aana journal course 5

6 CE Credits*

AANA Journal Course 5

*AANA Journal Course No. 25: The American Association of Nurse Anesthetists is accredited as a provider of continuing education in nursing by

the American Nurses Credentialing Center Commission on Accreditation. The AANA Journal course will consist of 6 successive articles, each with

objectives for the reader and sources for additional reading. At the conclusion of the 6-part series, a final examination will be printed in the AANA

Journal. Successful completion will yield the participant 6 CE credits (6 contact hours), code number: 27603, expiration date: July 31, 2006.

Update for nurse anesthetists

Anesthetic considerations for patients withamyloidosisJill M. Nisbit, CRNA, MNABradly J. Narr, MDMary E. Shirk Marienau, CRNA, MSChristopher K. Dietz, CRNA, MNARochester, Minnesota

ObjectivesAt completion of this course, the reader should beable to:

1. Describe the disease process of amyloidosis.2. Describe the complex symptoms and manifesta-

tions of amyloidosis that may involve every bodyorgan and tissue.

3. Incorporate the anesthetic considerations intothe care for a patient with amyloidosis.

4. Discuss stem cell transplantation and its use intreating amyloidosis.

5. Discuss the treatment options for primary andfamilial amyloidosis.

IntroductionAmyloidosis is a plasma cell dyscrasia with multipleanesthetic implications. Insoluble immunoglobulindeposits may involve virtually any organ system of thebody, leading to severe pathophysiologic changes.1,2

This article describes 2 cases of amyloidosis and dis-cusses the types of amyloidosis and anesthetic impli-cations.

Case 1A 46-year-old man was given a diagnosis of systemic

Amyloidosis is a rare disease process that results in the dep-osition of insoluble, fibrous amyloid proteins in extracellularspaces and tissues. Amyloid fibrils can be deposited locallyor may involve every organ system of the body. Advance-ments in the treatment for amyloidosis allow longer survival,and patients are being seen in our operating rooms for diag-nostic, interventional, and curative purposes. Amyloidosis

has numerous implications for anesthesia providers due to

the possibility of systemic involvement. This course describes

2 cases of amyloidosis and discusses the types of amyloido-

sis and their anesthetic implications.

Key words: Amyloidosis, anesthesia, hemodynamics, seda-

tion, transplant.

amyloidosis. The patient began to experience fatigue,dyspnea, and chest pain, and had 3 syncopal episodes14 months before initial examination. A diagnosis ofcardiomyopathy was made at that time. Cardiac mon-itoring revealed runs of nonsustained ventriculartachycardia with mild hypotension. The patient hadan arterial embolism in his right arm requiring anembolectomy and initiation of anticoagulant therapy.Throughout this period, the patient also experiencedsubconjunctival hemorrhages, voice changes, xeros-tomia, jaw claudication, decreased appetite, andweight loss.

The patient was referred to a tertiary center fortreatment and consideration of heart transplantation.The electrocardiogram revealed premature ventricularcomplexes and a low-voltage QRS complex. Anechocardiogram revealed normal left ventricular sizeand generalized left ventricular hypokinesis with anestimated ejection fraction of 40%. The ventricularseptum and right and left ventricular walls were thick-ened, and there was diastolic dysfunction. The find-ings were considered consistent with amyloid heartdisease. Cardiac catheterization revealed congestivecardiomyopathy and moderate pulmonary hyperten-sion. A right-sided myocardial biopsy was performed

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and was positive for amyloid heart disease. A bonemarrow biopsy revealed hypercellularity and 20%plasma cells in his bone marrow. An IgA lambda monoclonal protein was identified in his serum, andlambda light chains in his urine were consistent witha plasma cell dyscrasia. Pulmonary function testsrevealed mild restrictive lung disease.

The patient underwent internal cardiac defibrilla-tor placement due to several episodes of syncope withventricular tachycardia. Cardiac transplantation wasdelayed in lieu of autologous stem cell transplantationto treat amyloidosis. In preparation for the stem celltransplantation, the patient underwent Hickmancatheter placement without complications. This pro-cedure was completed with sedation using midazolamand fentanyl.

