are protein fragments used in type 1 collagen that make up nearly 90% of the bone matrix. The C and N terminals of these proteins are crosslinked to provide tensile strength to the bone. When bone breaks down, CTx and NTx are released into the bloodstream and excreted in the urine. Serum levels of these fragments have been shown to correlate well with urine measurements normalized to creatinine. Measurements of these fragments show early response to antire-sorptive therapy (within 3 to 6 months) and are good indicators of bone resorption. Normal levels may vary with the method of testing.Amino-terminal propeptide of type 1 procollagen (P1NP), like NTx, is directly proportional to the amount of new collagen 176 bone turnover markers produced by osteoblasts. Concentrations are increased in patients with various bone diseases that are characterized by increased osteoblastic activity. P1NP is the most effective marker of bone formation and is particularly useful for monitoring bone forma-tion therapies and antiresorptive therapies.Osteocalcin, or bone G1a protein (BGP), is a noncollagenous protein in the bone and is made by osteoblasts. It enters the cir-culation during bone resorption and bone formation; it is a good indicator of bone metabolism. Serum levels of BGP correlate with bone formation and destruction (turnover). Increased levels are associated with increased bone mineral density loss. BGP is a vitamin K–dependent protein. A reduced vitamin K intake is associated with reduced BGP levels. This probably explains the pathophysiology of vitamin K–dependent deficiency osteoporosis.Pyridinium (PYD) crosslinks are formed during maturation of the type 1 collagen during bone formation. During bone resorp-tion, these PYD crosslinks are released into the circulation.Bone-specific alkaline phosphatase (BSAP) is an isoenzyme of alkaline phosphatase (p. 29) and is found in the cell membrane of the osteoblast. It is, therefore, an indicator of the metabolic status of osteoblasts and bone formation.These BTMs cannot indicate the risk of bone fracture nearly as well as a bone density measurement scan. These markers can be used to monitor the activity and treatment of Paget disease, hyperparathyroidism, and bone metastasis.BTMs are normally high in children because of increased bone resorption associated with growth and remodeling of the ends of the long bones. The levels reach a peak at about age 14 and then gradually decline to adult values. Because estrogen is a strong inhibitor of osteoclastic (bone resorption) activity, loss of bone density begins soon after menopause begins. Marker levels therefore rise after menopause. Most urinary assays are correlated with creatinine excretion for normalization.Interfering factors• Measurements of these urinary markers can differ by as much as 30% in one person, even on the same day. Collecting double-voided specimens in the morning can minimize variability.• Bodybuilding treatments, such as testosterone, can cause reduced levels of NTx.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yesbone turnover markers 177B• Blood tube commonly used: verify with lab• It is important to obtain baseline levels before instituting therapy.• See inside front cover for Routine Urine Testing.Urine• Preferably, obtain a double-voided specimen.• Collect the urine specimen 30 to 40 minutes before the time the specimen is needed.• Discard this first specimen.• Give the patient a glass of water to drink.• At the requested time, obtain a second specimen.Blood• Collect a venous blood sample in a red-top tube for NTx •178 bone x-raybone x-rayType of test X-rayNormal findings No evidence of fracture, tumor, infection, or congenital abnormalitiesTest explanation and related physiologyX-ray images of the long bones are usually taken when the patient has complaints about a particular body area. Fractures or tumors are readily detectable by x-ray studies. In patients who have a severe or chronic infection overlying a bone (osteomyelitis), an x-ray image may detect the infection involving that bone. X-ray studies of the long bones also can detect joint destruction and bone spurring as a result of persistent arthritis. Growth patterns can be followed by serial x-ray studies of a long bone, usually the wrists and hands. Healing of a fracture can be documented and followed. X-ray images of the joints reveal the presence of joint effusions and soft tissue swelling as well. Calcifications in the soft tissue indicate chronic inflammatory changes of the nearby bursa or tendons. Soft tissue swelling also can be seen on these bone x-rays. Because the cartilage and tendons are not directly visualized, cartilage fractures, sprains, or ligamentous injuries cannot be seen.At least two x-rays at 90-degree angles are required so that the bone region being studied can be visualized from two differ-ent angles (usually anterior to posterior and lateral). Some bone studies (e.g., skull, spine, hip) require oblique views to visualize all the parts that need to be seen.Interfering factors• Jewelry or clothing can obstruct radiographic visualization of part of the bone to be evaluated.• Prior barium studies can diminish the full radiographic visual-ization of some of the bones surrounding the abdomen (e.g., spine and pelvis).Procedure and patient careBefore Explain the procedure to the patient.• Handle carefully any injured parts of the patient’s body. Instruct the patient that he or she will need to keep the extremity still while the x-ray image is being taken. This can sometimes be difficult, especially when the patient has severe pain associated with a recent injury.bone x-ray 179B• Shield the patient’s testes, ovaries, or pregnant abdomen to avoid exposure from scattered radiation. Tell the patient that no fasting or sedation is required.During• Note that, in the x-ray department, the patient is asked to place the involved extremity in several positions. An x-ray image is taken of each position.• Note that this test is routinely performed by a radiologic tech-nologist within several minutes. Tell the patient that no discomfort is associated with this test, except possibly from moving an injured extremity.After• Administer an analgesic for relief of pain if indicated.Abnormal findingsFracturesCongenital bone disorders (e.g., achondroplasia, dysplasia, dysostosis)Tumors (osteogenic sarcoma, Paget disease, myeloma, or metastatic)Infection/osteomyelitisOsteoporosis/osteopeniaJoint destruction (arthritis)Bone spurringAbnormal growth patternJoint effusionForeign bodiesnotes180 brain scanbrain scan (Cisternogram, Cerebral blood flow, DaT scan)Type of test Nuclear scanNormal findings No areas of altered radionuclide uptake within the brain.Test explanation and related physiologyThe usefulness of a nuclear brain scan is narrow when com-pared with computed tomography (CT), magnetic resonance imaging (MRI), and positron emission tomography (PET) scans of the brain. Primarily, a nuclear brain scan is used to indicate complete and irreversible cessation of brain function(brain death). This determination, when combined with appropriate clinical data, allows for cessation of medical therapy and opportu-nity for the harvest of potential donor organs. With brain death, there is complete absence of blood perfusion to the brain.The brain scan can also be used to indicate cerebral vascular occlusion or stenosis. With the use of Diamox (acetazolamide), an accurate assessment of local cerebral blood flow can be deter-mined. Diamox is a carbonic anhydrase inhibitor that results in the elevation of Pco2 in the bloodstream. Normally, this causes dilatation of the cerebral blood vessels. If asymmetric blood flow is noted after Diamox injection, cerebral vascular occlusion or stenosis can be suspected.Brain scans are also used to investigate the ventricular system (cisternogram) of the central nervous system. Normal pressure hydrocephalus and ventricular shunt dysfunction can be identi-fied and located.Contraindications• Patients who are pregnant unless the benefits outweigh the risk of fetal damage• Patients who cannot cooperate during the testingInterfering factors Many sedative drugs can affect brain nuclear imaging. Angiotensin-converting enzyme (ACE) inhibitors, vasocon-strictors, and vasodilators can alter blood flow distribution in nuclear brain imaging.Procedure and patient careBefore Explain the procedure to the patient.• Administer blocking agents as ordered before scanning.• Consider having a sedative ordered for agitated patients.brain scan 181BDuring• Note the following procedural steps:1. After administration of the radioisotope, the patient is placed in the supine position while planar and single-photon emis-sion computed tomography (SPECT) images are obtained.2. When cerebral flow studies are performed, the counter is immediately placed over the head.3. The counts are anatomically recorded in timed sequence to follow the isotope during its first flow through the brain.• Note that this study is performed by a technologist in the nuclear medicine department in approximately 35 to 45 minutes.AfterBecause only tracer doses of radioisotopes are used, inform the patient that no precautions need to be taken to prevent radioac-tive exposure to other personnel or family present.Encourage the patient to drink fluids to aid in the excretion of the isotope from the body.Abnormal findingsCerebral deathCerebral vascular stenosis/occlusionCerebral neoplasmCSF leakageHydrocephalusnotes182 breast cancer genomicsbreast cancer genomics (Oncotype DX, Genotyping, MammaPrint)Type of test Microscopic examinationNormal findings Recurrence score 5.5% is unfavorable.10% is unfavorable.10% is unfavorable.20% is unfavorable.10% to 20% is borderline.ploidy remains unchanged). This is usually reported as S-phase fraction (SPF), which is the number of cells in S phase divided by the total number of cancer cells in the particular specimen.Cathepsin DThis protein catabolic enzyme was found to be absent in rest-ing breast tissue but significantly elevated in malignant tissue. This protein exists on tumor cell membrane and is correlated with worse clinical outcomes. The exact cutoff point between a favorable prognosis and unfavorable prognosis has yet to be standardized.HER-2 (c erbB2, neu) proteinHER-2/neu, which stands for human epidermal growth factor receptor 2, is a protein associated with worse clinical outcomes. The HER-2/neu oncogene encodes a transmembrane tyrosine kinase receptor with extensive similarity to other epidermal growth factor receptors. It is normally involved in the pathways leading to cell growth and survival. Approximately 15% to 20% of breast cancers have an amplification of the HER-2/neu gene or overexpression of its protein product.There are two commonly used methods to measure HER-2/neu protein, immunohistochemistry (IHC) and fluorescence in situ hybrid-ization (FISH). HER-2 testing is also helpful in making treatment decisions. The HER-2 gene can act as a target for an antineoplastic monoclonal antibody drug such as trastuzumab (Herceptin).p53 proteinThe p53 gene is a tumor suppressor gene that is overex-pressed in more aggressive breast cancer cells. Mutation of the gene causes overexpression and a buildup of mutant proteins on the surface of the cancer cells.186 breast cancer tumor analysisKi67 proteinThe Ki67 gene encodes the synthesis for Ki67 protein that is associated with worse clinical outcomes.Interfering factors• Delay in tissue fixation may cause deterioration of marker pro-teins and may produce lower values. Preoperative use of some chemotherapy agents may cause decreased levels of some marker proteins.Procedure and patient careBefore Inform the patient that an examination for these tumor pre-dictor markers may be performed on their breast cancer tissue. Provide psychological and emotional support to the breast cancer patient.During• The surgeon obtains tumor tissue.