The International Student Journal of Nurse Anesthesia

VO LU M E 6 N U M B E R 2 2 0 0 7

Topics in This Issue

Difficult Airways

Ablation of Atrial Fibrillation

Jehovah’s Witness Patient

Angelman’s Syndrome

Carotid Endarterectomy

Obstetric Complications

Dexmedetomidine

Multiorgan Procurement

Post-Operative Pain Management

Pulmonary Edema

Hyponatremia

Acute Intermittent Porphyria

Elastic Gum Bougie

Pediatric Awake Craniotomy

Pulmonary Artery Catheter Criteria

Mid-cavity Ballooning Syndrome

Continuous Femoral Nerve Block

Colloid Replacement

ABSTRACT Projected CRNA Retirements

EDITOR IN CHIEFRonald L. Van Nest, CRNA, MA

ASSOCIATE EDITORJulie A. Pearson, CRNA, PhD

EDITORIAL BOARDKathy Wren, CRNA, PhD, Louisiana State UniversityJanet A. Dewan, CRNA, MS, Northeastern UniversityLadan Eshkevari, CRNA, MS, Georgetown UniversityDonna Jasinski, CRNA, PhD, Georgetown UniversityElizabeth Koop, CRNA, MS, Georgetown UniversityMichele Gold, CRNA, PhD, University of Southern CaliforniaJoseph E. Pellegrini CRNA, DNSc, CDR, NC, USN, Navy Nurse Corps

Anesthesia ProgramEdward Waters, CRNA, MN, Kaiser School of Anesthesia, California State

University Fullerton Vicki C. Coopmans, CRNA, PhD, Barnes - Jewish College of Nursing and Allied Health

CONTRIBUTING EDITORS and REVIEWERSGeorgetown University

Carrie Bowman, CRNA, MSU.S. Navy Nurse Corps Anesthesia Program

Lisa Osborne, CRNA, PhD, CDR, NC, USNGregory Nezat, CRNA, MS, LCDR, NC, USNRobert Hawkins, CRNA, MS, LCDR, NC, USN

Kaiser School of Anesthesia, California State University Fullerton John J. Nagelhout, CRNA, PhD Sass Elisha, CRNA, MSN

Wake Forest University Baptist Medical Center Nurse Anesthesia ProgramUniversity of North Carolina at Greensboro

Michael Rieker CRNA, DNPUnited States Navy

Jeanette Berry, CRNA, MS, LCDR, NC, USNNewman University

Sharon Niemann, CRNA, MHSUniversity of Pennsylvania

Russ Lynn, CRNA, MSNMaria Magro, CRNA, MSN, MS

University of North Carolina at GreensboroNancy Bruton-Maree, CRNA, MS

University of ScrantonJoAnn Platko CRNA, MSN

R & S Ouellette Inc;President International Federation of Nurse Anesthetists

Sandra M. Ouellette, CRNA, MEd, FAANMedical University of South Carolina

Anthony Chipas CRNA, PhDMichigan State University

Henry C Talley V, CRNA, PhDGooding Institute of Nurse AnesthesiaBay Medical Center

Charles A. Vacchiano, CRNA, PhDMidwestern University

Mary Wojnakowski, CRNA, PhDFlorida International University

W. Patrick Monaghan, CLS, SBB, Ph.D.Northeastern University

Nicola Ryding, CRNA, MSPaul Sawler, CRNALana Leinbach Yaney, CRNA, MS

The International Student Journal of Nurse Anesthesia

Cover Photo: Allison Daley,

University of Pennsylvania,Confirms placement of

double lumen endobrochial tube

University of Kansas, Bryan LGH School of Nurse Anesthesia

Sharon Hadenfeldt, CRNA, PhDTexas Christian University

Nelson L. Strother, CRNA, BSKristy Beaver, CRNA, MSN

Columbia UniversityMaribeth Massie, CRNA, MS

Barry UniversityPaul J. Safara, CRNA, MSNA

University of MichiganPatricia Klask, CRNA, MSLulu Bender CRNA, MS

Virginia Commonwealth UniversityCharles Reese, CRNA, PhD

Robert A. Roubik, CRNA, MS, Col, NC, USAF (Ret)Cynthia Cappello, CRNA, MAE, CAPT, NC, USN (Ret)

The opinions contained in this journal are those of the student and do not necessarily represent the opinions of the program or the University

Disclaimer for all articles authored by military personnel: The views expressed in this journal are those of the authors and do not necessarily reflect the official policy or position of their respective Military Department, Department of Defense, nor the U.S. Government. The work was prepared as part of the official duties of the military service member. Title 17 U.S.C. 105 provides that ‘Copyright protection under this title is not available for any work of the United States Government’. Title 17 U.S.C. 101 defines a United States Government work as a work prepared by a military service member or employee of the United States Government as part of that person’s official duties.

The International Student Journal of Nurse Anesthesia is produced and distributed through an Educational Grant from Baxter Healthcare Corporation.

Front Cover design: Ruth M. Moyer. Go For Joy.

EDITORIAL . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .49

CASE REPORTS

Difficult Airway in a Pediatric Patient with Spinal Curvature and Tracheal Esophageal Fistula . . . . . . . . . . . . . . 50Amy J. Granquist, University of Pennsylvania

Minimally Invasive Video-Assisted Thoracoscopic Approach to Ablation of Atrial Fibrillation . . . . . . . . . . . . . . . . 52Jennifer M. Judeikis, University of Pennsylvania

Anesthetic Management of a Jehovah’s Witness Patient Possessing Many Co-Morbidities . . . . . . . . . . . . . . . . . . . 57Michael S.K. Awai, Florida International University

Fiberoptic Nasal Intubation in the Case of Limited Mouth Opening . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .61Stephen E. Kushiner, University of Scranton

Genitourinary Surgery in a Patient with Angelman’s Syndrome . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .64Amy L Mancini, Northeastern University

Anesthesia for Carotid Endarterectomy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .67Christine Ramsden Jackson, Northeastern University

Anesthetic Management of Known Placenta Previa/Accreta . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .71Darin J. O'Brien, University of Kansas, Bryan LGH School of Nurse Anesthesia

Dexmedetomidine: Use as an Analgesic and Hemodynamic Stabilizer . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .74Kirsten H. Meister, University of Pennsylvania

Multiorgan Procurement Management . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .80Bhavika Patel, Northeastern University

Single-Shot Epidural for Post-Operative Pain Management in Colon Resection . . . . . . . . . . . . . . . . . . . . . . . . . . . .83Jessica D. Sherman, Northeastern University

Potential for Postobstructive Pulmonary Edema . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .86Angela D. Ewers, Texas Christian University

Hyponatremia Associated with Transurethral Resection of the Prostate . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .89Brandi L Lane, Texas Christian University

General Anesthesia in a Patient with History of Acute Intermittent Porphyria . . . . . . . . . . . . . . . . . . . . . . . . . . . . .92Chad A. Hinton, University North Carolina, Greensboro

Uterine Rupture in the Unscarred Uterus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .94Alison Daly, University of Pennsylvania

Use of An Elastic Gum Bougie During Silicone Stent Retrieval . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .97Serena Ackerman, University of Pennsylvania

Pediatric Awake Craniotomy for Pallidal Deep Brain Stimulator (DBS) Placement . . . . . . . . . . . . . . . . . . . . . . . . . .99Paul A. Gregor, Columbia University

Unanticipated Difficult Intubation . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .102Erika Murphey, University of Pennsylvania

Acute Post-Operative Laryngospasm With Negative Pressure Pulmonary Edema . . . . . . . . . . . . . . . . . . . . . . . . . .105Adam J. Durant, University of Pennsylvania

Pulmonary Artery Catheter Criteria in Abdominal Aortic Aneurysm Repairs . . . . . . . . . . . . . . . . . . . . . . . . . . . . .109Stacey Freda, Northeastern University

Mid-cavity Ballooning Syndrome Following Ondansetron . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .112Jeanne M. Antolchick, Barry University

Continuous Femoral Nerve Block for Total Knee Arthroplasty . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .115Amber Libby, Midwestern University

Intra-Operative Colloid Replacement Therapy . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .119Holly E. McGee, Wake Forest University, Baptist Medical Center

ABSTRACT: Projected CRNA Retirement in Michigan over the Next 20 Years . . . . . . . . . . . . . . . . . . . . . . . . . . . .123Laura Acosta, Scott Spiridigliozzi, University of Michigan

Guide for Authors can be found on the AANA web site. www.aana.com > Professional Development > Nurse AnesthesiaEducation > For Students (scroll to the bottom of the page) > Guide for Authors

49

As a policy we rarely reject an article,however, we have sent a number of articlesback to the author for repair to clarifysome ambiguity or to respond to questionsraised by the reviewers. Of those we havesent back, most are not returned for publi-cation. This is unfortunate for many rea-sons. First, the authors have put a lot oftime in writing the article in the first place.Secondly, program mentors have alsodevoted a considerable amount of time andeffort in guiding the author in the process.Thirdly, the reviewers have put a lot oftime and effort into reviewing the articles.