Stem cell mobilization with granulocyte colony-stimulating factor was initiated 1 day after catheterplacement. The granulocyte colony-stimulating factorcauses the release of large numbers of peripheralblood stem cells into the bloodstream.* After stem cellmobilization, significant weight gain and worseningdyspnea developed. A thoracentesis was completedand provided symptomatic relief. The patient was hos-pitalized due to severe episodes of syncope andhypotension. He then underwent 12 days of stem cellcollection. A repeated echocardiogram revealedseverely impaired cardiac function with an ejectionfraction of 10%. The patient died 23 days after initia-tion of stem cell transplantation.

Case 2A 49-year-old man with a family history of type Ifamilial amyloidosis sought care because of gastroin-testinal complaints, peripheral neuropathy, and visualchanges. Gastrointestinal symptoms included diffi-culty swallowing, abdominal cramps, nausea, andvomiting, with a 20-pound weight loss.

An electrocardiogram showed normal sinus rhythmwith low-voltage QRS complex with anteroseptal andinferior infarcts. An echocardiogram revealed normalsystolic function with a 60% ejection fraction; how-ever, there was a marked increase in the left ventricu-lar wall thickness. Diastolic dysfunction also wasnoted. DNA studies of the patient and 2 of his sisterswere positive for a tyrosine 77 mutation, an amyloidprecursor protein.2

The clinical findings suggested that this patient hadautonomic neuropathy with gastrointestinal symptoms

rather than amyloid deposition in the gastrointestinaltract. Autonomic neuropathy usually improves aftertransplantation, whereas peripheral neuropathy doesnot. Curative treatment for familial amyloidosis is livertransplantation.1,2,4-6 Even though the patient wasasymptomatic from a cardiac standpoint, inadequatecardiac reserve during the liver transplantation periodor progression of his cardiac disease despite liver trans-plantation was a concern. The patient was listed forheart and liver transplantation.

Heart transplantation occurred 1 year later. A livertransplant was not completed due to hemodynamicinstability during the cardiac procedure. A right ven-tricular assist device and an intra-aortic balloon pumpwere required postoperatively for hemodynamic sup-port. An echocardiogram on postoperative day 1showed an ejection fraction of 35%. Serial echocardio-grams revealed continued improvement to an ejectionfraction of 65%, at which time the intra-aortic balloonpump was discontinued. The right ventricular assistdevice was weaned and removed without complications1 week after transplantation. Dismissal echocardiogramresults revealed a normal left ventricle with an esti-mated ejection fraction of 61%. The patient is beingreevaluated for liver transplantation.

DiscussionAmyloidosis results from the deposition of insoluble,fibrous amyloid proteins in the extracellular spaces oforgans and tissues. Depending on the biochemicalnature of the amyloid precursor protein, amyloid fib-rils can be deposited locally or may involve everyorgan system of the body. There are multiple forms ofamyloid fibrils, which are classified according to theunique fibrous structure that they each possess. Thefollowing forms exist: (1) primary (AL) amyloidosis(no evidence of preexisting or coexisting disease); (2)amyloidosis associated with multiple myeloma (alsothe AL type); (3) secondary (AA) amyloidosis associ-ated with chronic infectious diseases or chronicinflammatory diseases; (4) heredofamilial amyloidosis(AF); (5) local (AE) amyloidosis (amyloid depositionlimited to a single organ); (6) senile (AS) associatedwith aging; (7) chronic hemodialysis–related amyloi-dosis (AH).2,6 (See Table 1.)

Amyloidosis is a rare disease, affecting about 8 per-sons per million annually. In patients with primaryamyloidosis, 15% to 20% have AL associated withmyeloma, 95% are older than 40 years, and 66% are

* Stem cells are immature cells that grow and divide into mature red blood cells, white blood cells, or platelets. When the white blood cell count has

increased to a sufficient level, stem cell collection begins. High-dose chemotherapy is a potential cure for this disease. However, high-dose chemother-

apy suppresses bone marrow production of stem cells, and mobilized peripheral blood stem cells are needed to restore bone marrow function. Before

the use of high-dose chemotherapy, peripheral blood stem cells are collected and frozen for storage. After chemotherapy, the peripheral blood stem

cells are thawed and transfused into the patient. The stem cells migrate to the bone marrow and begin the process of creating new blood cells.3

men.7 The average survival with primary amyloidosisis 12 months, and in familial amyloidosis, survival is7 to 15 years.1,8 The major causes of death are heartdisease and renal failure. Sudden death, presumablydue to arrhythmias, is common.5,7