• This tissue should be placed on ice or in formalin.• Part of the tissue is used for routine histology. A portion of the paraffin block is sent to a reference laboratory.After Explain to the patient that results are usually available in 1 week.Abnormal findingsUnfavorable test results indicating a risk of cancer reoccurrencenotesbreast ductal lavage 187Bbreast ductal lavageType of test Fluid analysisNormal findings No atypical cells in the effluentPossible critical values Cancer cells in the effluentTest explanation and related physiologyThe theory behind ductal lavage is that by washing out exfo-liated cells from a few breast ducts, the risk of breast cancer developing in the near future can be assessed. If atypical cells are obtained, the risk of breast cancer developing in the next decade may be as high as 4 to 10 times normal. Once that risk is identi-fied, the patient may choose to attempt to alter that risk by using chemopreventative medications (e.g., selective estrogen receptor modulators) or surgery.Initially, it was hoped that ductal lavage would be able to identify ductal carcinoma of the breast at its earliest stages. The results of several large studies did not support that fact. Its use has now been limited to women who have been found to be at a statistically higher risk for breast cancer by Gail or Claus breast cancer risk models. These statistical models are based on age at menarche, age at first pregnancy, prior breast surgery, family history, and history of atypical changes in previous breast biopsies. Many women found to be at increased risk would like more data before they decide to take a medication designed to reduce those risks. If these women were found to have atypical cells in the lavage, most would choose to take the medication. If no atypical cells were found, they might choose close observa-tion only.There are still no data to confirm that the findings do accu-rately reflect a true risk for breast cancer. Furthermore, there are no data to indicate what a negative lavage means.Contraindications• Patients with prior breast cancer surgery, because their risks are already known to be highPotential complications• Infection188 breast ductal lavageProcedure and patient careBefore Explain the procedure to the patient. Often these women have already received extensive counseling regarding their risk of breast cancer.• Be sure the breast exam and mammogram are normal.• Apply a topical anesthetic to the nipple area about ½ hour before the test.During• Note the following procedural steps:1. A suction apparatus is applied to the nipple area. Ducts that reveal fluid with the suction are then chosen for cannulation.2. A tiny catheter is gently placed into the nipple duct, and the duct is lavaged with 1 to 3 mL of saline.3. The effluent is collected in a small tube and sent for cytology.4. The procedure is then repeated for the other ducts that produced fluid with nipple suction.• This procedure is performed by a surgeon in the office. There is minimal to moderate discomfort associated with the nipple suction, duct cannulation, and lavage.After Inform the patient of the possibility of mild breast discomfort.• Arrange for follow-up to discuss test results. Provide counseling if results indicate atypical or malignant cells.Abnormal findingsAtypical cellsDuctal cancer cellsnotesbreast ultrasonography 189Bbreast ultrasonography (Ultrasound mammography, Breast sonogram)Type of test UltrasoundNormal findings No evidence of cyst or tumorTest explanation and related physiologyUltrasound examination of the breast is diagnostically per-formed to determine if a mammographic abnormality or a palpable lump is a cyst (fluid-filled) or a solid tumor (benign or malignant). It is also used in screening for breast cancer in women whose breasts are dense on mammography.In diagnostic real-time ultrasonography, harmless high- frequency sound waves are emitted and penetrate the breast. The sound waves are reflected back to the sensor and are arranged in a pictorial image by electronic conversion. Ultrasonography of the breast is used to:• Differentiate cystic from solid breast lesions.• Identify masses in women with breast tissue too dense for accurate mammography.• Monitor a cyst to determine whether it enlarges or disappears.• Measure the size of a tumor.• Evaluate the axilla in women who are newly diagnosed with breast cancer.Ultrasonography is also useful for examination of symptom-atic breasts in women in whom the radiation of mammography is potentially harmful. These include:• Pregnant women. Radiation may be harmful to the fetus.• Women younger than age 25, who may be at greater onco-logic risk from the radiation of mammography.• Women who refuse mammography because of unreason-able fear of diagnostic radiation.With high-quality diagnostic ultrasonography, the character-istics of an abnormality can be evaluated and a reasonable predic-tion can be made whether it is malignant. Diagnostic accuracy is improved when breast ultrasonography is combined with mam-mography (see p. 624). Ultrasound is especially useful in patients with an abnormal mass identified on a mammogram, because the nature (cystic or solid) of the mass can be determined. Most cysts are benign.Ultrasound can be used to locate and accurately direct percu-taneous biopsy probes to a nonpalpable breast abnormality for 190 breast ultrasonographybiopsy or aspiration. Ultrasound is painless, harmless, and with-out any radiation effects on the breast tissue.Procedure and patient careBefore Explain the procedure to the patient. Assure thepatient that no discomfort is associated with this study. Inform the patient that no fasting or sedation is required before the tests. Instruct the patient not to apply any lotions or powders to the breasts on the examination day.During• The patient is placed in the supine position, and the trans-ducer is directly applied to the breast using contact gel to improve sound transmission.• Note that this test is performed by an ultrasound technician in approximately 15 minutes.• There is no discomfort associated with this procedure.After• After the test is completed, the breasts are dried and the con-ductive paste is removed.Abnormal findingsCystHematomaCancerFibroadenomaFibrocystic diseaseAbscessnotesbronchoscopy 191BbronchoscopyType of test EndoscopyNormal findings Normal larynx, trachea, bronchi, and alveoliTest explanation and related physiologyBronchoscopy permits endoscopic visualization of the larynx, trachea, and bronchi by either a flexible fiberoptic bronchoscope or a rigid bronchoscope. There are many diagnostic and thera-peutic uses for bronchoscopy.Diagnostic uses of bronchoscopy include:• Direct visualization of the tracheobronchial tree for abnor-malities (e.g., tumors, inflammation, strictures)• Biopsy of tissue from observed lesions• Aspiration of deep sputum for culture, sensitivity, and cytology determinations• Direct visualization of the larynx for identification of vocal cord paralysis if presentTherapeutic uses of bronchoscopy include:• Aspiration of retained secretions in patients with airway obstruction or postoperative atelectasis• Control of bleeding within the bronchus• Removal of foreign bodies that have been aspirated• Brachytherapy, which is endobronchial radiation therapy using an iridium wire placed via the bronchoscope• Palliative laser obliteration of bronchial neoplastic obstructionThe flexible fiberoptic bronchoscope has accessory lumens through which cable-activated instruments can be used for remov-ing biopsy specimens of pathologic lesions. Also, the collection of bronchial washings (obtained by flushing the airways with saline solution), pulmonary toilet, and the instillation of anesthetic agents can be carried out through these extra lumens. Double-sheathed, plugged-protected brushes also can be passed through this accessory lumen. Specimens for cytology and bacteriology can be obtained with these brushes. This allows more accurate determination of pulmonary infectious agents. Needles can be placed through the scope to obtain biopsies from tissue immedi-ately adjacent to the bronchi. Laser therapy to burn out endotra-cheal lesions can now be performed through the bronchoscope.Laryngoscopy is often performed through a short bron-choscope to allow inspection of the larynx and paralaryngeal structures. This is most commonly performed by an ENT 192 bronchoscopy surgeon. Cancers, polyps, inflammation, and infections of those structures can be identified. The vocal cord motion can be eval-uated also. Anesthesiologists use laryngoscopy to visualize the vocal cord structures on patients who are difficult to intubate for general anesthesia. In this instance, the laryngoscope is shaped very much like a rigid scope routinely used to see the vocal cords under direct visualization using retraction of the anterior neck during intubation. This endoscopic laryngoscope, however, is attached to a camera that projects the image of the vocal cords onto a monitor.Contraindications• Patients with hypercapnia and severe shortness of breath who cannot tolerate interruption of high-flow oxygen. However, bronchoscopy can be performed through a special oxygen mask or an endotracheal tube so that the patient can receive oxygen if required.• Severe tracheal stenosis may make it difficult to pass the scope.Potential complications• Fever• Hypoxemia• Laryngospasm• Bronchospasm• Pneumothorax• Aspiration• Hemorrhage (after biopsy)Procedure and patient careBefore Explain the procedure to the patient. Allay any fears and allow the patient to verbalize any concerns.• Obtain informed consent for this procedure.• Keep the patient NPO for 4 to 8 hours before the test to reduce the risk of aspiration. Instruct the patient to perform good mouth care to mini-mize the risk of introducing bacteria into the lungs during the procedure.• Remove and safely store the patient’s dentures, glasses, or contact lenses before administering the preprocedure medications.• Administer the preprocedure medications as ordered. Reassure the patient that he or she will be able to breathe dur-ing this procedure.bronchoscopy 193B Instruct the patient not to swallow the local anesthetic sprayed into the throat. Provide a basin for expectoration of the lidocaine.• Have emergency resuscitation equipment available.During• Note the following procedural steps for fiberoptic bronchoscopy:1. This test is performed by a pulmonary specialist or a sur-geon at the bedside or in an appropriately equipped room.2. The patient’s nasopharynx and oropharynx are anesthe-tized topically with lidocaine spray before insertion of the bronchoscope.3. The patient is placed in a sitting or supine position, and the tube is inserted through the nose or mouth and into the pharynx (Figure 7).4. After the tube is passed into the larynx and through the glottis, more lidocaine is sprayed into the trachea to pre-vent the cough reflex.5. The tube is passed farther, well into the trachea, bronchi, and first- and second-generation bronchioles, for system-atic examination of the bronchial tree.6. Biopsy specimens and washings are taken if pathology is suspected.7. If bronchoscopy is performed for pulmonary toilet (removal of mucus), each bronchus is aspirated until it is clear.• Note that this procedure is performed by a physician in approximately 30 to 45 minutes. Tell the patient that because of sedation, no discomfort is usu-ally felt.After Instruct the patient not to eat or drink anything until the tra-cheobronchial anesthesia has worn off and the gag reflex has returned, usually in approximately 2 hours.• Observe the patient’s sputum for hemorrhage if biopsy specimens were removed. A small amount of blood streak-ing may be expected and is normal for several hours after the procedure. Large amounts of bleeding can cause a chemical pneumonitis.