Our biggest concern as editors is the timespent and wasted by reviewers. Yourreviewers are program directors and facul-ty from other programs who are giving uptheir time to help you, the author, not onlyto get published, but to publish a qualityarticle. If the article is not repaired andresubmitted a sad waste has taken place.

We ask all authors to do your best to sub-mit a publishable quality paper. We ask thementors to wear two hats before authoriz-ing the submission – one as advocate foryour student author and then the hat of areviewer reading it on behalf of theJournal, answering the question – is thispublication quality? Both persons canimprove that performance by checking thework against the check off sheet found inthe Guide for Authors (found on theAANA web site in the student section).

Ronald L. Van Nest, CRNA, MAJulie A. Pearson, CRNA, PhD

EditorialThank You

Revising Your Articles

A special Thank You to KaiserPermanente School of Anesthesia/California State University, Fullerton forits financial support. The program made a

generous donation to the AANAFoundation that is particularly allocated toencouraging and assisting nurse anesthesiastudent writing and publication.

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Keywords: anesthesia, trachealesophageal fistula, difficult airway,pediatric airway, esophageal atresia

Tracheal esophageal fistula (TEF) occurs inapproximately 1 out of every 3000 births.TEF exists in 5 different forms with 87% ofthe cases presenting in the form ofesophageal atresia with a distal trachealesophageal fistula. Corrective repair is typically done within the first few days oflife.1 Tracheal intubation prior to repair canbe difficult due to the need to place theendotracheal tube distal to the tracheoe-sophageal fistula to avoid ventilating thestomach and to adequately ventilate thelungs. The neonate with TEF is at a greaterrisk for aspiration due to the direct connec-tion of the esophagus to the trachea.2

Case Report

A 7 year old, 23.3 kg, ventilator dependentmale with a long standing tracheotomy, ahistory of spinal muscle atrophy type I(SMA I), and repaired TEF presented for aposterior spinal fusion with unit rod placement. The patient presented with anuncuffed 5.5 bovine tracheotomy tube andan audible leak.

It was decided that the anesthesia teamwould utilize a cuffed 5.5 mmID endotra-cheal tube during the surgery and stitch itinto place prior to turning the patient prone.The patient was taken to the operating roomand an inhalational induction with sevoflu-rane 4% was performed through theuncuffed 5.5 mmID tracheostomy tube.Tracheal intubation through the tracheosto-

my stoma was performed without difficultywith a cuffed 5.5 mmID endotracheal tube.The ability to ventilate was easily estab-lished. Adequate ventilation was confirmedwith a sustained ETCO2 and bilateral breathsounds. The endotracheal tube was suturedinto place, the sevoflurane was turned off,and an infusion of propofol was started at arate of 200 ug/kg/min along with an infu-sion of sufentanil at 0.2 ug/kg/min.

During the preparation for the placement ofa right subclavian central line, the patient’stidal volumes decreased from approximate-ly 180 mL to approximately 30 mL. We dis-connected the ventilator and began manualventilation. Manual ventilation allowed for40-60 mL tidal volumes with peak inspira-tory pressures of 30-40 mmHg. The endo-tracheal tube sutures were cut and the endo-tracheal tube was repositioned severaltimes before ventilation became adequate.After completion of re-suturing to securethe endotracheal tube, manual ventilationagain became difficult as evidenced bypeak inspiratory pressures of greater than30 mmHg and tidal volumes ranging from20-60 mL. The cuffed endotracheal tubewas removed, a cuffed 5.5 mmID bovinetracheostomy tube was placed. There wasno audible leak and adequate ventilationwas established.

Preparation for surgery continued withoutany further problems. A right subclaviancentral line, left radial arterial line, andFoley catheter were placed. The patient wasturned prone onto the operating room table.At this point ventilation became difficultagain and an audible leak around the

Difficult Airway in a Pediatric Patientwith Spinal Curvature and Tracheal Esophageal Fistula

Amy J. Granquist, B.S.N.University of Pennsylvania

51

tracheostomy tube was noted. Tidal volumes were maintained with high oxygenflows and oxygen saturations remainedgreater than 95%. After discovering that the leak became significantly better if posterior pressure was applied to the tracheostomy tube, the patient’s tracheosto-my ties were replaced to facilitate the maintenance of this position. Although theleak was improved, a small audible leakstill existed. The air was removed from thecuff of the tracheostomy tube and replacedwith 2.5 mL of sterile water. The leak completely resolved.

Discussion

Scoliosis can lead to respiratory problemsthat are directly associated with the degreeof spinal curvature. As the curvature of the spine increases, functional residualcapacity (FRC), diffusion capacity, chestwall compliance, and PaO2 decrease.3 Anangle of curvature greater than 45 degreesis typically treated with surgical interven-tion due to respiratory compromise.4 Thepatient presented in this case study had acurvature of 73 degrees. An inability to ventilate a patient with this degree of curva-ture will result in a rapid decrease in oxy-gen saturation due to a decrease in FRC.

This patient’s pre-operative assessmentalerted us to the possibility of a difficult airway. Difficulty with ventilation did notarise until after the placement of the cuffed5.5 mmID endotracheal tube. It was notedthat the cuffed 5.5 endotracheal tube hadless of a curve than either the uncuffed orcuffed 5.5 mmID bovines. It was postulatedthat, due to the patient’s history of TEF, thisdifference in curvature may have caused thecuffed 5.5 mmID endotracheal tube to fallinto a blind esophageal pouch. A rigidfiberoptic scope may have been helpful in

positively identifying the problem with thecuffed endotracheal tube.

Difficulty with airway management is themost common cause of adverse outcomesduring anesthesia. The inability to ventilatecoupled with the inability to intubate occursin as many as 1 in 5000 anesthetics.5

Although the difficult airway algorithmdoes not encompass the difficult airway asit occurred in this case study, a plan of action should always be established preoperatively in order to avoid adverseoutcomes.6

References

1. Orenstein S, Peters J, Khan S, Youssef N, Hussain SZ. Congenital anomalies: Esophageal atresia and tracheoesophageal fistula. In: Behrman RE, Kleigman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, PA: Saunders; 2004:1219-1220.

2. Tobias JD, Maxwell LG. Anesthesia for pediatric thoracic surgery. In: Litman RS, ed. Pediatric Anesthesia: The Requisites in Anesthesiology.Philadelphia, PA: Mosby, Inc.; 2004: 297-301.

3. Lestrud S. Bronchopulmonary dysplasia. In: Behrman RE, Kleigman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed. Philadelphia, PA:Saunders; 2004: 1469.

4. Thompson GH. Growth and development. In: Behrman RE,Kleigman RM, Jenson HB, eds. Nelson Textbook of Pediatrics. 17th ed.Philadelphia, PA: Saunders; 2004: 2282.

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5. Miller RD. Anesthesia for nose and throat surgery. In: Miller RD, ed. Miller’s Anesthesia. 6th ed. Philadelphia, PA: Elsevier Inc.; 2005: 2545.

6. Morgan GE, Mikhail MS, Murray MJ. Airway management. In: Foltin J,Lebowitz H, Boyle PJ, eds. Clinical Anesthesiology. 3rd ed. New York, NY:McGraw-Hill Companies, Inc.; 2002: 75.

Mentor: Maria Magro, CRNA, MS, MSN

Minimally Invasive Video-Assisted Thoracoscopic Approach to Ablation of Atrial Fibrillation

Jennifer M. Judeikis, B.S.N.University of Pennsylvania

Keywords: Atrial fibrillation, ablation,thoracoscopic, anesthesia

Atrial fibrillation (AF) is the most commonsustained cardiac arrhythmia, affectingapproximately 2.5 million patients in theUnited States. An estimated 300,000 newcases are diagnosed each year.1 It is predi-cated that by the year 2050 5.6 millionpatients will be diagnosed with AF.1 AF isassociated with increased mortality, exacer-bation of heart failure, and a seven-foldincreased risk of stoke.1 Optimal therapyfor AF has been a challenge. Standard medical management of AF involves heartrate control plus blood thinners. Thisapproach utilizes antiarrhythmic medications to treat the symptoms of AF and anticoagulants to minimize the riskof stroke.3 However, antiarrhythmic medications have limited efficacy in maintaining sinus rhythm and might have serious adverse effects,2 as do anticoagulants. Achieving and maintainingsinus rhythm could result in fewer symptoms, lower stroke risk, eventual discontinuation of anticoagulants, betterexercise tolerance, improved quality of life, and lower mortality.2 Until recently,nonpharmacological surgical approaches

for the treatment of AF have proven effective, but require an extremely invasive sternotomy incision, and the risksassociated with cardiopulmonary bypass. A new, minimally invasive, video-assistedthoracoscopic (VATS) surgical techniquehas been demonstrated to be safe and effec-tive in the treatment of AF.2 The followingcase report describes the intraoperativemanagement of a patient undergoing bilat-eral VATS pulmonary vein isolation with excision of the left atrial appendage (LAA),or Minimaze procedure for the treatment of AF.