AL amyloidosis is a disease process in which amonoclonal population of bone marrow plasma cellsproduces small lambda or kappa fragments that areprocessed in an abnormal manner by macrophageenzymes. The enzymes produce the partially degradedlight chains responsible for AL amyloidosis. Theinsoluble amyloid fibril, or light chain, deposits in theextracellular spaces of organs and tissues lead to organfailure and, eventually, death.1-3,5-7,9

Primary amyloidosis related to multiple myelomais a relatively rare disease with 3,000 cases reportedannually in the United States.9 Multiple myeloma is acancer of the plasma cells. Plasma cells, which arelocated in the bone marrow, function as part of theimmune system by producing antibodies. Normalbone marrow contains only about 2% plasma cells.With multiple myeloma, increased abnormal plasmacells produce increased numbers of antibodies. Theseadditional antibodies do not function normally andare thought to prevent the body from making normalinfection-fighting antibodies.10 Multiple myelomaassociated with amyloidosis is a rapidly progressivedisease once symptoms occur, and life expectancy isusually less than 6 months. Diagnosis often is madelate in the course of the disease, and cardiac failure isthe most common initial symptom.1,2

Familial amyloidosis involves a mutant transthyretinprotein that forms amyloid fibrils, leading to polyneu-ropathy, cardiomyopathy, or both. The mutant proteins,although present from birth, are associated with a

delayed onset of symptoms, usually after 3 to 7 decadesof life.1,2,4,6,9 The amyloid fibrils are characterized bysingle amino acid substitutions within the transthyretinmolecule. The liver produces transthyretin (normal orabnormal amyloid) almost exclusively; therefore, livertransplantation has been successful in the treatment offamilial amyloidosis.1,4-6

Anesthetic implicationsThe clinical manifestations of amyloidosis are variedand depend entirely on the area of the body that isinvolved. In many cases, amyloid fibrils deposit in theheart (Table 2). The myocardium involved with amy-loid deposition is usually firm, thickened, and non-compliant, which can result in restrictive cardiomyopa-thy with systolic or diastolic impairment (Figures 1Aand Figure 2). Cardiac manifestations consist primarilyof congestive heart failure, cardiomegaly, and a varietyof arrhythmias. Echocardiography reveals thickening ofthe left ventricular wall and interventricular septum,hypokinesia, and decreased systolic contraction. Elec-trocardiogram abnormalities include low-voltage QRScomplex and conduction abnormalities, often resultingin varying degrees of heart block.1,2,6 Syncope is com-mon and is a strong predictor of sudden death.7

Anesthesia providers must be aware of the cardiacmanifestations of amyloidosis and the associatedimplications. In patients with cardiac involvement, thereduced stroke volume due to diastolic dysfunctionproduces systolic hypotension.4,7 It can be difficult tomaintain hemodynamic stability during induction andthroughout the surgical period. The cardiac depressanteffects of anesthetic drugs enhance amyloid-relateddysfunction.4,5 The need for invasive monitoring andcentral venous access should be determined on a case-


Classification Associated diseases Chemically related precursor protein

Primary amyloidosis No evidence of preexisting or coexisting Immunoglobulin kappa and lambda light chainsdisease

Primary amyloidosis Multiple myeloma Immunoglobulin kappa and lambda light chainsrelated to multiple myeloma

Secondary/reactive Chronic infections or inflammatory Serum amyloid A (SAA)conditions

Heredofamilial Genetically predisposed Transthyretin (more than 50 known mutations)

Local Deposits limited to a single organ Amyloid proteins seem to be derived frompolypeptide hormones or unique proteins

Senile Alzheimer disease Amyloid precursor protein (APP)

Chronic hemodialysis– Chronic renal failure β2-microglobulin related amyloidosis

Table 1. Classification of amyloidosis*

* Compiled from Wilson et al,2 Lee et al,6 and Kumar et al.9


Body system Manifestations Anesthetic considerations for each body system

Cardiac

Kidney

Respiratory

Gastrointestinal

Nervous system

Skin

Hepatic

Table 2. Systemic effects of amyloidosis*

* Compiled from entire list of references.1-11

Restrictive cardiomyopathy

Systolic or diastolic dysfunction

Cardiomegaly

Arrhythmias

Syncope

Congestive heart failure

Echocardiogram: thickening of the leftventricular wall and interventricular septum,hypokinesia, and decreased systolic contraction