• Observe the patient closely for evidence of impaired respira-tion or laryngospasm. The vocal cords may go into spasms after intubation.194 bronchoscopy Inform the patient that postbronchoscopy fever often devel-ops within the first 24 hours. High, persistent fever should be reported immediately.• If a tumor is suspected, collect a postbronchoscopy sputum sample for a cytology determination. Inform the patient that warm saline gargles and lozenges may be helpful if a sore throat develops. Inform the patient that biopsy or culture reports will be avail-able in 2 to 7 days.FIGURE 7 Bronchoscopy. A bronchoscope is inserted through the trachea and into the bronchus.bronchoscopy 195BAbnormal findingsInflammationStricturesTuberculosisCancerHemorrhageForeign bodyAbscessInfectionnotes196 CA 15-3 and CA 27.29 tumor markersCA 15-3 and CA 27.29 tumor markers (Cancer antigen 15-3, Cancer antigen 27.29)Type of test BloodNormal findingsCA 15-3:antigen tests as a screening technique in early breast cancers is quite limited. Benign breast disease and nonbreast malignancies also can cause elevation of these antigen levels.Interfering factors• Other benign and malignant diseases associated with eleva-tions include cancer of the lung, ovary, pancreas, prostate, and colon; fibrocystic disease of the breast; cirrhosis; and hepatitis.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no.• Blood tube commonly used: red.• The blood sample may be sent to a central diagnostic labora-tory. The results may not be available for 7 to 10 days.Abnormal findings Increased levelsMetastatic breast cancernotesCCA 19-9 tumor marker 197CA 19-9 tumor marker (Cancer antigen 19-9)Type of test BloodNormal findingslevels should be followed with further provocative testing using pentagastrin or calcium to stimulate calcitonin secretion. Pentagastrin stimulation involves an IV infusion with blood samples drawn before the injection and at 90 seconds, 2 minutes, and 5 minutes after the infusion. The calcium infusion test can be performed in a variety of ways but is most commonly administered with baseline and 5- and 10-minute postinfusion blood levels.Elevated levels of calcitonin also may be seen in people with cancer of the lung, breast, or pancreas. This is probably a form of paraneoplastic syndrome in which there is an ectopic production of calcitonin by the nonthyroid cancer cells.202 calcitoninInterfering factors• Levels are often elevated in pregnancy and in newborns. Drugs that may cause increased levels include calcium, chole-cystokinin, epinephrine, glucagon, pentagastrin, and oral contraceptives.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes.• Blood tube commonly used: green or red.• Collect a venous sample of blood in a heparinized green-top tube or a chilled red-top tube according to the laboratory’s protocol.• The specimen should be placed on ice immediately. The blood may be frozen and sent to a reference laboratory. Tell the patient that results may not be available for several days.Abnormal findings Increased levelsMedullary carcinoma of the thyroidC-cell hyperplasiaOat cell carcinoma of the lungBreast carcinomaPancreatic cancerPrimary hyperparathyroidismSecondary hyperparathyroidism because of chronic renal failurePernicious anemiaZollinger-Ellison syndromeAlcoholic cirrhosisThyroiditisnotescalcium 203Ccalcium (Total/ionized calcium, Ca, Serum calcium)Type of test Blood; urineNormal findingsAge mg/dL mmol/LTotal calcium13 mg/dLIonized calcium: 7 mg/dLTest explanation and related physiologyThe serum calcium test is used to evaluate parathyroid func-tion and calcium metabolism by directly measuring the total amount of calcium in the blood. Determination of serum cal-cium is used to monitor patients with renal failure, renal trans-plantation, hyperparathyroidism, and various malignancies. It is also used to monitor calcium levels during and after large-volume blood transfusions.About half the total calcium in the blood exists in its free (ionized) form, and about half exists in its protein-bound form (mostly with albumin). The serum calcium level is a measure of both. As a result, when the serum albumin level is low (as in malnourished patients), the serum calcium level will also be low and vice versa. As a rule of thumb, the total serum calcium level decreases by approximately 0.8 mg for every 1-g decrease in the serum albumin level. Serum albumin should be measured with serum calcium. An advantage of measuring only the ionized form is that it is unaffected by changes in serum albumin levels.When the serum calcium level is elevated on at least three sepa-rate determinations, the patient is said to have hypercalcemia. The most common cause of hypercalcemia is hyperparathyroidism. 204 calciumParathyroid hormone (see p. 689) causes elevated calcium lev-els by increasing gastrointestinal absorption, decreasing urinary excretion, and increasing bone resorption. Malignancy, the second most common cause of hypercalcemia, can cause ele-vated calcium levels in two main ways. First, tumor metastasis (myeloma, lung, breast, renal cell) to the bone can destroy the bone, causing resorption and pushing calcium into the blood. Second, the cancer (lung, breast, renal cell) can produce a para-thyroid hormone–like substance that drives the serum calcium up (ectopic PTH). Excess vitamin D ingestion can increase serum calcium by increasing renal and gastrointestinal absorp-tion. Granulomatous infections, such as sarcoidosis and tubercu-losis, are associated with hypercalcemia.Hypocalcemia occurs in patients with hypoalbuminemia. The most common causes of hypoalbuminemia are malnutrition (espe-cially in alcoholics) and large-volume IV infusions. Large blood transfusions are associated with low serum calcium levels because the citrate additives used in banked blood for anticoagulation bind the free calcium in the recipient’s bloodstream. Intestinal malabsorption, renal failure, rhabdomyolysis, alkalosis, and acute pancreatitis (caused by saponification of fat) are also known to be associated with low serum calcium levels. Hypomagnesemia can be associated with refractory hypocalcemia.Urinary calcium can also be measured. Excretion of cal-cium in the urine is increased in all patients with hypercalcemia. Urinary calcium levels are decreased in patients with hypocal-cemia. The test is helpful in determining the cause of recurrent nephrolithiasis.Interfering factors• Vitamin D intoxication may cause increased calcium levels.• Excessive ingestion of milk may cause increased levels.• Serum pH can affect calcium values. A decrease in pH causes increased calcium levels.• Prolonged tourniquet time will lower pH and falsely increase calcium levels.• There is normally a small diurnal variation in calcium, with peak levels occurring around 9 pm.• Hypoalbuminemia is artifactually associated with decreased levels of total calcium. Drugs that may cause increased serum levels include alkaline antacids, androgens, calcium salts, ergocalciferol, hydralazine, lithium, parathyroid hormone (PTH), thiazide diuretics, thy-roid hormone, and vitamin D.calcium 205C Drugs that may cause decreased serum levels include acetazol-amide, albuterol, anticonvulsants, asparaginase, aspirin, calci-tonin, cisplatin, corticosteroids, diuretics, estrogens, heparin, laxatives, loop diuretics, magnesium salts, and oral contra-ceptives.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: verify with lab.• Blood tube commonly used: red.Abnormal findings Increased levels (hypercalcemia) Decreased levels (hypocalcemia)HyperparathyroidismNonparathyroid PTH- producing tumor (e.g., lung or renal carcinoma)Metastatic tumor to the bonePaget disease of boneProlonged immobilizationMilk-alkali syndromeVitamin D intoxicationLymphomaGranulomatous infections (e.g., sarcoidosis and tuberculosis)Addison diseaseAcromegalyHyperthyroidismHypoparathyroidismRenal failureHyperphosphatemia secondary to renal failureRicketsVitamin D deficiencyOsteomalaciaMalabsorptionPancreatitisFat embolismAlkalosisHypoalbuminemianotes206 caloric studycaloric study (Oculovestibular reflex study)Type of test ElectrodiagnosticNormal findings Nystagmus with irrigationTest explanation and related physiologyCaloric studies are used to evaluate the vestibular portion of the eighth cranial nerve (CN VIII) by irrigating the external auditory canal with hot or cold water. This is considered a part of a complete neurological exam. Normally stimulation with cold water causes rotary nystagmus (involuntary rapid eye movement) away from the ear being irrigated; hot water induces nystagmus toward the side of the ear being irrigated. If the labyrinth is dis-eased or CN VIII is not functioning (e.g., from tumor compres-sion), no nystagmus is induced. This study aids in the differential diagnosis of abnormalities that may occur in the vestibular sys-tem, brainstem, or cerebellum.Contraindications• Patients with a perforated eardrumCold air may be substituted for the fluid, although this method is much less reliable.• Patients with an acutedisease of the labyrinth (e.g., Ménière syndrome)The test can be performed when the acute attack subsides.Interfering factors Drugs such as sedatives and antivertigo agents can alter test results.Procedure and patient careBefore Explain the procedure to the patient. Instruct the patient to avoid solid foods before the test to reduce the incidence of vomiting.During• Although the exact procedures for caloric studies vary, note the following steps in a typical test:1. Before the test, the patient is examined for the presence of nystagmus, postural deviation (Romberg sign), and past-pointing. This examination provides the baseline values for comparison during the test.caloric study 207C2. The ear canal should be examined and cleaned before test-ing to ensure that the water will freely flow to the middle ear area.3. The ear on the suspected side is irrigated first because the patient’s response may be minimal.4. After an emesis basin is placed under the ear, the irrigation solution is directed into the external auditory canal until the patient complains of nausea and dizziness or nystag-mus is seen. Usually this occurs in 20 to 30 seconds.5. If after 3 minutes no symptoms occur, the irrigation is stopped.6. The patient is tested again for nystagmus, past-pointing, and Romberg sign.7. After approximately 5 minutes, the procedure is repeated on the other side.• Note that this procedure is usually performed by a physician or technician in approximately 15 minutes. Tell the patient that he or she will probably experience nausea and dizziness during the test.After• Usually place the patient on bed rest for approximately 30 to 60 minutes until nausea or vomiting subsides.• Ensure patient safety related to dizziness.Abnormal findingsBrainstem inflammation, infarction, or tumorCerebellar inflammation, infarction, or tumorVestibular or cochlear inflammation or tumorAcoustic neuromaEighth nerve neuritis/neuropathynotes208 carbon dioxide contentcarbon dioxide content (CO2 content, CO2 combining power)Type of test BloodNormal findingsAdult/elderly: 23-30 mEq/L or 23-30 mmol/L (SI units)Child: 20-28 mEq/LInfant: 20-28 mEq/LNewborn: 13-22 mEq/LPossible critical values 20%Test explanation and related physiologyThis test is used to detect carbon monoxide poisoning. It measures the amount of serum COHb, which is formed by the combination of carbon monoxide (CO) and hemoglobin (Hb). CO combines with Hb 200 times more readily than oxygen (O2) can combine with Hb; thus fewer Hb bonds are available to combine with O2. Furthermore, when CO occupies the O2 binding sites, Hb is changed to bind the remaining O2 more tightly. This greater affinity of CO for Hb and this change in O2 binding strength do not allow O2 to pass readily from RBCs to tissue. Less O2 is therefore available for tissue cell respiration. This results in hypoxemia.CO poisoning is documented by Hb analysis for COHb. A specimen should be drawn as soon as possible after exposure because CO is rapidly cleared from Hb by breathing normal air. O2 saturation studies and oximetry are inaccurate in CO-exposed patients because they measure all forms of oxygen-saturated Hb, including COHb. In these circumstances, the patient’s oximetry will be good, yet the patient will be hypoxemic.This test can also be used to evaluate patients with com-plaints of headache, irritability, nausea, vomiting, and vertigo, who unknowingly may have been exposed to CO. Its greatest use, however, is in patients exposed to smoke inhalation, exhaust fumes, and fires. Other sources of CO include tobacco smoke, petroleum and natural gas fuel fumes, automobile exhaust, unvented natural gas heaters, and defective gas stoves. The treat-ment of CO toxicity is administration of high concentrations of O2 to displace the COHb.