Case Report

A 60-year-old male patient presented to the hospital for minimally invasive video-assisted bilateral pulmonary vein isolation and ablation of AF, with removalof the LAA, also known as a Minimaze procedure. This patient had a three-yearhistory of AF with two failed cardioversionattempts within the last six months. Since diagnosis he had been medicallymanaged with atenolol, dofetilide,warfarin, and aspirin. Despite taking antiarrhythmic medications for the management of AF, the patient continued

53

to have episodic symptomatic paroxysmalAF, and reported poor tolerance and dislikeof the drug’s side effects. After learning ofthe Minimaze on a local news channel, thepatient sought to have the procedure per-formed to treat his arrhythmia.

Preoperative evaluation of the patient deter-mined he would be an excellent candidatefor the Minimaze. Preoperative trans-esophageal echocardiogram (TEE) revealednormal left ventricular systolic function, anestimated ejection fraction of 55%, mild tomoderate mitral regurgitation, trace tricuspid regurgitation, and mild atrialenlargement (left greater than right). Chestx-ray was normal, and the patient was freefrom any pulmonary disease according topulmonary function testing. Coagulationstudies had normalized since discontinuingwarfarin one week prior to the scheduledoperation. Aspirin was discontinued at the same time. Preoperative electrocardio-gram demonstrated normal sinus rhythm(NSR), and the patient remained in NSRduring the majority of the intraoperativeperiod. (For the Minimaze procedure, it isnot necessary for AF to be occurring inorder to properly identify the arrhythmiatriggering regions.1)

On the day of surgery, two large boreperipheral intravenous lines and a radialarterial line were placed preoperatively.Standard induction of general anesthesiawas followed by placement of a 39 Frenchleft-sided double lumen tube (DLT), whichwas confirmed by fiberoptic bronchoscopy.Standard measures to minimize hypoxemiadue to one lung ventilation (OLV) were utilized intraoperatively, including positiveend-expiratory pressure (PEEP) to thedependent lung, continuous positive airwaypressure (CPAP) to the nondependent lung,and fraction of inspired oxygen of 100%.

These measures helped to maintain pulseoximetry readings above 95% and arterialpartial pressure of oxygen greater than 80mmHg throughout the procedure. All intraoperative arterial blood gas measureswere within normal range limits. TEE wasperformed in the operating room prior toincision to verify absence of any left atrialthrombi, which would prohibit exclusion ofthe LAA and therefore require procedurecancellation.2 The patient did not have anyleft atrial clots. Also, transcutaneous pacerpads were placed on the patient in prepara-tion for an intraoperative need for pacing.

Surgical approach for the Minimaze proce-dure was via small bilateral thoracotomies.There were two additional small incisionsbilaterally for insertion of assistive surgicaldevices. Initially the patient was positionedwith the left side down and the right armabducted so that the right pulmonary veinscould be accessed first. This required OLVto the dependent left lung and deflation ofright lung to allow surgical exposure. Uponcompletion of the right-sided portion of theprocedure, the patient was repositionedwith the right side down and the left armabducted. At this time, OLV occurred to thedependent right lung and the left lung wasnow deflated for surgical exposure. Thesame ablation technique completed on theright was repeated on the left with the addition of removing the LAA. The additional excision of the LAA was incor-porated into this procedure because it was the major source of thromboemboliassociated with AF.2

The patient tolerated all aspects of the surgery. With completion of the procedureon each side, the incisions were closed andchest tubes were inserted for lung re-expan-sion. On-Que® pain management devicesfilled with Marcaine 0.25% were placed in

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bilateral chest walls for postoperative painmanagement. The DLT was changed without difficulty to a 8.0 mm oral endotracheal tube over an airway exchangecatheter. The patient was then transportedto the intensive care unit (ICU) paralyzedand sedated. He was extubated uneventful-ly after a few hours of positive pressuremechanical ventilation and successfulweaning from the ventilator. This was todecrease the atelectasis that ensued intraoperatively from bilateral OLV. Onpostoperative day one, the bilateral chesttubes were removed and the patient report-ed his pain management to be satisfactory.The remainder of his postoperative periodwas uneventful and he remained in normalsinus rhythm without any episodes of AF.

Discussion

There exist a few invasive methods for thetreatment of AF, including catheter ablationand the original MAZE procedure. The goalof all these procedures is to permanentlydisable the region of the heart responsiblefor this aberrant rhythm. Catheter ablationis noted to have limited success and a highincidence of recurrence associated withserious complications.2 Although the original MAZE procedure does have a highsuccess rate, its usefulness is limited due toassociated surgical complexity and morbidity. The MAZE procedure requiresan open chest via sternotomy and a stillheart, necessitating cardiopulmonarybypass (CPB).3 For these reasons, this procedure is considered too invasive to beused in patients with lone AF, and is only sometimes performed simultaneouslyon those having cardiac surgery thatrequires CPB.2

Recent improved understanding of thepathogenesis of AF has prompted efforts todevelop a less invasive surgical approach to

cure AF. The anatomical region where thepulmonary veins connect with the left atrium has been identified as the majororiginating locale of AF.2 Most AF comesfrom the left atrium and usually originatesfrom within or near the area where the pulmonary veins converge on the left atrium. Autonomic nervous system fibersalso connect to the heart in this area.Abnormal electrical impulses from thenerves and pulmonary veins in this region isthe cause of AF in many patients.3

The Minimaze procedure uses small incisions between the ribs by which the surgeon places a clamp like tool on the leftatrium near the pulmonary veins.Cauterizing the desired atrial tissue localized by the clamp causes the ablation.The nerves that contribute to the cause ofAF in this region are also eliminated.3

This new technique enables a surgical cureof AF through an epicardial approach on abeating heart. A bipolar radiofrequencyablation device is the key tool for perform-ing this procedure. This device createsbilateral, transmural, linear lesions aroundthe atrial cuff of the right and left pulmonary veins, effectively achievingelectrical isolation of the pulmonary veinswithout any need for CPB.2

The Minimaze approach to the ablation ofAF was determined safe and effective atintermediate follow up. The Minimaze reliably and rapidly achieves ablation of thesource of AF in the heart. This technique isan attractive, safe and effective alternativeto antiarrhythmic and anticoagulant medications, and other invasive means to curing AF.2

Transderm ScopFor postoperative nausea and vomiting (PONV)

The patch that deliversPONV prevention for 24 hours 1

• 2 out of 3 patients had no retching or vomiting for 24 hours following recovery from anesthesia and surgery1

• 3 out of 4 patients had no need for additional antiemetics1

IndicationsTransderm Sco–p is indicated in adults for prevention of nausea and vomiting associated with recovery from anesthesia and surgery.

Safety InformationTransderm Sco–p is contraindicated in:• Pediatric patients• Persons who are hypersensitive to the drug scopolamine or to

other belladonna alkaloids or to any ingredient or component in the formulation or delivery system

• Patients with angle-closure (narrow-angle) glaucoma

Transderm Sco–p should be used with caution in the elderly or in individuals with impaired liver or kidney function.

In clinical studies, the most commonly reported adverse events were dry mouth (29%) and dizziness (12%).

While using this product one should not drive, operate dangerousmachinery, or do other things that require alertness. One should not use alcohol.

Baxter is a registered trademark of Baxter International Inc.Transderm Scop is a registered trademark of Novartis.

Baxter Healthcare Corporation95 Spring Street, New Providence, NJ 079741-800-ANA-DRUG (1-800-262-3784)www.baxter.com

References: 1. Transderm Scop (scopolamine 1.5 mg) [package insert]. Parsippany, NJ: Novartis Consumer Health, Inc.2. Bailey PL, Streisand JB, Pace NL, et al. Transdermal scopolamine reduces nausea and vomiting after outpatientlaparoscopy. Anesthesiology. 1990;72:977-980.

Please refer to Full Prescribing Information on adjacent page.

The 24-hour patch for prevention

For PONV

Printed in USA 720199 02/07

In two pivotal clinical trials with OB/GYN patients

T

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References

1. Wolf MiniMaze. Minimally invasive treatment for atrial fibrillation. Available at: www.wolfminimaze.com. Accessed July 7, 2006.

2. Wolf RK, Schneeberger EW, Osterday R,et al. Video-assisted bilateral pulmonary vein isolation and left atrial appendage exclusion for atrial fibrillation. J Thorac Cardiovasc Surg. 2005;130:797-802.