Electrocardiogram: low-voltage QRS complexwith conduction abnormalities; heart blocksand arrhythmias common

Anesthetic plan according to cardiac dysfunction

Hemodynamic challenges during induction andthroughout the perioperative period

Enhancement of amyloid-related dysfunction bythe cardiac depressant effects of anestheticdrugs

Immediate availability of emergency drugs anddefibrillator due to the risk of cardiac arrthymias

Range from proteinuria to nephrotic syndrome

Elevated creatinine level

Hypoalbuminuria

Increased proteinuria

Decreased renal function and renal blood flow

Influence of impaired renal function on drugselection

Reduced protein binding of drugs

Maintain perfusion pressure and adequatehydration.

Larynx most common site in respiratory tract;amyloid deposits of tumorous masses ordiffuse infiltration; signs and symptoms:hoarseness, dyspnea, and dysphagia

Macroglossia

Salivary gland involvement

Possible blockage of ducts or the air passagesin the nasal sinuses, larynx, and trachea byaccumulation of amyloid fibrils

Progressive stenosis of the airways due todeposition of amyloid fibrils in thetracheobronchial tree

Thorough airway examination before any sedationor anesthetic: hoarseness, voice changes,enlarged or swollen tongue, dry mouth, difficultybreathing, and wheezing

Macroglossia: patent airway obstruction anddirect laryngoscopy interference

Difficult intubation; possible complications,airway obstruction and hemorrhage

Prevention of airway obstruction and anunprotected airway if laryngeal or respiratoryamyloidosis is diagnosed or suspected by carefultitration of sedation

Difficulty with ventilation, wheezing, and/orbronchospasm due to airway stenosis

Gastrointestinal involvement common in allforms; occurs at all levels of the gastrointestinaltract. Symptoms: obstruction, hemorrhage,diarrhea, malnutrition, and dehydration

Gastric reflux

Delayed gastric emptying

Proper intravenous hydration

Monitoring of electrolytes and hemoglobin

Rapid-sequence induction

Raised waxy papules or plaques, usually in theface or neck or clustered in the folds of the axil-lary, anal, or inguinal regions; periorbitalecchymoses

Vigilant positioning to prevent skin breakdown

Peripheral neuropathy

Autonomic neuropathy

Postural hypotension

Carpal tunnel syndrome

Visual changes

Alzheimer disease

Neuropathy a relative contraindication to regionalanesthesia

Vigilant positioning to prevent nerve damage andfurther exacerbate neuropathies

Significant hypotension and delayed gastricemptying due to autonomic neuropathy

Hematological changes: increased fibrinolysisand selective deficiency of clotting factors

Acquired factor X deficiency

Hepatomegaly

Preoperative and perioperative monitoring ofcomplete blood cell count, prothrombin time,activated partial thromboplastin time,international normalized ratio, and bleeding time


by-case basis. Emergency drugs and a defibrillatorshould be immediately available due to the risk of car-diac arrhythmias and dysfunction.1,2,4,5 The cause ofdeath in most patients with amyloidosis is cardiac—progressive cardiomyopathy with heart failure or sud-den death due to ventricular arrhythmias.1,2,5,7,9

Renal involvement is common and potentially themost serious manifestation of amyloidosis.5,7,9 Amy-loid involvement in the kidney may range from mildproteinuria to nephrotic syndrome.1,2,7 Renal tubularacidosis and renal vein thrombosis may occur.1,2,5-7,9

Impaired renal function and clearance may influencedrug selection.5

The respiratory system and gastrointestinal tractare commonly affected by amyloidosis. The larynx isthe most common site for amyloidosis in the respira-tory tract. Symptoms consist mainly of hoarseness,but dyspnea and dysphagia may be present.11 Thenasal sinuses, larynx, and trachea may be involved,causing obstruction, hemorrhage, or difficult intuba-tion. Thick, immobile tongues classically develop,leading to macroglossia.1,2,5,11 Macroglossia and sali-vary gland involvement can produce upper airwayobstruction; therefore, sedation must be titrated care-fully when the airway is unprotected.1,2,5,6,9,11 Amyloiddeposits can extend into the tracheobronchial tree andmay result in progressive stenosis of the airways lead-ing to difficulty with ventilation.1,2,11