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no.• Blood tube commonly used: lavender or green.carboxyhemoglobin 211C• Obtain the patient’s history for possible sources of CO.• Assess the patient for signs and symptoms of mild CO toxic-ity (e.g., headache, weakness, dizziness, malaise, dyspnea) and moderate to severe CO toxicity (e.g., severe headache, bright red mucous membranes, cherry-red blood). Maintain patient safety precautions if confusion is present.• Treat the patient as indicated by the physician. Usually the patient receives high concentrations of O2. Encourage respirations to allow the patient to clear CO from the Hb.Abnormal findingsCarbon monoxide poisoningnotes212 carcinoembryonic antigencarcinoembryonic antigen (CEA)Type of test BloodNormal findingsCEA levels.Because the CEA level can be elevated in both benign and malignant diseases, it is not considered to be a specific test for colorectal cancer. As a result, CEA is not a reliable screening test for the detection of colorectal cancer in the general population. Its use is limited to determining the prognosis and monitoring the response of tumor to antineoplastic therapy in a patient with cancer. This is especially helpful in patients with breast and gas-trointestinal cancers. The CEA level on the initial test is an indi-cator of tumor burden and prognosis. Smaller and earlier-staged tumors are likely to have minimal CEA elevations, if not normal CEA levels. A drastic reduction of normal CEA levels is expected with complete eradication of tumor. Therefore, this test is used to determine the adequacy of treatment.This test also is used in the surveillance of patients with can-cer. A steadily rising CEA level is occasionally the first sign of tumor recurrence. This makes CEA testing very valuable in the follow-up of patients who have had potentially curative ther-apy. It is important to note that many patients with advanced breast or gastrointestinal tumors may not have elevated CEA levels.CEA can also be detected in bodily fluids other than blood. Its presence in those bodily fluids indicates metastasis. This antigen is commonly measured in peritoneal fluid or chest effusions. An elevated CEA in these fluids indicates metastasis to the peritoneum or pleurae, respectively. Likewise, elevated CEA levels in the CSF would indicate central nervous system metastasis.carcinoembryonic antigen 213CInterfering factors• Smokers tend to have higher CEA levels than nonsmokers.• Benign diseases (e.g., cholecystitis, colitis, diverticulitis) are associated with elevated CEA levels.• Liver diseases (e.g., hepatitis, cirrhosis) are associated with elevated CEA levels.• Results may vary considerably depending on the method used for quantification. Because of this, results from different labo-ratories cannot be compared or interchangeably interpreted.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no.• Blood tube commonly used: verify with lab.• Indicate on the laboratory slip if the patient smokes or has diseases that can affect test results.Abnormal findings Increased levelsCancer (gastrointestinal, breast, lung, pancreatic, hepatobiliary)Inflammation (colitis, cholecystitis, pancreatitis, diverticulitis)CirrhosisPeptic ulcerCrohn diseasenotes214 cardiac catheterizationcardiac catheterization (Coronary angiography, Ventriculography)Type of test X-ray with contrast dyeNormal findings Normal heart-muscle motion, normal coro-nary arteries, normal great vessels, and normal intracardiac pres-sures and volumesTest explanation and related physiologyCardiac catheterization is used to visualize the heart chambers, arteries, and great vessels. It is used most often to evaluate patients with chest pain. Patients with a positive stress test are also studied to locate the region of coronary occlusion. This test is also used to determine the effects of valvular heart disease. Right heart cathe-terization is performed to calculate cardiac output and to measure right heart pressures. This is the most accurate method to deter-mine cardiac output. Right heart catheterization is also used to identify pulmonary emboli (see pulmonary angiography, p. 771).For cardiac catheterization, a catheter is passed into the heart through a peripheral vein or artery, depending on whether cathe-terization of the right or left side of the heart is being performed. Pressures are recorded through the catheter, and radiographic dyes are injected. With the assistance of a computer, cardiac out-put and other measures of cardiac functions can be determined. Cardiac catheterization is indicated for the following reasons:• To identify, locate, and quantitate the severity of athero-sclerotic, occlusive coronary artery disease• To evaluate the severity of acquired and congenital cardiac valvular or septal defects• To detect congenital cardiac abnormalities, such as trans-position of great vessels, patent ductus arteriosus, and anomalous venous return to the heart• To evaluate the success of previous cardiac surgery or bal-loon angioplasty• To evaluate cardiac muscle function• To identify and quantify ventricular aneurysms• To detect disease of the great vessels, such as atheroscle-rotic occlusion or aneurysms within the aortic arch• To evaluate and treat patients with acute myocardial infarction• To insert a catheter to monitor right-sided heart pressures, such as pulmonary artery and pulmonary wedge pressures (Table 6 provides pressures and volumes used in cardiac monitoring.)cardiac catheterization 215CTABLE 6 Pressures and volumes used in cardiac monitoringPressures/Volumes Description Normal valuesPressuresRoutine blood pressure Routine brachial artery pressure 90-140/60-90 mm HgSystolic left ventricular pressure Peak pressure in the left ventricle during systole 90-140 mm HgEnd-diastolic left ventricular pressurePressure in the left ventricle at the end of diastole 4-12 mm HgCentral venous pressure Pressure in the superior vena cava 2-14 cm H2OPulmonary wedge pressure Pressure in the pulmonary venules, an indirect measurement of left atrial pressure and left ventricular end-diastolic pressureLeft atrial: 6-15 mm HgPulmonary artery pressure Pressure in the pulmonary artery 15-28/5-16 mm HgAortic artery pressure Same as routine blood pressure VolumesEnd-diastolic volume (EDV) Amount of blood present in the left ventricle at the end of diastole 50-90 mL/m2End-systolic volume (ESV) Amount of blood present in the left ventricle at the end of systole 25 mL/m2Stroke volume (SV) Amount of blood ejected from the heart in one contraction (SV = EDV – ESV)45 ± 12 mL/m2Ejection fraction (EF) Proportion (fraction) of EDV ejected from the left ventricle during systole (EF = SV/EDV)0.67 ± 0.07Cardiac output (CO) Amount of blood ejected by the heart in 1 minute 3-6 L/minCardiac index (CI) Amount of blood ejected by the heart in 1 minute per square meter of body surface area (CI = CO/body surface area)2.8-4.2 L/min/m2 for a patient with 1.5 m2 of body surface area216 cardiac catheterization• To perform dilation of stenotic coronary arteries (angio-plasty), place coronary artery stents, or perform laser atherectomyCardiac catheterization is performed under sterile condi-tions. In right-sided heart catheterization, usually the jugular, subclavian, brachial, or femoral vein is used for vascular access. In left-sided heart catheterization, usually the right femoral artery is cannulated; alternatively, however, the radial or brachial artery may be chosen (Figure 8). As the catheter is placed into the great vessels of the heart chamber, pressures are monitored and recorded. Blood samples for analysis of O2 content are also obtained. The catheter is advanced with appropriate guidance into the desired position. After pressures are obtained, angio-graphic visualization of the heart chambers, valves, and coronary arteries is achieved with the injection of radiographic dye.Groin insertionArm insertionFIGURE 8 Cardiac catheterization. Brachial (arm) or femoral (groin) arterial insertion for cardiac catheterization.cardiac catheterization 217CPercutaneous transluminal coronary angioplasty and intra-coronary stents are therapeutic procedures that can be performed during cardiac catheterization in medical centers where open heart surgery is available. During this procedure, a specially designed balloon catheter is introduced into the coronary arter-ies and placed across the stenotic area of the coronary artery. This area can then be dilated by controlled inflation of the bal-loon and subsequently stented. The coronaryarteriogram is then repeated to document the effects of the forceful dilation of the stenotic area. Coronary arterial stents can be placed at the site of previous stenosis after angioplasty to maintain patency for longer periods of time.Likewise, atherectomy of coronary arterial plaques can be performed to more permanently open some of the hard, ath-eromatous plaques. There are certain occlusive lesions with char-acteristics unfavorable for balloon angioplasty that appear to be ideally suited for atherectomy. Rotational atherectomy is most commonly used. A tiny, rotating knife inside a catheter is moved to the arterial obstruction. A balloon is inflated to position the knife precisely on the fatty deposit, and the fatty deposit is then shaved off the wall of the artery. The shavings are collected in the catheter and removed.Contraindications• Patients who are unable to cooperate during the test• Patients with an iodine dye allergy who have not received pre-ventive medication for allergy• Patients who are pregnant because of radiation exposure to the fetus• Patients with renal disorders because iodinated contrast is nephrotoxic• Patients with a bleeding propensityPotential complications• Cardiac arrhythmias (dysrhythmias)• Perforation of the heart myocardium• Catheter-induced embolic stroke (cerebrovascular accident) or myocardial infarction• Complications associated with the catheter insertion site (e.g., arterial thrombosis, embolism, or pseudoaneurysm)• Infection at the catheter insertion site• Pneumothorax following subclavian vein catheterization of the right side of the heart218 cardiac catheterization• Lactic acidosis in patients who are taking metformin and receiving iodine contrast. Metformin should be held the day of the test to prevent this complication.Procedure and patient careBefore Explain the procedure to the patient.• Obtain written permission from the fully informed patient.• Allay the patient’s fears and anxieties regarding this test. Although this test creates tremendous fear in a patient, it is performed often and complications are rare. Instruct the patient to abstain from oral intake for at least 4 to 8 hours before the test.• Prepare the catheter insertion site as per protocol.• Mark the patient’s peripheral pulses with a pen before cath-eterization. This will facilitate postcatheterization assessment of the pulses at the affected and nonaffected extremities.