3. Oregon Cardiology. Advanced therapy for cure of atrial fibrillation. Available at: www.minimaze.org/Assets/Advanced_AF.pdf. Accessed July 7, 2006.

Mentor: Russ Lynn, MSN, CRNA

Anesthetic Management of a Jehovah’s Witness Patient Possessing Many Co-Morbidities

Michael S.K. Awai, B.S.N.Florida International University

Keywords: Jehovah’s Witness,Autologous blood, Aortic stenosis, Heartfailure, Anesthesia

Providing anesthesia for a patient who is aJehovah’s Witness is challenging, especial-ly in the event that large amounts of bloodare lost. Jehovah’s Witnesses believe thatwhen blood has left the body, it is consid-ered impure and it should be disposed.Most Jehovah’s Witnesses refuse transfu-sion of primary blood components whichincludes red blood cells, white blood cells,platelets and plasma.1 Some however,accept albumin and other fractionatedblood components. Still others agree withreceiving cell saver autologous blood aslong as the blood has not left the closed sys-tem.2 Therefore each Jehovah’s Witnesspatient must be approached as an individualand not as a member of a group. A thoroughpreoperative assessment by the nurse anes-thetist which takes into account the individ-ual patient’s beliefs is essential in providingthe most considerate care.

Case Report

A 58 year old, 150 kg female gravida 3 para3 presented with abdominal pain and with alarge pelvic mass. She was scheduled for anexploratory laparotomy. The patient haddocumented allergies to penicillin and eggyolk which caused itching, and shellfishwhich caused nausea and vomiting. Theonly significant past surgical history was anappendectomy which had no anestheticcomplications documented. Some of thepatient’s comorbidities included a historyof restrictive pulmonary disease, severeaortic stenosis, depression, morbid obesity,chronic anemia, and congestive heart fail-ure. Also there was a 10 pack-year smokinghistory. The patient denied alcohol andillicit drug use. The patient was also a prac-ticing Jehovah’s Witness. The increasedrisk of potential blood loss was discussed indetail with the patient. The patient refusedto receive allogenic packed red blood cellsbut did consent to intraoperative salvage ofautologous blood by cell saver protocol andalbumin colloid solutions.

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The patient was classified as an AmericanSociety of Anesthesiologist (ASA) 4 withan airway evaluation which revealed aMallampati class II, three fingerbreadththyromental distance, and a full range ofmotion of the neck. Preoperative bloodpressure was 142/81 mmHg with a heartrate of 110 beats per minute. Oxygen satu-ration with two liters of O2 via nasal cannu-la was 96%. Hemoglobin was 11.7grams/deciliter and hematocrit was 39%.Physical examination revealed S1S2 with aIII/VI systolic ejection murmur. Lungswere clear to auscultation bilaterally. Nopulmonary function tests or arterial bloodgases were obtained preoperatively. Thepatient reported being able to ambulatewith a walker but tired easily and was most-ly confined to bed. The head of the bed waselevated and the patient was further positioned by the use of folded blankets tofacilitate intubation. A slow, smooth intravenous induction with fentanyl 150mcg, esmolol 100 mg, and etomidate 20 mgwas administered.

Anesthesia was maintained with 1.2-1.5%isoflurane and 50% oxygen and 50% air.Fentanyl 100 mcg was given after the firsthour of surgery, for a total of 250 mcg tomaintain arterial blood pressure and heartrate within 20% of baseline. A sufentanildrip at 0.3 mcg/kg was maintained through-out the procedure for a total dose of 150mcg. 12 Liters of lactated Ringer’s, 3250ml of Albumin 5% and 200 ml Albumin25% were also given. Urine output was1775 ml, the total estimated blood loss(EBL) was 1800 ml, and 500 ml of autolo-gous red blood cell concentrate collected bycell saver was provided. End tidal CO2 wasmaintained between 30-32 mm Hg byadjusting the tidal volume between 450-500ml and respiratory rate between 14-16breaths per minute. Neuromuscular block-

ade was maintained for the 6.5 hour surgerywith vecuronium every 1-1.5 hours in 2-3mg boluses titrated to 2 twitches using thetrain of four measurement for a total doseof 45 mg. An arterial blood gas was report-ed within normal limits and the HCT of34% was noted approximately 30 minutesafter surgical incision.

About 30 minutes before the end of surgery,an ABG was reported within normal limitsand the HCT was 25%. The patient wastransferred to the surgical ICU while intu-bated. Neuromuscular blockade was main-tained with another 10 mg of vecuronium.The patient was transferred with standardmonitors and was hand ventilated enroute.The patient's ventilation was then con-trolled by mechanical ventilation with thefollowing settings: SIMV/PS 14, TV 500,PS 10, PEEP 5, and 100% FIO2. Vital signsupon arrival to the ICU were as follows:BP-156/67 mmHg, HR-111, SPO2 96%.The patient's airway was extubated the nextday and she was discharged from the hospi-tal four days later without any complica-tions reported.

Discussion

It is well known and documented thatJehovah’s Witnesses do not normally acceptwhole blood transfusions. They believe thatonce blood has left the body, it is consid-ered unhealthy.3,4 A written waiver is oftensigned relieving the anesthetist of anyresponsibility or consequences of bloodrefusal. The patient did consent for albuminand the use of cell saver autologous bloodproducts as long as it was maintained in aclosed sterile system. The decision toaccept blood derivatives was made by thepatient. Other known co-morbidities suchas aortic stenosis, congestive heart failure,and morbid obesity existed and were

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considered as potential factors in establish-ing the anesthetic plan.

Autologous blood donation could be analternative if the patient needed blood during surgery.5-7 This option was not presented to the patient because of theemergent situation. There are several waysto collect autologous blood. Autologousblood donation usually is collected three tofive weeks prior to elective surgery.Intraoperative hemodilution is usually collected at the beginning of surgery andthe fluid lost is replaced with intravenoussolution. Then the blood is stored and rein-fused during or at the end of surgery.Intraoperative blood salvage is collectedfrom the surgical area during the surgeryand re-infused during or after surgery. Post-operative blood salvage is collectedafter the surgery and re-infused at the com-pletion of surgery.8

The only method that was used in this casewas intraoperative blood salvage by cellsaver. Aortic stenosis presents another chal-lenge to the anesthesia provider. Thispatient had severe aortic stenosis with anarea of 0.9 cm2. The normal aortic valvearea is 3.0-4.0 cm2.

9 The stenosis and thebuild up of pressure is gradual which allowsthe ventricle to initially compensate andmaintain stroke volume. Concentric hypertrophy enables the left ventricle tomaintain stroke volume by generating avalvular gradient and reduce ventricularwall tension.10-11

Documented congestive heart failure cancause eccentric or concentric hypertro-phy.12-14 Eccentric hypertrophy is a result ofthe left ventricle’s inability to pump or con-tract effectively. The patient’s concentrichypertrophy may have been the result ofaortic stenosis. Usually there is a build upof pressure in the left ventricle because the

aortic valvular opening narrows. The leftventricle then becomes thickened and muscular in order to maintain the normalblood pressure.

Morbid obesity is usually considered to bea body mass index (BMI) greater than40.15,16 Obese patients present major pulmonary and ventilatory challenges during the intraoperative period. Ourpatient had a BMI calculated to be > 40. Inthe obese patient, excessive adipose tissueover the chest decreases lung complianceleading to a decrease in functional residualcapacity (FRC). The decrease in FRC canrapidly lead to hypoxia. The increase inabdominal mass pushes the diaphragmcephalad further decreasing FRC and issuggestive of restrictive pulmonary disease.Even though pre-oxygenation with 100%FIO2 prior to induction is the usual standard, it is of the utmost importance inthe obese patient.

Anesthesia care for the Jehovah’s Witnesspatient involves the preoperative discussionwith the individual patient to determine thelevel of knowledge of options available andthe desire to accept transfusion of blood orfractionations of blood.17 Providing ade-quate amounts of intraoperative crystalloidsand colloids is essential for the mainte-nance of tissue perfusion. An understandingof the preoperative alternatives to increasered cell production is essential in providingthe best anesthesia possible. Co-morbiditiessuch as aortic stenosis, congestive heartfailure, and morbid obesity further compli-cate surgery and increase the anestheticrisk. All of these co-morbidities may con-tribute to clinical complications andincrease the potential blood loss. The over-all status of the patient who is a Jehovah’sWitness including all co-morbidities mustbe fully analyzed in order to minimize thisblood loss and assure a successful outcome.

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References

1. Sniecinski R, Levy JH. What is blood and what is not? Caring for the Jehovah’s Witness patient undergoing cardiac surgery. Anesth Analg. 2007; 753-754.

2. Jehovah’s witness. Available at http://www.watchtower.org/library/hb/index.htm?article=article_06.htm.Accessed April 2, 2006.