Gastrointestinal involvement is common in allforms of amyloidosis and can occur at all levels of thegastrointestinal tract.1,2,5,6,9 Malnutrition, dehydra-tion, and gastric reflux are common; therefore, proper

intravenous hydration and rapid-sequence inductionare recommended.5

Pathology related to the nervous system and tissueinfiltration of amyloid fibrils presents numerousanesthetic implications. Amyloid fibrils may depositalong peripheral nerves, in autonomic ganglia, insenile plaques, or in blood vessels of the central nerv-ous system.1,2,4-6 Peripheral neuropathy, prominent inheredofamilial amyloidosis, is a relative contraindica-tion to regional anesthesia.5 Care with positioning isessential to prevent nerve damage and breakdowndue to skin fragility and peripheral neuropathy.5 Infil-tration of the autonomic nervous system may mani-fest as delayed gastric emptying or postural hypoten-sion.1,2,4,5 As a result of autonomic dysfunction, theadministration of anesthetic drugs to patients withfamilial amyloidosis increases the risk of producingsignificant hypotension.4-7

Involvement of the skin is one of the most character-istic manifestations of primary amyloidosis. The face,neck, and mucosal areas may be affected, causing symp-toms of hoarseness, dyspnea, and dysphagia. Thesesymptoms may be an indicator of possible laryngeal ortracheal involvement and should be investigated further.Infiltrates of the cornea or vitreous body may be presentin hereditary amyloidosis, causing visual changes.1,2

Although liver involvement is common, liver func-tion abnormalities are minimal and occur late in thedisease. Hematologic changes may include increasedfibrinolysis and selective deficiency of clotting factors,

Figure 1. Heart in primary amyloidosis Figure 2. Hypertrophic cardiomyopathy is common inamyloidosis

A, Markedly thickened left ventricular wall, withdisproportionate thickening of the ventricular septum,simulating hypertrophic cardiomyopathy (short-axisslice at the midventricular level, viewed from the apextoward the base). B, Light microscopy showing amyloidin green and myocytes in yellow (sulfated Alcian bluestain, medium power).

(Courtesy of William D. Edwards, MD, Division of Anatomical Pathology,Mayo Clinic College of Medicine, Rochester, Minn.)

Note the left ventricular and intraventricular septal wallthickness. Concentric thickening of the left ventricularwall in primary amyloidosis (short-axis view at thebase of the heart).

(Courtesy of William D. Edwards, MD, Division of Anatomical Pathology,Mayo Clinic College of Medicine, Rochester, Minn.)


leading to an increased risk of bleeding.1,2,5,6 Bleedingdisorders are common in patients with amyloidosis,most commonly due to infiltration of blood vessels byamyloid fibrils. Acquired factor X deficiency isuncommon but is a well-documented complication ofAL amyloidosis.6 Coagulopathy may contraindicateregional anesthesia.5

Anesthetic and surgical stress cause tremendousimplications for patients with amyloidosis, even dur-ing minor surgical procedures. Viana et al4 comparedhemodynamics during liver transplantation in patientswith familial amyloidosis with the hemodynamics in acontrol group. Comparison of the 2 groups revealedthat standardized identical anesthetics produce signifi-cant hypotension in patients with familial amyloidosis.These patients are very sensitive to decreases in pre-load and require vigilant monitoring with rapid inter-vention. Hypotension also occurred despite adequatepreload, which was treated most effectively by a vaso-constrictor infusion. Despite the decreased use ofinhalation agents and opioids and increased use ofvasoconstrictors, the patients with familial amyloidosishad more significant hypotensive episodes.4

Amyloid fibrils are identified by biopsy of the sus-pected organ, abdominal fat, and renal or rectal tissuespecimens, and patients often require anesthetic care.All tissues obtained must be stained with Congo redand examined under a polarizing microscope. TheCongo red stain develops into a unique green whenamyloid fibrils are present.1,2,5,6,9 See Figure 1B.