• Provide appropriate precatheterization sedation as ordered by the physician. Instruct the patient to void before going to the catheteriza-tion laboratory.• Remove all valuables and dental prostheses before transport-ing the patient to the catheterization laboratory.• Obtain IV access for delivery of IV fluids and cardiac drugs if necessary.During• Take the patient to the cardiac catheterization laboratory.• Note the following procedural steps:1. The chosen catheter insertion site is prepared and draped in a sterile manner.2. The desired vessel is punctured with a needle.3. A wire is placed through the needle and a sheath is placed over the wire and into the vessel.4. The angiographic catheter is threaded through the sheath over a guidewire.5. When the catheter is in the desired location, the appro-priate cardiac pressures and volumes are measured.6. Cardiac ventriculography is performed with controlled injection of contrast.7. Each coronary artery is catheterized. Cardiac angiogra-phy is then carried out with a controlled injection of con-trast material.8. During the injection, x-ray images are rapidly made.cardiac catheterization 219C9. The patient’s vital signs must be monitored constantly during this procedure.10. If angioplasty is performed, the cardiologist appropriately places the catheter and balloon at the stenotic area. Note the following procedural steps:a. As the ECG tracing is observed, the balloon is inflated and the stenotic areas are forcefully dilated.b. If signs of myocardial ischemia develop, the balloon is immediately deflated.c. Usually inflation of the balloon is continued only for 10 seconds.11. After obtaining all the required information, the catheter is removed and a vascular closure device may be placed.12. A chemical vascular closure device designed to seal the arterial puncture is often placed.• Note that this test is usually performed by a cardiologist in approximately 1 hour. Tell the patient that during the injection he or she may experience a severe hot flush. This is uncomfortable but lasts only 10 to 15 seconds.• Note that some patients have a tendency to cough as the cath-eter is placed into the pulmonary artery.• Verbally support the patient as the x-ray images are taken because the loud noises may be frightening.After• Monitor the patient’s vital signs to check for bleeding.• Apply pressure to the site of vascular access.• Keep the patient on bed rest for 4 to 8 hours to allow for complete sealing of the arterial puncture.• Keep the affected extremity extended and immobilized with sandbags to decrease bleeding.• Assess the puncture site for signs of bleeding, hematoma, or absence of pulse.• Assess the patient’s pulses for both extremities. Compare with preprocedure baseline values. Encourage the patient to drink fluids to maintain adequate hydration. Dehydration may be caused by the diuretic action of the dye. Monitor urinary output. Instruct the patient to report any signs of numbness, tingling, pain, or loss of function in the involved extremity.• See p. xviii for appropriate interventions concerning care of patients with iodine allergy.220 cardiac catheterization Instruct the patient that the test will be reviewed by the cardi-ologist and the results will be available in 1 or 2 days.Abnormal findingsAnatomic variation of the cardiac chambers and great vesselsCoronary artery occlusive diseaseCoronary aneurysmCoronary fistulaCardiomyopathyVentricular aneurysmVentricular mural thrombiIntracardiac tumorAortic root arteriosclerotic or aneurysmal diseaseAnomalies in pulmonary venous returnAcquired or congenital septal defects and valvular abnormalitiesPulmonary emboliPulmonary hypertensionnotescardiac nuclear scan 221Ccardiac nuclear scan (Myocardial perfusion scan, Myocardial perfusion imaging, Myocardial scan, Cardiac scan, Heart scan, Thallium scan, MUGA scan, Isonitrile scan, Sestamibi cardiac scan, Cardiac flow studies, and Nuclear stress test)Type of test Nuclear scanNormal FindingsHeterogeneous uptake of radionuclide throughout the myocar-dium of the left ventricleLeft ventricular end-diastolic volume ≤70 mLLeft ventricular end-systolic volume ≤25 mLLeft ventricular ejection fraction >50%Right ventricular ejection fraction >40%Normal cardiac wall motionNo muscle wall thickeningTest explanation and related physiologyA cardiac perfusion scan measures the coronary blood flow at rest and during exercise. It is often used to evaluate the cause of chest pain. It may be done after a coronary ischemic event to evaluate coronary patency or heart muscle function.In this test, a radionuclide is injected intravenously into the patient. Myocardial perfusion images are then obtained while the patient is lying down under a single-photon emission computed tomography (SPECT) camera that generates a picture of the radioactivity coming from the heart. This scan can be performed at rest or with exercise such as treadmill or bicycling (myocar-dial nuclear stress testing). Medications may be administered that duplicate exercise stress testing. Vasodilators (dipyridamole, adenosine, and regadenoson) or chronotropic agents (dobuta-mine) are commonly used. Regadenoson is the most recent A2A adenosine receptor agonist that instigates coronary vasodilata-tion. It is associated with fewer side effects (e.g., heart block, bronchospasm) and can be injected more quickly.The initial radioisotope used was thallium (thus the name thal-lium scan). Technetium agents such as tetrofosmin and sestamibi (isonitrile) are now more commonly used. The uptake of these agents is proportional to the myocardial coronary flow. At rest, a coronary stenosis must exceed 90% of the normal diameter before blood flow is impaired enough to see it on the perfusion scan. With exercise stress testing, however, stenosis of 50% becomes obvious. Often, stenosis or coronary obstruction is noted by a normal resting perfusion scan followed by stress perfusion scan 222 cardiac nuclear scanthat demonstrates cold spots compatible with decreased coro-nary perfusion. Myocardial perfusion scans can be synchronized by gating the images with the cardiac cycle and thereby allow-ing the visualization and evaluation of cardiac muscle function. The contractility of the muscle wall can be evaluated at the same time. Prior muscle injury is demonstrated by reduced muscle wall motion. Most times, nuclear myocardial scans include both per-fusion and gated wall motion images. Cardiac ejection fraction, the end-systolic volume of the left ventricle, can be calculated.Cardiac nuclear imaging when gated to the cardiac cycle (multigated acquisition scan [MUGA], gated blood pool scan) can provide an accurate measure of ventricular function through the calculation of the ventricular ejection fraction. In this scan, the patient’s red blood cells are tagged with technetium. Ventricular volumes can be calculated and used to accurately calculate the amount of blood that is ejected from the ventricle with each contraction (ejection fraction). This is used in the initial assess-ment of cardiac function and subsequently to monitor therapy designed to improve cardiac function. Patients with cardiomy-opathies (ischemic, infiltrative, inflammatory), cardiac transplant, or drug-induced cardiac muscle toxicity (from doxorubicin or Herceptin) require frequent evaluation of ventricular ejection fraction.Contraindications• Patients who are uncooperative or medically unstable• Patients with severe cardiac arrhythmia.• Patients who are pregnant, (unless the benefits outweigh the risks) because of fetal exposure to radionuclide material (unless the benefits outweigh the risks)Interfering factors• Myocardial trauma• Cardiac flow studies can be altered by excessive alterations in chest pressure (as exists with excessive crying in children).• Recent nuclear scans (e.g., thyroid or bone scan) Drugs, such as long-acting nitrates, may only temporarily improve coronary perfusion and cardiac function.Procedure and patient careBefore Explain the procedure to the patient. Instruct the patient that a short fasting period may be required, especially when using sestamibi or tetrofosmin.cardiac nuclear scan 223C Tell the patient that the only discomfort associated with this test is the venipuncture required for injection of the radioisotope.• Be sure all jewelry is removed from the chest wall.• Obtain a consent form if stress testing is to be performed.During• Take the patient to the nuclear medicine department. Depending on the type of nuclear myocardial scan, each scan-ning protocol is different.• Note the following general procedural steps:1. One or more intravenous (IV) injection of radionuclide material is performed.2. Electrocardiographic (EKG) leads may be applied.3. Depending on the radionuclide used, scanning is per-formed 15 minutes to 4 hours later.4. SPECT camera is placed at the level of the precordium.5. If a single gamma camera is used, the patient is placed in a supine position, then may be repositioned to the lat-eral position or in the right and left oblique positions. In some departments, the detector can be rotated around the patient, who remains in the supine position.6. The gamma ray scanner records the image of the heart, and an image is immediately developed.7. For an exercise stress test, additional radionuclide is injected during exercise when the patient reaches a maximum heart rate. The patient then lies on a table, and scanning is done. A repeat scan may be done 3 to 4 hours later.8. If an isonitrile stress test is needed, the radionuclide material is injected and a scan performed 30 to 60 minutes later for the resting phase. Four hours later, cardiac stress testing is done. After a second injection, scanning is repeated.• Note that myocardial scans are usually performed in less than 30 minutes by a nuclear medicine technician.• If nuclear cardiac stress testing is performed, follow routine protocol described on page 225.After Inform the patient that because only tracer doses of radioiso-topes are used, no precautions need to be taken against radio-active exposure to personnel or family. Instruct the patient to drink fluids to aid in the excretion of the radioactive substance.• Apply pressure or a pressure dressing to the venipuncture site.• Assess the venipuncture site for bleeding.224 cardiac nuclear scan• If stress testing was performed, evaluate the patient’s vital signs at frequent intervals (as indicated).• Remove any applied EKG leads.Abnormal findingsCoronary artery occlusive diseaseDecreased myocardial function associated with ischemia, myo-carditis, cardiomyopathy, or congestive heart failureDecreased cardiac outputnotescardiac stress testing 225Ccardiac stress testing (Exercise stress testing; Nuclear stress testing; Echo stress testing)Type of test Electrodiagnostic; nuclearNormal findings Patient able to obtain and maintain maximal heart rate of 85% for predicted age and gender with no cardiac symptoms or ECG change. No cardiac muscle wall dysfunction present.Test explanation and related physiologyStress testing is used in the following situations:• To evaluate chest pain in a patient suspected of having coronary disease• To determine the limits of safe exercise during a cardiac rehabilitation program or to assist patients with cardiac disease in maintaining good physical fitness• To detect labile or exercise-related hypertension• To detect intermittent claudication in patients with sus-pected vascular occlusive disease in the extremities• To evaluate the effectiveness of treatment in patients who take antianginal or antiarrhythmic medications• To evaluate the effectiveness of cardiac intervention (e.g., bypass grafting or angioplasty)Stress testing is a noninvasive study that provides information about the patient’s cardiac function. In stress testing, the heart is stressed in some way and then evaluated during the stress. Changes indicating ischemia suggest coronary occlusive disease. By far the most commonly used method is exercise stress testing. Chemical stress testing methods are becoming more commonly used because of their safety and increased accuracy. A third method, less commonly used, is pacer stress testing.During exercise stress testing, the ECG, heart rate, and blood pressure are monitored while the patient engages in some type of physical activity (stress). The treadmill test is the most fre-quently used because it is the most easily standardized and reproducible.The usual goal of exercise stress testing is to increase the heart rate to just below maximal levels or to the target heart rate. Usually this target heart rate is 80% to 90% of the maxi-mal heart rate. The test is usually discontinued if the patient reaches that target heart rate or develops any symptoms or ECG changes. The maximal heart rate is determined by a chart that takes into account the patient’s age and gender. (Target rate 226 cardiac stress testingis about 220 minus the patient’s age.) Patients taking calcium channel blockers and sympathetic blockers have a lower-than-expected maximal heart rate.Exercise stress testing is based on the principle that occluded arteries will be unable to meet the heart’s increasedx-ray procedures.