3. Jehovah’s witness. Available at http://www.watchtower.org/library/hb/index.htm?article=article_07.htm.Accessed April 8, 2006.

4. Gyamfi C, Yasin, SY. Preparation for an elective surgery procedure in a jehovah’s witness: a review of the treatments and alternatives for anemia. Prim Care Update Ob/Gyns. 2000;7:266-268.

5. Sparling EA, Nelson CL, Lavender R,Smith J. The use of erythropoietin in the management of jehovah’s witness who have revision total hip arthroplasty. JBone Joint Surg Am. 1996;78:1548-1552.

6. Pierson J, Hannon T, Earles D. A blood-conservation algorithm to reduce blood transfusions after total hip and knee arthroplasty. J Bone Joint Surg Am. 2004;86:1512-1518.

7. Beholz S, Liu J, Thoelke R, Spiess C,Konertz W. Use of desmopressin and erythropoietin in an anemic jehovah’s witness patient with severely impaired coagulation capacity undergoing stentess aortic valve replacement. Perfusion. 2001;16:485-489.

8. American Association of Blood Banks. Available at http://www.aabb.org/Content/About_Blood/Facts_About_Blood_and_Blood_Banking/aabb_faqs.htm#4. Accessed July 9, 2006.

9. Istaphaneous G. The patient with aortic stenosis. Int Anesthesiol Clin. 2005;43:21-31.

10. Stewart BF, Siscovick D, Lind BK, et al. Clinical factors associated with aortic valve disease. J Am Coll Cardiol.1997;29:630-634.

11.Dare AJ, Veinot JP, Edwards WD,Tazelaar HD, Schaff HV. New observations on the etiology of aortic valve disease: a surgical pathologic study of 236 cases form 1990. Hum Pathol. 1993;24:1330-1338.

12. Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesia. 3rd ed. New York:McGraw-Hill; 2002;379-381.

13.Figueroa MS, Peters JI. Congestive heart failure: diagnosis,pathophysiology, therapy, and implications for respiratory care. Respiratory Care. 2006;51:403-412.

14.Vanky F, Hakanson E, Tamas E,Svedjeholm R. Ann Thorac Surg. 2006;81:1297-1304.

15. Todd DW. Anesthetic considerations for the obese and morbidly obese oral and maxillofacial surgery patient. J Oral Maxillofac Surg. 2005;63:1348-1353.

16. Adams JP, Murphy PG. Obesity in anesthesia and intensive care. Br J Anesth. 2000;85:91.

17. Schiller HJ. Optimal care for patients who are Jehovah’s Witnesses. Anesth Analg. 2007;104: 755-756.

Mentor: W. Patrick Monaghan, CLS,SBB, Ph.D.

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Fiberoptic Nasal Intubation in the Case of Limited Mouth OpeningStephen E. Kushiner, B.S.N.

University of Scranton

Keywords: Craniotomy, Tumor, Awakefiberoptic intubation, Difficult airway,Limited mouth opening, Anesthesia

Some patients have severely limited mouthopening secondary to injury, surgery orsimply due to abnormal anatomy.Occasionally these patients require elective,but necessary procedures. In the event thatone of these patients presents for a surgicalprocedure requiring a secure airway andgeneral anesthesia, a carefully prepared airway management plan must be in placeto protect the airway and patient safety. Thedifficult airway algorithm is quicklyexhausted of options that are useful in thispopulation.1 The impossibility of directvision laryngoscopy or laryngeal mask airway (LMA) placement requiresanesthesia professionals to be prepared foran awake fiberoptic nasal intubation,cricothyrotomy or tracheostomy.

Case Report

A 49 year old, 82 kilogram male diagnosedwith right temporal meningioma wasscheduled for a craniotomy and right tem-poral tumor excision. The tumor was diag-nosed after the patient developed frequentheadache and left sided weakness.

The patient history included tonsillectomy,right knee surgery, left modified radicalneck dissection with forearm flap for glottic neoplasm six months prior, a historyof smoking 2 packs of cigarettes a day for25 years, as well as insulin dependent diabetes. Medications included fentanylpatch 75 mcg, acetaminophen 500 mg,hydrocodone bitartrate 5 mg, and interme-

diate acting insulin. The patient reported noknown allergies.

Physical examination revealed no currentneurological symptoms. Assessment of theairway showed extremely limited mobilityof the neck and mouth opening limited to 2centimeters secondary to previous modifiedradical neck dissection. The patient wasedentulous. The mouth opening was so lim-ited that a Mallampati classification couldnot be assigned and direct vision laryn-goscopy was not deemed possible. Anawake fiberoptic nasal intubation wasplanned. An ear, nose and throat (ENT) surgeon was available in the event thatemergent tracheostomy was needed. A rightradial arterial line was placed in the pre-operative holding area after midazolam2 mg was administered intravenously (IV).At this time, neosynephrine spray wasadministered into the patient’s nasal passages through each nare. A swab soakedwith 4% lidocaine was then inserted into each nare and the patient was asked to hold them in place for approximately five minutes.

The patient was transported to the operatingroom where standard monitors were placedand oxygen was applied. Fentanyl 100 mcgIV was slowly administered to achievepatient comfort while maintaining sponta-neous ventilation. The patient was placed inslight reverse Trendelenburg position. Thetrachea was intubated using a nasal fiberop-tic approach. Upon confirmation of nasotra-cheal tube placement with the presence ofend-tidal CO2 s and equal bilateral breathsounds, anesthesia was induced with

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sodium thiopental 500 mg IV.Neuromuscular relaxation was providedwith rocuronium 50 mg IV. Anesthesia wasmaintained with desflurane at an end tidalconcentration of 4.2-6.5% and 1 liter floweach of air and oxygen. Fentanyl wasadministered incrementally throughout thecase for a total of 350 mcg. An additionaldose of rocuronium 20 mg was given uponthe return of four twitches to train-of-fourstimulation shortly after surgical incision.The intraoperative course was uneventful.

At the conclusion of the surgical procedure,neuromuscular blockade was antagonizedwith neostigmine and glycopyrrolate.Lidocaine 50 mg IV was administered 30minutes prior to the end of surgery toreduce airway irritability upon emergencefrom anesthesia. After the return of sponta-neous ventilation at a rate of 12 breaths perminute, a tidal volume of 550 mL, and ademonstrated ability to sustain head lift forfive seconds, the trachea was extubated.Neurological examination was withoutdeficit post operatively. The patient wastransported to the post-anesthesia care unitwith nasal oxygen at 4 liters per minute.The patient had no complaints of nausea orpain.

Discussion

The responsibility of anesthesia profession-als to safely manage the airway is of primary importance. This requires that avariety of skills and knowledge of the difficult airway algorithm be developed tomeet the many challenges that can be presented by difficult airways. In the caseof a patient with limited or absent mouthopening due to deformities, surgicalchanges, trismus, or any other reason it isnecessary to establish a secure airwayeither nasally or percutaneously.

In order to insert an endotracheal tube usingnasal fiberoptic technique, the anesthesiaprofessional must pass the endoscope intothe nasal passage, past the epiglottis,through the larynx, and into the tracheauntil tracheal rings and the carina are visu-alized. To accomplish this passage in apatient who is awake and spontaneouslybreathing requires proper preparation of thepatient prior to the start of the procedure.

Preparation of the nasal airway passagestarts with application of a topical vasocon-strictor to the nasal mucosa in order to pre-vent epistaxis which can lead to aspirationand/or obscure the endoscopic view. 1 Oncethe bronchoscope is in the trachea, theendotracheal tube is advanced into the tra-chea over the bronchoscope.2 It is alsoimportant to anesthetize the airway topical-ly with a local anesthetic in order to mini-mize airway reactivity. This can be accom-plished with transtracheal injection of localanesthetic, local anesthetic spray, or withthe use of viscous lidocaine.3

It is almost always necessary for patients tobe sedated in order to tolerate this prepara-tion as well as the intubation procedureitself. The most common method selectedfor sedation for this procedure, and the oneused in the case study described, is a com-bination of IV midazolam and fentanyl.3

Several other pharmacological regimenshave been suggested as potentially bettermethods of controlling the hemodynamicresponse to awake tracheal intubation. Inone study of 74 patients where remifentanilwas used as the sole sedative drug forawake fiberoptic intubation there was areduction in pain and coughing as well asbetter attenuation of the hemodynamicresponse in the patients receiving remifen-tanil versus those in the control group whoreceived midazolam and fentanyl. It is

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worth noting that a higher incidence ofrecall was present in the remifentanilgroup.4 The addition of midazolam to aremifentanil infusion can help to eliminatethis problem. Case reports have shown thatanother option for sedation with less poten-tial for respiratory depression and a greaterattenuation of the hemodynamic responseto intubation is the use of a dexmedetomi-dine infusion as the sole agent.5

In the event that nasal intubation of the tra-chea proves impossible it may be necessaryto perform a cricothyrotomy or tracheosto-my. A cricothyrotomy becomes an option inthe event that spontaneous ventilation islost during an unsuccessful nasal intubationattempt and mask ventilation attempts areunsuccessful.6 For this reason, anesthesiaprofessionals should consider taking thetime to place a mark on the patients’ skin atthe level of the cricothyroid membraneprior to any attempt to intubate the trachea.In the case study described above care wastaken to secure the presence of an ENTsurgeon in the operating theatre so that atracheostomy could be performed in theevent that tracheal intubation was unsuccessful. It is also important to verifythat the operating room nursing staff isaware of the possible need for an emer-gency tracheostomy and that the appropri-ate equipment is immediately available.