ConclusionAmyloidosis is a complex, progressive disease, andtreatment options vary depending on the type of amy-loidosis present and extent of organ involvement.Liver transplantation has been available since 1990 forthe treatment of familial amyloidosis. In successfultransplants, normal transthyretin gradually replacesthe circulating abnormal protein, followed by a grad-ual reduction of the existing amyloid fibrils.1,2,4,6 Themost effective form of treatment for patients with ALamyloidosis is chemotherapy with stem cell trans-plantation. Destruction of plasma cells, with concur-rent decreases in light chain production, may furtherprevent deposition of amyloid or even reverse theprocess.1,2,6 Studies have shown that outcome isrelated to the extent of cardiac involvement and thenumber of organs involved at the time of transplanta-tion.8,9 Cardiac transplantation for severe cardiacinvolvement in AL and AF amyloidosis also has beensuccessful.1,2,6,7 Subsequent stem cell transplantation

is indicated after cardiac transplantation in an effort toprevent recurrent amyloid.7

Amyloidosis has multiple implications for anesthesiaproviders due to the possibility of multiorgan involve-ment. Patients with amyloidosis are seen in the operat-ing rooms for diagnostic, interventional, and curativepurposes. Anesthesia providers must be aware of themultisystem involvement of amyloidosis and therelated anesthetic implications. Each amyloidosis caseis unique, and the anesthetic must be determined on acase-by-case basis and tailored to the individual signsand symptoms the patient is experiencing.REFERENCES1. Sipe JD, Cohen AS. Amyloidosis. In: Braunwald E, Fauci A, Kasper

D, Hauser S, Longo D, Jameson JL, eds. Harrison’s Principles ofInternal Medicine. 15th ed. New York, NY: McGraw Hill;2001:1974-1979.

2. Cohen AS. Amyloidosis. In: Wilson J, Braunwald E, Isselbacher K,Peterdorf R, Martin J, Fauci A, Root R, eds. Harrison’s Principles ofInternal Medicine. 12th ed. New York, NY: McGraw Hill; 1991;1417-1421.

3. Gertz M, Lacy M, Gastineau D, et al. Amyloid: blood stem celltransplantation as therapy for primary systemic amyloidosis (AL).Bone Marrow Transplant. 2000;26:963-969.

4. Viana J, Bento C, Vieira H, et al. Haemodynamics during livertransplantation in familial amyloidotic polyneuropathy: study ofthe intraoperative cardiocirculatory data of 50 patients. Rev PortCardiol. 1999;18:689-697.

5. Stoelting RK, Dierdorf SF. Anesthesia and Co-existing Disease. 4thed. Philadelphia, Pa: Churchill Livingstone; 2002:623-624.

6. Lee GR, Foerster J, Lukens J, Paraskevas F, Greer JP, Rodgers GM.Wintrobe’s Clinical Hematology. 10th ed. Baltimore, Md: LippincottWilliams & Wilkins; 1999.

7. Gertz M, Lacy M, Dispenzieri A. Immunoglobulin light chain amy-loidosis and the kidney. Kidney Int. 2002;61:1-9.

8. Reich G, Held T, Siegert W, Kampf D, Dorken B, Maschmeyer G.Four patients with AL amyloidosis treated with high-dosechemotherapy and autologous stem cell transplantation. BoneMarrow Transplant. 2001;27:341-343.

9. Kumar V, Cotran RS, Robbins SL. Robbins Basic Pathology. 7th ed.Philadelphia, Pa: Saunders; 2003.

10. University of Maryland Medicine. Multiple Myeloma Treatments atthe University of Maryland Greenebaum Cancer Center. Availableat: http://www.umm.edu/cancer/canc_multmyel.html. AccessedOctober 23, 2002.

11. Takashi N, Kouichiro M, Iwagaki T, Takara H, Sata T, ShigematsuA. Anesthetic management of a patient with laryngeal amyloidosis.J Clin Anesth. 1999;11:339-341.

AUTHORSJill M. Nisbit, CRNA, MNA, is a nurse anesthetist at Rusk CountyMemorial Hospital, Lady Smith, Wis. When this article was written,she was a nurse anesthesia student at the Mayo Clinic College of Med-icine, School of Health Sciences Master of Nurse Anesthesia Program,Rochester, Minn.

Bradly J. Narr, MD, is associate professor of anesthesiology and chairof the Department of Anesthesiology, Mayo Clinic, Rochester, Minn.

Mary E. Shirk Marienau, CRNA, MS, is assistant professor of anes-thesiology and program director, Mayo Clinic College of Medicine,School of Health Sciences Master of Nurse Anesthesia Program,Rochester, Minn.

Christopher K. Dietz, CRNA, MNA, is instructor of anesthesiologyand assistant program director, Mayo Clinic College of Medicine, Schoolof Health Sciences Master of Nurse Anesthesia Program, Rochester, Minn.

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