• Evaluate the patient for allergies to iodine dye. Carefully consider the following points:◦ Many types of contrast media are used in radiographic studies. For example, organic iodides and iodized oils are frequently used.◦ Allergic reactions to iodinated dye may vary from mild flushing, itching, and urticaria to severe, life-threatening anaphylaxis (evidenced by respiratory distress, drop in blood pressure, or shock). In the unusual event of anaphylaxis, the patient is treated with diphenhydramine (Benadryl), steroids, and epinephrine. Oxygen and endotracheal equipment should be on hand for immediate use.◦ The patient should always be assessed for allergies to iodine dye before it is administered. Inform the radiologist if an allergy to iodinated contrast is suspected. The radiologist may prescribe Benadryl and steroid preparation to be administered before testing. Usually, hypoallergenic nonionic contrast will be administered to allergic patients during the test.◦ After the x-ray procedure, evaluate the patient for a delayed reaction to dye (e.g., dyspnea, rashes, tachycardia, hives). This usually occurs within 2 to 6 hours after the test. Treat with antihistamines or steroids.• Assess the patient for any evidence of dehydration or renal disease. Usually blood urea nitrogen (BUN) and creati-nine tests are obtained prior to administration of iodine- containing intravenous contrast. Hydration may be required prior to the administration of iodine.• Assess the patient for diabetes. Diabetics are particularly susceptible to renal disease caused by the administra-tion of iodine-containing intravenous contrast. Diabetic patients who take metformin (Glucophage) or glyburide user’s guide to test preparation and procedures xixuser’s guide to test preparation and procedures(Micronase) are particularly susceptible to lactic acidosis and hypoglycemia. These medications may be discontin-ued for 1 to 4 days prior to and 1 to 2 days after the admin-istration of iodine. Check with the x-ray department.• Women in their childbearing years should have x-ray examinations during menses or within 10 to 14 days after the onset of menses to avoid possible exposure to a fetus.• Pregnant women should not have x-ray procedures unless the benefits outweigh the risk of damage to the fetus.• Note whether other x-ray studies are being planned; sched-ule them in the appropriate sequence. For example, x-ray examinations that do not require contrast should precede examinations that do require contrast. X-ray studies with barium should be scheduled after ultrasonography.• Note the necessary dietary restrictions. Such studies as barium enema and intravenous pyelogram (IVP) are more accurate if the patient is kept NPO (fasting from food and liquids) for several hours before the test.• Determine whether bowel preparations are necessary. For example, barium enemas and IVPs require bowel-cleansing regimens.• Determine whether signed consent forms are required. These are necessary for most invasive x-ray procedures.• Remove metal objects (e.g., necklaces, watches) because they can hinder visualization of the x-ray field.• Patient aftercare is determined by the type of x-ray proce-dure. For example, a patient having a simple chest x-ray study will not require postprocedure care. However, inva-sive x-ray procedures involving contrast dyes (e.g., cardiac catheterization) require extensive nursing measures to detect potential complications.Nuclear scanningOverviewWith the administration of a radionuclide and subsequent mea-surement of the radiation of a particular organ, functional abnor-malities of various body areas (e.g., brain, heart, lung, bones) can be detected. Because the half-lives of the radioisotopes are short, only minimal radiation exposure occurs.Guidelines• Radiopharmaceuticals concentrate in target organs by vari-ous mechanisms. For example, some labeled compounds (e.g., hippuran) are cleared from the blood and excreted xx user’s guide to test preparation and proceduresby the kidneys. Some phosphate compounds concentrate in the bone and infarcted tissue. Lung function can be studied by imaging the distribution of inhaled gases or aerosols.• Note whether the patient has had any recent exposure to radionuclides. The previous study could interfere with the interpretation of the current study.• Note the patient’s age and current weight. This informa-tion is used to calculate the dose of radioactive substances.• Nuclear scans are contraindicated in pregnant women and nursing mothers.• Many scanning procedures do not require special prepara-tion. However, a few have special requirements. For exam-ple, for bone scanning, the patient is encouraged to drink several glasses of water between the time of the injection of the isotope and the actual scanning. For some studies, blocking agents may need to be given to prevent other organs from taking up the isotope.• For most nuclear scans, a small amount of an organ-specific radionuclide is given orally or injected intravenously. After the radioisotope concentrates in the desired area, the area is scanned. The scanning procedure usually takes place in the nuclear medicine department.• Instruct the patient to lie still during the scanning.• Usually encourage the patient to drink extra fluids to enhance excretion of the radionuclide after the test is finished.• Although the amount of radionuclide excreted in the urine is very low, rubber gloves are sometimes recommended if the urine must be handled. Some hospitals may advise the patient to flush the toilet several times after voiding.Ultrasound studiesOverviewIn diagnostic ultrasonography, harmless high-frequency sound waves are emitted and penetrate the organ being studied. The sound waves bounce back to the sensor and are electronically converted into a picture of the organ. Ultrasonography is used to assess a variety of body areas, including the pelvis, abdomen, breast, heart, and pregnant uterus.Guidelines• Most ultrasound procedures require little or no preparation. However, the patient having a pelvic sonogram needs a full bladder, and the patient having an ultrasound examination of the gallbladder must be kept NPO before the procedure.user’s guide to test preparation and procedures xxiuser’s guide to test preparation and procedures• Ultrasound examinations are usually performed in an ultrasound room; however, they can be performed in the patient unit.• For ultrasound, a greasy paste is applied to the skin overly-ing the desired organ. This paste is used to enhance sound transmission and reception because air impedes transmis-sion of sound waves to the body.• Because of the noninvasive nature of ultrasonography, no special measures are needed after the study except for help-ing the patient remove the ultrasound paste.• Ultrasound examinations have no radiation risk.• Ultrasound examinations can be repeated as many times as necessary without being harmful to the patient. No cumu-lative effect has been seen.• Barium has an adverse effect on the quality of abdominal studies. For this reason, schedule ultrasound of the abdo-men before barium studies.• Large amounts of gas in the bowel obstruct visualization of the bowel. This is because bowel gas is a reflector of sound.Endoscopy proceduresOverviewWith the help of a lighted, flexible instrument, internal structures of many areas of the body (e.g., stomach, colon, joints, bronchi, urinary system, and biliary tree) can be directly viewed. The spe-cific purpose and procedure should be reviewed with the patient.Guidelines• Preparation for an endoscopic procedure varies according to the internal structure being examined. For example, examination of the stomach (gastroscopy) will require the passage of an instrument through the esophagus and into the stomach. The patientdemand for blood during the testing. This may become obvious with symptoms (e.g., chest pain, fatigue, dyspnea, tachycardia, car-diac arrhythmias [dysrhythmias], fall in blood pressure) or ECG changes (e.g., ST-segment variance >1 mm, increasing premature ventricular contractions, or other rhythm disturbances). Besides the electrodiagnostic method of cardiac evaluation, the stressed heart can also be evaluated by nuclear scanning or echocardiog-raphy (which are more sensitive and accurate).When exercise testing is not advisable or the patient is unable to exercise at a level adequate to stress the heart (e.g., patients with an orthopedic, arthritic, neurologic, vascular, or pulmonary limi-tation), chemical stress testing is recommended. Although chemi-cal stress testing is less physiologic than exercise testing, it is safer and more controllable. Dipyridamole (Persantine) is a coronary vasodilator. If one coronary artery is significantly occluded, the coronary blood flow is diverted to the opened vessels. Adenosine works similarly to dipyridamole. Dobutamine is another chemical that can stress the heart. Dobutamine stimulates the heart muscle function. The normal heart muscle increases (augments) its con-tractility (wall motion). Ischemic muscle has no augmentation. In fact, in time the ischemic area becomes hypokinetic. Infarcted tissue is akinetic. In chemical stress testing, the stressed heart is evaluated by nuclear scanning or echocardiography.Pacing is another method of stress testing. In patients with permanent pacemakers, the rate of capture can be increased to a rate that would be considered a cardiac stress. The heart is then evaluated electrodiagnostically or with nuclear scanning or echocardiography.The methods of evaluation of the heart are electrophysiologic parameters (e.g., ECG, blood pressure, and heart rate), cardiac nuclear scanning, and echocardiography. These other tests are discussed separately (see pp. 221 and 356). Echocardiography is fast becoming the method of choice for urgent and elective cardiac evaluation with or without stress testing.Contraindications• Patients with unstable angina• Patients with severe aortic valvular heart diseasecardiac stress testing 227C• Patients who have recently had a myocardial infarction ( however, limited stress testing can be done)• Patients with severe congestive heart failure• Patients with severe left main coronary artery diseasePotential complications• Fatal cardiac arrhythmias• Severe angina• Myocardial infarction• FaintingInterfering factors• Heavy meals before testing can divert blood to the gastroin-testinal tract.• Nicotine from smoking can cause coronary artery spasm.• Caffeine blocks the effect of dipyridamole.