There are difficulties associated withattempting tracheal intubation in a patientpopulation requiring a nasal approach. The limitations placed on the anesthesiaprofessional’s airway management optionsrequire skill and preparation when confronted with these difficulties. However,with teamwork, planning, and care these cases can be managed safely and successfully.

References

1. Barash PG, Cullen BF, Stoelting RK. Clinical Anesthesia. 5th ed. Philadelphia:Lippincott Williams and Wilkins; 2006:618-628.

2. Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology. 4th ed. New York: McGraw-Hill; 2006:106-107.

3. Jaffe RA, Samuels SI. Anesthesiologist’s Manual of Surgical Procedures. 3rd ed. Philadelphia: Lippincott Williams and Wilkins; 2004:Appendix B.

4. Puchner W, Egger P, Puhringer F,Lockinger A, Obwegeser J, Gombotz H. Evaluation of remifentanil as single drug for awake fiberoptic intubation. Acta Anesthesiol Scand. 2002; 46:350-354.

5. Grant SA, Breslin DS, MacLeod DB,Gleason D, Martin G. Dexmedetomidine infusion for sedation during fiberoptic intubation: A report of three cases. JClin Anesth. 2004; 16:124-126.

6. Practice guidelines for the management of the difficult airway: An updated report by the American Society of Anesthesiologists Task Force on Management of the Difficult Airway. Anesthesiology. 2003, 98:1269-1277.

Mentor: JoAnn K. Platko CRNA, MSN

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Genitourinary Surgery in a Patient with Angelman’s SyndromeAmy L Mancini, B.S.N.Northeastern University

Keywords: Angelman’s Syndrome, pedi-atric airway, prognathia, macroglossia,anticonvulsants, neuromuscular blockade,anesthesia

Angelman’s Syndrome was first diagnosedin 1965 by Dr. Harold Angelman. It is a disease that causes neurological problemsas a result of a deletion or inactivation ofspecific genes on chromosome 15q11-13.Most cases of Angelman’s can be linked tothe maternal inheritance of an abnormalchromosome and the remaining cases aredue to a genetic mutation of unknown ori-gin.1 The incidence of Angelman’s syn-drome is small, 1:15,000-1:20,000.2

However, these patients often suffer fromstrabismus, seizure disorders and hyperac-tive lower limb deep tendon reflexes andfrequently present for surgery and anesthe-sia care.3 This potential need for anesthesiawarrants further research by anesthesia pro-fessionals on how to best prepare and carefor this unique pediatric population.

Case Report

A 12 year old male presented for rightorchiopexy and cystoscopy. He weighed 35kilograms and his past medical historyconsisted of aspiration pneumonia,horseshoe kidney, seizure disorder,microcephaly, hypothyroidism and devel-opmental delay which rendered him nonverbal. ASA physical status at the timeof the surgery was II and his past surgicalhistory consisted of myringotomy, leftorchiopexy and eyelid surgery, all of whichwere uneventful. The patient lived in ahousehold where one parent smoked tobac-co and he had a sibling who also suffered

from Angelman’s syndrome. He had noknown drug allergies and his daily medica-tion regimen included levothyroxine,phenytoin and valproic acid.

The anesthesia care team met the patient forthe first time on the day of surgery. He waslying on a stretcher with his legs bent at theknees and crossed, and with his arms flap-ping and waving in the air. He was laughingloudly and smiling while he crumpledpieces of paper. He was nonverbal andmade incomprehensible sounds. The anesthesia providers introduced themselvesto the patient and the patient’s mother. Abrief physical exam was performed. Thechild’s jaw was large for his body size andhe had prognathia and macroglossia. Hemade constant chewing motions with hismouth and tongue. He could not cooperatefor an open mouth airway exam but hismother stated that all teeth were intact. Hisairway mobility appeared normal. Thepatient entered the operating room and apulse oximeter and pre cordial stethoscopewere applied. An inhalation induction usingnitrous oxide five liters, oxygen two litersand sevoflurane 1% were administered. Thesevoflurane was increased incrementally.Standard monitors were applied after thepatient became unresponsive to stimulationand the eyelid reflex was lost. An intra-venous catheter was placed in the left handand an 80 millimeter oral airway wasplaced in the patient’s mouth. Breaths wereprovided to the patient at a rate of 18breaths per minute. Once the intravenouscatheter access was established, the oral airway was removed and a #3 LaryngealMask Airway (LMA) was placed without

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difficulty. Ventilation was confirmed byauscultation of clear bilateral breath soundsand a positive end tidal carbon dioxide trac-ing was noted on the capnograph. At thispoint, the volatile anesthetic was changedto isoflurane 0.6% and the nitrous oxideand oxygen flows were decreased to 1 literand 0.6 liters, respectively. The patient’sventilation was manually assisted until adequate spontaneous effort returned. Thepatient was placed in the lithotomy positionand the procedure began. During the case,dexamethasone four milligrams, cefazolin850 milligrams, Ketorolac 15 milligramsand ondansetron two milligrams were givenintravenously. Fentanyl (total 62.5 micro-grams) IV and propofol (10 milligrams) IVwere titrated according to patient conditionand comfort level. The patient received 500milliliters of intravenous lactated ringer’ssolution. After the procedure was completethe LMA was removed, the patient wasspontaneously breathing but was still unre-sponsive to verbal stimulation. An 80 mil-limeter oral airway was placed. The oralairway and a jaw lift were required forapproximately five minutes to maintainclear bilateral breath sounds. Once thepatient was awake and able to protect hisairway without a jaw lift he was transferredto the recovery room and was discharged tohome later that day.

Discussion

This case study brings up three areas for consideration by the anesthesia professional. First, chronic use of the anti-convulsants phenytoin and valproic acidcause interactions with anesthetic medica-tions. These medications cause druginduced enzyme induction and therefore,alter the metabolism of some drugs such asmidazolam and neuromuscular blockers(NMB). The concurrent use of atracurium

and these anticonvulsants can causeatracurium resistance.4 Larger doses ofsome medications such as atracurium andother NMB as well as midazolam may beneeded.5 On the other hand, the sedationthat occurs with anticonvulsants is additiveto the sedative effects of anesthesia medica-tions like opioids and barbiturates.Therefore, smaller doses of these sedativesmay be required. Angelman’s patients whopresent with seizure disorders requiringchronic use of phenytoin and valproic acidare also at a higher risk for organ toxicitydue to altered drug metabolism. Liver failure, anemia and pancreatitis can beassessed through lab work and a thoroughphysical exam can detect depression ofcerebral function, ataxia and dyskinesis ofthe tongue, face and limbs all of which aresigns of antiepileptic medication organ tox-icity. In this patient population it is crucialto titrate all medications to patient effect.We avoided NMB and because spontaneousrespiration was maintained it was possible to titrate sedation to the patient'srespiratory rate. Valproic acid can alsocause thrombocytopenia and this could leadto bleeding problems and potentialhematoma formation if bleeding duringsurgery were to occur.6

The second area for concern in Angelman’spatients is positioning. As previously stated, a symptom of Angelman’s syndromeis hyperactive lower extremity deep tendonreflexes.3 Cystoscopy required the patientto be in the lithotomy position and a poten-tial complication of this position is com-partment syndrome of one or both legs.Care was taken to avoid over stretching theligaments of the lower extremities. Thesupport devices for each leg were carefullymeasured to fit the patient’s height and theedges were padded to avoid pressure to anybony prominences.7 Proper positioning and

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padding is extremely important to protectthese nonverbal highly contracted patientsfrom avoidable harm. Positioning was carefully accomplished with our patient andinvolved the entire operating room team.

Finally, prognathia and macroglossiaincrease the risk of encountering a difficultairway.3,8 These congenital malformationscan cause upper and lower airway obstruc-tion. Fortunately, the prognathia andmacroglossia in our patient were offset by awide jaw and mouth also characteristic ofpatients with Angelman’s syndrome.3

We chose to use a #3 LMA for the case andutilized an 80 millimeter oral airway forventilation before placement of the LMAand also after the LMA was removed toensure adequate oxygenation and ventila-tion for the patient. We were prepared toplace an endotracheal tube if the LMA wasnot adequate to support ventilation. Afterassessing the patient we did not anticipate adifficult intubation but a bougie and rocuro-nium were available. If a difficult intuba-tion was anticipated a fiberoptic bron-choscopy could have been in the operatingroom as well.