• Medical problems, such as left ventricular hypertrophy, hyper-tension, valvular heart disease, left bundle-branch block, severe anemia, hypoxemia, and chronic pulmonary disease, can affect results. Drugs that can affect test results include beta-blockers, cal-cium channel blockers, digoxin, and nitroglycerin.Procedure and patient careBefore Explain the procedure to the patient. Instruct the patient to abstain from eating, drinking, and smoking for 4 hours prior to testing. Inform the patient about the risks of the test and obtain informed consent. Instruct the patient to bring comfortable clothing and athletic shoes for exercise. Slippers are not acceptable. Inform the patient if any medications should be discontinued for a time period before testing.• Obtain a pretest ECG.• Record the patient’s vital signs for baseline values.• Apply and secure appropriate ECG electrodes.During• Note that a physician usually is present during stress testing.• After the patient begins to exercise, adjust the tread-mill machine settings to apply increasing levels of stress. Encourage and support the patient at each level of increased stress. Encourage patients to verbalize any symptoms.228 cardiac stress testing• Note that during the test the ECG tracing and vital signs are monitored continuously.• Terminate the test if the patient complains of chest pain, exhaustion, dyspnea, fatigue, or dizziness.• Note that testing usually takes approximately 45 minutes. Inform the patient that the physician in attendance usually interprets and explains the results.After• Place the patient in the supine position to rest after the test.• Monitor the ECG tracing and record vital signs at poststress intervals until recordings and values return to pretest levels.• Remove electrodes and paste. Tell the patient when the test results will be available.Abnormal findingsCoronary artery occlusive diseaseExercise-related hypertension or hypotensionIntermittent claudicationAbnormal cardiac rhythms: stress inducedArrhythmias (e.g., ventricular tachycardia or supraventricular tachycardia)notescarotid artery duplex scanning 229Ccarotid artery duplex scanning (Carotid ultrasound)Type of test UltrasoundNormal findings Carotid artery free of plaques and stenosisTest explanation and related physiologyCarotid duplex scanning is a noninvasive ultrasound test used on the vertebral and extracranial carotid artery to detect occlu-sive disease directly. It is recommended for patients with periph-eral vascular disease, headaches, and neurologic symptoms (e.g., transient ischemic attacks [TIAs], hemiparesis, paresthesia, and acute speech or visual deficits).This scan is called duplex because it combines the benefits of two methods of ultrasonography—Doppler and B-mode. With the use of the transducer, a B-mode ultrasound grayscale image of the carotid vessel is obtained. A pulsed Doppler probe within the transducer is used to evaluate blood flow velocity and direction in the artery and to measure the amplitude and waveform of the carotid arterial pulse. A computer combines that information and provides a two-dimensional image of the carotid artery along with an image of blood flow. With this technique, one is able to directly visualize areas of stenotic or occluded arteries and arterial flow disruption. The degree of occlusion is measured in the percentage of the entire lumen that is occluded.Color Doppler ultrasound (CDU) can be added to duplex scanning. CDU assigns color for direction of blood flow within the vessel, and the intensity of that color is dependent on the mean computed velocity of blood traveling in the vessel. This allows visualization of stenotic areas by seeing slowing or rever-sal of direction of blood flow at a particular area of the artery. Reversal of blood flow is sometimes associated with contralateral arterial occlusion, which can be easily demonstrated by using this technique.Measurement of the thickness of the wall of the carotid artery (carotid intima–media thickness [CIMT]) is used as a measure-ment of cerebrovascular atherosclerosis specifically and is a pre-dictor of coronary atherosclerosis in general. CIMT is also used to monitor progression of atherosclerosis (particularly in diabet-ics). It is used to monitor atherosclerotic regression in patients who are undergoing a treatment for atherosclerosis.230 carotid artery duplex scanningProcedure and patient careBefore Explain the procedure to the patient. Tell the patient that no special preparation is required. Assure the patient that the test is painless.During• Place the patient in the supine position with the head sup-ported to prevent lateral motion.• Note the following procedural steps:1. A water-soluble gel is used to couple the sound from the transducer to the skin surface.2. Images of the carotid artery and pulse waveform are obtained.• Note that this test is performed by an ultrasound technologist in the ultrasound or radiology department in approximately 15 to 30 minutes. Tell the patient that no discomfort is associated with this test.After• Remove the water-solubleis kept NPO for 8 to 12 hours before the test to prevent gagging, vomiting, and aspira-tion. For colonoscopy, an instrument is passed through the rectum and into the colon. Therefore, the bowel must be cleansed and free of fecal material to afford proper visual-ization. Arthroscopic examination of the knee joint is usu-ally done with the patient under general anesthesia, which necessitates routine preoperative care.• Schedule endoscopic examinations before barium studies.• Obtain a signed consent for endoscopic procedures.xxii user’s guide to test preparation and procedures• Endoscopic procedures are preferably performed by a physician in a specially equipped endoscopy room or in an operating room. However, some kinds can safely be per-formed at the bedside.• Air is instilled into the bowel during colon examinations to maintain patency of the bowel lumen and to afford better visualization. This sometimes causes gas pains.• In addition to visualization of the desired area, special pro-cedures can be performed. Biopsies can be obtained, and bleeding ulcers can be cauterized. Also, knee surgery can be performed during arthroscopy.• Specific postprocedure interventions are determined by the type of endoscopic examination performed. All pro-cedures have the potential complication of perforation and bleeding. Most procedures use some type of sedation; safety precautions should be observed until the effects of the sedatives have worn off.• After colonoscopy and similar studies, the patient may complain of rectal discomfort. A warm tub bath may be soothing.• Usually keep the patient NPO for 2 hours after endoscopic procedures of the upper gastrointestinal system. Be certain that swallow, gag, and cough reflexes are present before permitting fluids or liquids to be ingested orally.abdominal ultrasound 1Aabdominal ultrasound (Abdominal sonogram)Type of test UltrasoundNormal findings Normal abdominal aorta, liver, gallbladder, bile ducts, pancreas, kidneys, ureters, and bladderTest explanation and related physiologyThrough the use of reflected sound waves, ultrasonography provides accurate visualization of the abdominal aorta, liver, gallbladder, pancreas, bile ducts, kidneys, ureters, and bladder. The technique of ultrasonography requires the emission of high- frequency sound waves from a transducer to penetrate the partic-ular organ being studied. The sound waves are bounced back to the transducer and are then electronically converted into a picto-rial image (Figure 1). Real-time ultrasound provides an accurate picture of the organ being studied. Doppler ultrasound provides information concerning blood flow to those organs.The kidney is ultrasonographically evaluated to diagnose and locate renal cysts, to differentiate renal cysts from solid renal tumors, to demonstrate renal and pelvic calculi, to docu-ment hydronephrosis, to guide a percutaneously inserted needle for cyst aspiration or biopsy, and to place a nephrostomy tube. Ultrasound of the urologic tract is also used to detect malformed or ectopic kidneys and perinephric abscesses. Renal transplanta-tion surveillance is possible with ultrasound. One advantage of a kidney sonogram over intravenous pyelography (see p. 778) is that it can be performed on patients with impaired renal func-tion because no intravenous contrast is required.Endourethral urologic ultrasound can also be performed through a stent that has a transducer at its end. The stent probe is placed into the urethra to examine that segment for diverticula. The stent probe can then be advanced into the bladder where the depth of a tumor into the bladder wall can be measured. With the use of wire lead guidance, the stent probe can be passed into the ureter where stones (especially those embedded into the sub-mucosa), tumors, or extraurethral compression can be identified and localized. Finally, as the probe is advanced in the proximal ureter, renal tumors or cysts can be better delineated.The prostate and the testes are discussed on pp. 754 and 816.Another use of sonography is in the assessment of the abdominal aorta for aneurysmal dilation. Sonographic evi-dence of an aortic aneurysm greater than 5 cm or any size aneurysm that is documented to be significantly enlarging is an 2 abdominal ultrasound indication for abdominal aorta aneurysm resection. Ultrasound is also an ideal way to evaluate aneurysm patients before and after surgery.Ultrasound is used to detect cystic structures of the liver (e.g., benign cysts, hepatic abscesses, and dilated hepatic ducts) and solid intrahepatic tumors (primary and metastatic). Hepatic ultrasound also can be performed intraoperatively by using a ster-ile probe. This technique allows for accurate location of small, nonpalpable hepatic tumors or abscesses. The gallbladder and bile ducts can be visualized and examined for evidence of gall-stones, polyps, or dilation secondary to obstructive strictures or tumors. The pancreas is examined for evidence of tumors, pseu-docysts, acute inflammation, chronic inflammation, or pancreatic abscesses. Ultrasound of the pancreas is frequently performed serially to document and demonstrate resolution of acute pan-creatic inflammatory processes.FIGURE 1 Ultrasound of the abdomen.abdominal ultrasound 3ABecause this study requires no contrast material and has no associated radiation, it is especially useful in patients who are allergic to contrast and in those who are pregnant. Fasting may be preferred, but it is not mandatory. (See discussion of pelvic ultrasonography [p. 697] for sonographic evaluation of pelvic organs.)Interfering factors• Air impedes transmission of ultrasonic waves into the body. The use of a lubricant is essential to ensure good transmission of sound waves to and from the body.• Barium blocks transmission of ultrasonic waves. For this rea-son, ultrasonography of the abdomen should be performed before any barium contrast studies.• Large amounts of gas in the bowel distort visualization of abdominal organs because bowel gas reflects sound. Likewise, ultrasonic evaluation of the lungs yields poor results.• Obesity may affect the results of the study because sound waves are altered by fatty tissue.• Movement causes artifacts. Some patients may need to be sedated to remain still. Uncooperative patients (especially children) may not be candidates for ultrasonography.• Because ultrasonography requires direct contact of the trans-ducer and the skin, it may not be possible to perform this study in postoperative patients with dressings.• The quality of the ultrasound image and the sufficiency of the study depend to a very large part on the abilities of the ultra-sound technologist performing the study.Procedure and patient careBefore Explain the procedure to the patient. Tell the patient that fasting may or may not be required, depending on the organ to be examined. No fasting is required for ultrasonography of the abdominal aorta, kidney, liver, spleen, or pancreas. Fasting, however, is preferred for ultrasound of the gallbladder and bile ducts.During• Note the following procedural steps:1. The patient is placed on the ultrasonography table in the prone or supine position, depending on the organ to be studied.4 abdominal ultrasound2. A greasy conductive paste (coupling agent) is applied to the patient’s skin. This paste is used to enhance sound wave transmission and reception.3. A transducer is placed over the skin.4. Pictures are taken of the reflections from the organs.• The test is completed in approximately 20 minutes, usually by an ultrasound technologist, and is interpreted by a radiologist. Tell the patient that this procedure causes no discomfort.After• Remove the coupling agent from the patient’s skin.• Note that if a biopsy is done, refer to biopsy of the specific organ (e.g., liver or kidney biopsy).Abnormal findingsKidneyRenal cystsRenal tumorRenal calculiHydronephrosisUreteral obstructionPerirenal abscessGlomerulonephritisPyelonephritisPerirenal hematomaGallbladderPolypsTumorGallstoneLiverTumorAbscessIntrahepatic dilated bile ductsPancreasTumorCystsPseudocystsAbscessInflammationBile ductsGallstoneDilationStrictureTumorAbdominal aortaAneurysmAbdominal cavityAscitesAbscessnotesacetylcholine receptor antibody panel 5Aacetylcholine receptor antibody panel (AChR Ab, Anti–AChR antibody)Type of test BloodNormal findingsACh receptor (muscle) binding antibodies: ≤0.02 nmol/LACh receptor (muscle) modulating antibodies: 0 to 20% (reported as % loss of AChR)Striational (striated muscle) antibodies:high-dose heparin, such as during CPB, when high-dose anticoagulation is necessary at levels 10 times those used for venous thrombosis. The APTT is not measurable at these high doses. The accepted goal for the ACT is 400 to 480 seconds during CPB.Second, the ACT is both less expensive and more easily per-formed, even at the bedside. This allows for immediate accessibil-ity and decreased turnaround time. The capability to perform the ACT at the point of care makes the ACT particularly useful for patients requiring angioplasty, hemodialysis, and CPB.A nomogram is often used as a guide to reach the desired level of anticoagulation. This nomogram is used in determining the dose of protamine to neutralize the heparin upon completion of these procedures. The ACT is used in determining when it is safe to remove the vascular access upon completion of these proce-dures. The benefits of the modified ACT test are that it requires a smaller-volume blood specimen; it can be automated; it can use 10 activated clotting timestandardized blood/reagent mixing; and it provides faster clot-ting time results than the conventional ACT. The modified ACT is now being used more frequently.Interfering factors• The ACT is affected by biologic variables, including hypo-thermia, hemodilution, and platelet number and function.• Factors affecting the pharmacokinetics of heparin (e.g., kid-ney or liver disease) and heparin resistance can affect ACT measurements.• A clotted specimen can increase ACT measurements.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: no• Blood tube commonly used: verify with lab• Less than 1 mL of blood is collected and placed in a machine at the bedside. When a clot forms, the ACT value is displayed.• If the patient is receiving a continuous heparin drip, the blood sample is obtained from the arm without the intravenous catheter.• The bleeding time will be prolonged because of anticoagula-tion therapy.• Assess the patient to detect possible bleeding. Check for blood in the urine and all other excretions, and assess the patient for bruises, petechiae, and low back pain.Abnormal findings Increased levels Decreased levelsHeparin administration ThrombosisClotting factor deficiencies Cirrhosis of the liver Lupus inhibitor Warfarin administration notesadrenocorticotropic hormone 11Aadrenocorticotropic hormone (ACTH, Corticotropin)Type of test BloodNormal findingsAdult/elderly:Female: 19 years and older: 6-58 pg/mLMale: 19 years and older: 7-69 pg/mLChildren:Male and female: 10-18 years: 6-55 pg/mLMale and female: 1 week-9 years: 5-46 pg/mLTest explanation and related physiologyThe ACTH tests the anterior pituitary gland function and provides the greatest insight into the causes of either Cushing syndrome (overproduction of cortisol) or Addison disease (underproduction of cortisol). An elaborate feedback mechanism for cortisol exists to coordinate the function of the hypothala-mus, pituitary gland, and adrenal glands. ACTH is an impor-tant part of this mechanism. Corticotropin-releasing hormone (CRH) is made in the hypothalamus. This stimulates ACTH production in the anterior pituitary gland. This, in turn, stimu-lates the adrenal cortex to produce cortisol. The rising levels of cortisol act as negative feedback and curtail further production of CRH and ACTH.In the patient with Cushing syndrome, an elevated ACTH level can be caused by a pituitary or a nonpituitary (ectopic) ACTH-producing tumor, usually in the lung, pancreas, thymus, or ovary. ACTH levels over 200 pg/mL usually indicate ecto-pic ACTH production. If the ACTH level is below normal in a patient with Cushing syndrome, an adrenal adenoma or carci-noma is probably the cause of the hyperfunction.In patients with Addison disease, an elevated ACTH level indicates primary adrenal gland failure, as in adrenal gland destruction caused by infarction, hemorrhage, or autoimmunity; surgical removal of the adrenal gland; congenital enzyme defi-ciency; or adrenal suppression after prolonged ingestion of exog-enous steroids. If the ACTH level is below normal in a patient with adrenal insufficiency, hypopituitarism is most probably the cause of the hypofunction.One must be aware that there is a diurnal variation of ACTH levels that corresponds to variation of cortisol levels. Levels in evening (8 pm to 10 pm) samples are usually one half to two thirds those of morning (4 am to 8 am) specimens. This diurnal variation 12 adrenocorticotropic hormoneis lost when disease (especially neoplasm) affects the pituitary or adrenal glands. Likewise, stress can blunt or eliminate this nor-mal diurnal variation.Interfering factors• Stress (trauma, pyrogens, or hypoglycemia) and pregnancy can increase levels.• Recently administered radioisotope scans can affect levels. Drugs that may cause increased ACTH levels include amino-glutethimide, amphetamines, estrogens, ethanol, insulin, metyrapone, spironolactone, and vasopressin. Corticosteroids may decrease ACTH levels.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes• Blood tube commonly used: green• Evaluate the patient for stress factors that could invalidate the test results.• Evaluate the patient for sleep pattern abnormalities. With a normal sleep pattern, the ACTH level is the highest between 4 am and 8 am and the lowest around 9 pm.• Chill the blood tube to prevent enzymatic degradation of ACTH.• Place the specimen in ice water and send it to the chemistry laboratory immediately. ACTH is a very unstable peptide in plasma and should be stored at −20 ° C to prevent artificially low values.Abnormal findings Increased levels Decreased levelsAddison disease (primary adrenal insufficiency)Cushing syndrome ( pituitary-dependent adrenal hyperplasia)Ectopic ACTH syndromeStressAdrenogenital syndrome (congenital adrenal hyperplasia)Secondary adrenal insufficiency (pituitary insufficiency)Cushing syndromeHypopituitarismAdrenal adenoma or carcinomaSteroid administrationnotesAACTH stimulation test with cosyntropin 13adrenocorticotropic hormone stimulation test with cosyntropin (ACTH stimulation test, Cortisol stimulation test)Type of test BloodNormal findingsRapid test: cortisol levels increase more than 7 mcg/dL above baseline24-hour test: cortisol levels greater than 40 mcg/dL3-day test: cortisol levels greater than 40 mcg/dLTest explanation and related physiologyThis test is performed on patients found to have an adrenal insufficiency. An increase in plasma cortisol levels after the infu-sion of an ACTH-like drug indicates that the adrenal gland is normal and is capable of functioning if stimulated. In that case, the cause of the adrenal insufficiency would lie within the pitu-itary gland (hypopituitarism, which is called secondary adrenal insufficiency). If little or no rise in cortisol levels occurs after the administration of the ACTH-like drug, the adrenal gland is the source of the problem and cannot secrete cortisol. This is called primary adrenal insufficiency (Addison disease), which may be caused by adrenal hemorrhage, infarction, autoimmunity, meta-static tumor, surgical removal of the adrenal glands, or congeni-tal adrenal enzyme deficiency.This test can also be used in the evaluation of patients with Cushing syndrome. Patients with Cushing syndrome caused by bilateral adrenal hyperplasia have an exaggerated cortisol eleva-tion in response to the administration of the ACTH-like drug. Those experiencing Cushing syndrome as a result of hyperfunc-tioning adrenal tumors (which are usually autonomous and rela-tively insensitive to ACTH) have little or no increase in cortisol levels over baseline values.Cosyntropin (Cortrosyn) is a synthetic subunit of ACTH that has the same corticosteroid-stimulating effectas endog-enous ACTH in healthy persons. During this test, cosyntropin is administered to the patient, and the ability of the adrenal gland to respond is measured by plasma cortisol levels.The rapid stimulation test is only a screening test. A normal response excludes adrenal insufficiency. An abnormal response, however, requires a 24-hour to 3-day prolonged ACTH stimu-lation test to differentiate primary insufficiency from secondary insufficiency. It should be noted that the adrenal gland can also be stimulated by insulin-induced hypoglycemia as a stressing 14 ACTH stimulation test with cosyntropinagent. When insulin is the stimulant, cortisol and glucose levels are measured.Interfering factors Drugs that may cause artificially increased cortisol levels include corticosteroids, estrogens, and spironolactone.Procedure and patient care• See inside front cover for Routine Blood Testing.• Fasting: yes• Blood tube commonly used: redRapid test• Obtain a baseline plasma cortisol level. This should be done 30 minutes before cosyntropin (ACTH-like drug) administration.• Administer an IV injection of cosyntropin over a 2-minute period as prescribed.• Measure plasma cortisol levels 30 and 60 minutes after drug administration.24-hour test• Obtain a baseline plasma cortisol level.• Start an IV infusion of synthetic cosyntropin.• Administer the solution as prescribed for 24 hours.• After 24 hours, obtain another plasma cortisol level.3-day test• Obtain a baseline plasma cortisol level.• Administer the prescribed dose of cosyntropin IV over an 8-hour period for 2 to 3 consecutive days.• Measure plasma cortisol levels at 12, 24, 36, 48, 60, and 72 hours after the start of the test.AACTH stimulation test with cosyntropin 15Abnormal findingsIn adrenal insufficiencyIncrease above normal response (secondary adrenal insufficiency)HypopituitarismExogenous steroid ingestionEndogenous steroid production from a nonendocrine tumorNormal or below normal response (primary adrenal insufficiency)Addison diseaseAdrenal infarction/hemorrhageMetastatic tumor to the adrenal glandCongenital enzyme adrenal insufficiencySurgical removal of the adrenal glandIn Cushing syndromeIncrease above normal responseBilateral adrenal hyperplasiaNormal or below normal responseAdrenal adenomaAdrenal carcinomaACTH-producing nonadrenal tumorChronic steroid usenotes16 ACTH stimulation test with metyraponeadrenocorticotropic hormone stimulation test with metyrapone (ACTH stimulation test with metyrapone, Metyrapone test)Type of test Blood; urine (24-hour)Normal findingsBlood11-deoxycortisol increased to >7 mcg/dL and cortisol
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