Like many patients with Angelman’s syn-drome, our patient’s seizure disorderrequired him to take daily phenytoin andvalproic acid both of which alter the metab-olism of anesthetic medications. By usingan LMA and allowing the patient to main-tain spontaneous respirations, the anesthe-sia professional could get a better sense ofhow well anesthetized the patient was.Patient respiratory rate can be a helpfulindicator of pain and sedation level. In thefuture, a bispectral monitor may also havebeen an informative device in determininganesthetic level. The patient seemed comfortable and appropriately anesthetizedduring the case but due to his nonverbalcommunication and developmental delay

this is impossible to truly assess.Angelman’s syndrome is one of the congenital diagnoses found in the pediatricpopulation that holds implications for anes-thesia care and planning. With knowledge,planning and individualization of manage-ment anesthesia practitioners can optimizeoutcomes in this unique population.

References

1. Williams CA, Angelman H, Clayton-Smith J, et al. Angelman Syndrome:Consensus for diagnostic criteria. Angelman Syndrome Foundation. Available at http://www.angelman.org/angel/index.php?id=65. Accessed September 26, 2006.

2. Williams C, Philips RC, Wagstaff J. Facts about Angelman Syndrome. Angelman Syndrome Foundation, INC. Available at http://www.angelman.org/angel/index.php?id=75. Accessed October 3, 2006.

3. Office of Communications and Public Liaison. Angelman Syndrome information page. National Institute of Neurological Disorders and Stroke. Available at http://www.ninds.nih.gov/disorders/angelman/angelman.htm?css=print. Accessed October 3, 2006.

4. Tempelhoff R, Modica PA, Jellish WS,Sp i t znage l EL . Res i s t ance to Atracurium-induced neuromuscular blockade in patients with intractable seizure disorder treated withanticonvulsants. Anesth Analg.

1990;71:665-669.

5. Bardas SL. Appendix F: Table of drug interactions. In: Jaffe RA, Samuels SI. eds. Anesthesiologist’s Manual of Surg ica l Procedures . 3 rd ed .Philadelphia: Lippincott Williams & Wilkins; 2004:F1-F11.

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6. Stoelting RK, Dierdorff SF. Anesthesia and Co-existing Disease. 4th ed. Philadelphia: Churchill Livingstone; 2002:284.

7. Warner MA. Patient positioning. In:Barash PG, Cullen BF, Stoelting RK. eds. Clinical Anesthesia. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2001:646.

8. Butler MG, Hayes BG, Hathaway MM,Begleiter ML. Specific genetic diseases a t r i s k f o r s e d a t i o n / a n e s t h e s i acomplications. Anesth Analg.

2000;91:837-855.

Mentors: Janet Dewan, MS, CRNA,Nicola Ryding, MS, CRNA

Anesthesia for Carotid EndarterectomyChristine Ramsden Jackson, B.S.N.

Northeastern University

Keywords: carotid endarterectomy,desflurane, remifentanil, carotid arterystenosis, opioid, anesthesia

Anesthesia for the surgical treatment ofhigh-grade carotid artery stenosis presentsmany challenges. The main goals are toprotect cerebral perfusion while guardingagainst cardiac ischemia.1 The most com-mon morbidity in the perioperative periodof carotid endarterectomy (CEA) in symp-tomatic and asymptomatic patients is strokeand is related to many patient characteris-tics.2 In some cases, the post-operative mor-bidity can be significantly reduced ifdetected early and treated immediately.3

This case describes the management of anasymptomatic patient with high gradecarotid artery stenosis.

Case Report

A 76 year old female asymptomatic patientdiagnosed by duplex scan with 95% rightcarotid stenosis presented for right-sidedcarotid endarterectomy. The patient’s med-ical history included hypertension, coro-nary artery disease without angina, hyper-lipidemia, tobacco use, and hypothy-roidism. Her past surgical history included

a 2-vessel coronary artery bypass graft, acoronary artery stent placement, and bilat-eral cataract extractions. The patient’s med-ications consisted of: metoprolol, isorbide,lisinopril, aspirin, hydrochlorothiazide,atorvastatin calcium, and levothyroxine.The patient was instructed to take all med-ications except aspirin on the day of sur-gery.

The patient weighed 76 kilograms and was64 inches tall. Her preoperative heart ratewas 60 beats per minute, blood pressurewas 136/60 mmHg, oxygen saturation onroom air was 98%, and respiratory rate was14 breaths per minute. A recent 12-leadelectrocardiogram showed left ventricularhypertrophy with old ST segment abnor-mality. A 3 year old dobutamine stress testwas negative for ischemia and showed anejection fraction of 48%. Physical examrevealed a pleasant, alert and orientedfemale in no acute distress. Breath soundswere diminished with mild rales in the rightlower lobe. Heart rate and rhythm were reg-ular. Her physical status was classified asASA III and general anesthesia wasplanned.

A radial arterial line was placed in the pre-

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operative area after midazolam 1 mg andfentanyl 50 mcg sedation. The patient wasthen taken to the operating room and moni-tors applied including a bispectral index(BIS) monitor. Her first vital signs in theoperating room were as follows: bloodpressure 143/62, heart rate 64, ECG normalsinus rhythm, and room air oxygen satura-tion 95%. After preoxygenation, anesthesiawas induced with lidocaine 80 mg,propofol 100 mg, and remifentanil infusionstarted without bolus at 0.125 mcg/kg/min.Esmolol 40 mg, rocuronium 40 mg, and anadditional propofol 40 mg dose were givenprior to laryngoscopy. The patient’s vitalsigns remained stable throughout inductionand intubation. After the trachea was intubated, oxygen was decreased to a 2 literflow, nitrous oxide added at 2 liters, anddesflurane introduced at 2%.

Prior to carotid artery cross-clamping, adose of ephedrine 5 mg was given and aphenylephrine infusion was initiated andtitrated to maintain systolic arterial bloodpressure above 130 mmHg during shuntplacement. BIS values were monitored andremained between 40 and 60. Followingclosure of the carotid artery with a patch,the surgeon requested that the patientsblood pressure be increased to near her preoperative level and the phenylephrinedrip was titrated to raise the systolic arteri-al blood pressure to 140-150. After per-formance of an arteriogram to evaluate thepatency of the vessel, the phenylephrinedrip was titrated down and discontinued.When closure reached skin level, theremifentanil drip was discontinued,esmolol 50 mg given (in divided doses),and the neuromuscular blockade antago-nized with neostigmine and glycopyrrolate.After wound closure, the desflurane andnitrous oxide were discontinued. The dress-ing was placed and the patient opened her

eyes and calmly followed commands andthe trachea was extubated. At this pointneurological examination was preformedby the surgeon and found to be intact. Thepatient transferred herself to a stretcher andwas taken to the post-anesthesia care unit.

In the PACU fentanyl 50 mcg was given formoderate surgical site discomfort. Vitalsigns were stable without pharmacologicsupport. Total fluid administration was lac-tated Ringer’s 600 cc and estimated bloodloss was 50 cc. Operative time was 1 hour.The patient was alert and oriented and noneurological deficits appreciated. She wastransferred to the intensive care unit anddischarged the next afternoon after anuneventful postoperative course.

Discussion

CEA is being performed increasingly inpatients with carotid artery stenosis who areasymptomatic and studies have shown thatstrokes can be reduced by surgical treat-ment in these patients. The operative risk ofstroke and death in symptomatic patients is5.1% versus 2.8% in asymptomaticpatients.2 Ischemic events are usually thecause of intraoperative stroke and embolicevents are most common in the postopera-tive period. Therefore, rapid recovery andearly perioperative neurological assessmentare practical goals in the management ofpatients undergoing CEA.1

Many methods of anesthesia for CEA areused according to patient characteristics,surgeon’s skill and comfort level, and institutional convention. Regional anesthe-sia has been increasingly advocated toallow for rapid detection of intraoperativeneurological symptoms, stable hemody-namics, and adequate operating conditions.4

This technique has disadvantages includinglack of airway control and need for a

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cooperative patient.1 The literature does notyet support a clear advantage of one anesthetic technique over another for CEA.In this case, regional anesthesia for CEA is not a method customarily used atthis institution.

To facilitate the rapid emergence requiredfor these cases Wilhelm, et. al. proposedremifentanil-desflurane or fentanyl-desflu-rane anesthesia. In a small randomized trialthese methods were evaluated for times toearly recovery and response to simple neurological tests at 30, 60, and 90 minutesafter operation. Patients in the remifentanil-desflurane group had faster times to extuba-tion, stated their names faster, and preformed neurological tests significantlyearlier than those in the fentanyl-desfluranegroup. The remifentanil group maintainedhemodynamic stability better during intu-bation. Hemodynamic characteristics weresimilar during maintenance of anesthesia inboth groups. They concluded that this anes-thetic method is a suitable alternative tostandard fentanyl-based general anesthetictechnique in patients undergoing CEA. Alimitation of this study was the inability tocompare depth of anesthesia in the twogroups.3 We addressed the issue of depth ofanesthesia by using a BIS monitor as anadditional assessment tool.

Remifentanil is an opioid agonist with analgesic potency similar to fentanyl. It ismetabolized by hydrolysis by nonspecificesterases to inactive metabolites. Becauseof this remifentanil has a short duration ofaction, rapid onset, noncumulative effects,and rapid recovery. Remifentanil is able tobe precisely and rapidly titrated, has lowinterindividual variability, and has similarpharmacokinetics in obese and leanpatients. High dose remifentanil decreasescerebral blood flow and cerebral metabolic

oxygen requirements without impairingcarbon dioxide reactivity and is not associ-ated with histamine release.5 In addition tothese properties, better hemodynamic con-trol during laryngoscopy and maintenancewith remifentanil versus fentanyl has beenshown. The use of remifentanil titrated topatient need has been shown to decreaseintraoperative bradycardia and hypotensionepisodes that may be side effects of higherthan required dosing.7 In this case the dosewas not titrated and vasopressors used asneeded for hemodynamic control. Titrationmay have decreased the requirement ofphenylephrine.

Desflurane is a fluorinated methyl ethylether with a blood:gas partition coefficientof 0.45 and MAC of 6%. These propertiesallow for rapid achievement of anestheticlevels and timely awakening.5 When opioids and nitrous oxide are given with desflurane there is a dose dependantdecrease in the MAC. Midazolam premedication also decreases the MACof desflurane.6

Early detection and intervention is vitalshould complications arise after CEA.Patients require careful monitoring in thepost operative period. A new major neurologic deficit in the immediate postop-erative period represents a surgical emer-gency and early detection effects outcome.Immediate reexploration may be indicatedin these patients. The anesthetic manage-ment is similar to the technique used inelective situations. If a hematoma necessi-tates neck exploration following CEA a dif-ficult intubation should be anticipated andemergency tracheostomy or cricothyroido-tomy equipment available.1

CEA is a commonly performed surgery thatcarries the risk of substantial complica-tions. In some cases these may be amelio-

70

rated if diagnosed early and treated quickly.The use of short acting anesthetic drugssuch as remifentanil and desflurane may besuperior to other general anesthesia tech-niques in allowing reliable neurologicalassessment immediately post operatively.As with any case, a plan should be formu-lated based on the patient’s individual char-acteristics along with team experience andcomfort levels.

References

1. Ellis JE, Roizen MF, Mantha S,Schwarze ML, Lubarsky DA, Kenaan

CA. Anesthesia for vascular surgery. In: Barash PG, Cullen BF, Stoelting RK. eds. Clinical Anesthesia, 4th ed.Philadelphia: Lippincott Williams & Wilkins; 2001: 946-954.

2. Bond R, Rerkasem K, Rothwell PM. Systematic review of the risks of carotid endarterectomy in relation to the clinical indication for and timing of surgery. Stroke 2003;34:2290-2301.

3. Wilhelm W, Schlaich N, Harrer J,Kleinschmidt S, Muller M, Larson R. Recovery and neurological examination after remifentanil-desflurane or fentanyl-desflurane anaesthesia for carotid artery surgery. Br J Anaesth 2001;86:44-49.

4. Morgan GE, Mikhail MS, Murray MJ. Clinical Anesthesiology, 3rd ed. New York: The McGraw Hill Companies,Inc; 2002: 626-629.

5. Stoelting RK, Hillier SG. Pharmacology & Physiology in Anesthetic Practice. 4th ed.Philadelphia: Lippincott Williams & Wilkins; 2006:42-123.

6. Eger EI, Eisenkraft JB, Weiskopf RB. The Pharmacology of Inhaled Anesthetics. 3rd ed. USA: Edmond I Eger II, M.D.; 2003: 21-40.

7. Castro VD, Godet G, Mencia G, Raux M, Coriat P. Target-controlled infusion for remifentanil in vascular patients improves hemodynamics and decreases remifentanil requirement. Anesth Analg 2003;96:33-38.

Mentor: Janet A. Dewan, CRNA, MS

71

Anesthetic Management of Known Placenta Previa/AccretaDarin J. O'Brien, ADN, BHS

Bryan LGH School of Nurse Anesthesia

Keywords: Placenta previa, accreta,abnormal pregnancy, gravid hysterectomy,cesarean hysterectomy, anesthesia

Placenta previa is an abnormal condition ofpregnancy in which the placenta implantsin the lower segment of the uterus and maycover the internal cervical os.1,2 Placentaaccreta is an abnormal invasion of the placental trophoblast through the normallyprotective decidua basalis of the uterus andadherence of the placenta to the myometri-um.3,4,5,6 Either condition can lead to cata-strophic hemorrhage during childbirth.Careful surgical and anesthetic planningand management is required to anticipateintraoperative problems. This case reportdescribes anesthetic management of apatient diagnosed with placenta previa andsuspected placenta accreta during cesareansection (CS) and subsequent cesarean hys-terectomy (CH).

Case Report

A 25 year-old female gravida/parity 3-2-0-0-2, 69.5 kg, 62 in. presented for CS andlikely CH. The patient had two prior CSwithout complications. Estimated gesta-tional age was 36 weeks and one day. Thepregnancy had been relatively benign withminimal uterine activity, good fetal move-ments, and normal fetal growth noted ontwice weekly antepartum testing. Completeplacenta previa had been diagnosed byultrasonography (US), and magnetic reso-nance imaging (MRI) studies revealed like-ly accreta. The medical history included a10 pack-year history of cigarette smoking.The patient reported no known drug allergies and denied any current medica-

tions. Her most recent hemoglobin meas-urement was 11.0 gm/dL.

On the morning of surgery an epiduralcatheter was placed successfully, andadvanced approximately 3 cm into theepidural space. The patient was then trans-ported to interventional radiology wheretemporary balloon occlusion catheters weresuccessfully placed in the right and leftinternal iliac arteries under fluoroscopy forcontrol of intraoperative bleeding. Uponarrival to the preoperative holding area, asecond large-bore IV was placed, thepatient was preloaded with 1000 cc of LRintravenously (IV), and the epidural wasdosed in an incremental manner with 2%lidocaine and 1:200,000 epinephrine to atotal volume of 16 cc. In the operatingroom, routine monitors were placed andfour liters of oxygen were administered vianasal cannula.

A six pound male infant was deliveredbreech by CS uneventfully, with APGARscores of 8 and 8 at one and five minutes.Following delivery, the definitive diagnosesof accreta was made, and CH ensued. Theinternal iliac balloons were inflated by theinterventional radiologist to control uterineblood loss. Toward the completion of thehysterectomy, the patient began to experi-ence mild nausea, and described discomfortand pressure in the rectal area. She deniedany pain, but the discomfort worsened asthe surgery proceeded. Fentanyl 100 mcg,ondansetron 4 mg, and metoclopramide 10 mg were given IV. A low-dose propofoldrip IV was started as well. The patient’sdiscomfort persisted, and ketorolac 30 mgand meperidine 25 mg were given IV. The

72

discomfort became intense the patientbegan to move her legs on the table weakly,but uncooperatively. An additional 4 cc of2% lidocaine with epinephrine was placedin the epidural catheter, and general anes-thesia was administered with nitrous oxideand sevoflurane. No additional blood losswas noted when the iliac balloons weredeflated. Following closure of the surgicalwound, the patient was transported torecovery without complications or com-plaints. Estimated blood loss was 900cc,crystalloid fluid replacement was 3400ccand no blood products were transfused. Shewas discharged to home four days later witha healthy infant.

Discussion

Placenta previa is described as marginal (low-lying), partial (incomplete) or total (completeor central) depending on the amount of cervical os involvement.1,7 The incidence is0.1-1.0 %1,2,8 with a maternal mortality rate of0.03%.2,8 While the etiology is unknown, thereare several risk factors associated with placen-ta previa. There is a six-fold increase in risk forplacenta previa for women who have had aprevious lower segment CS.1 Multiparity,multigravida, frequent pregnancy (brief non-pregnant states), smoking, advanced maternalage and previous placenta previa are also asso-ciated with elevated risk.1,4,8 Diagnosis is usu-ally by serial US.1,7

Placenta accreta is a rare complication of preg-nancy now occurring in 0.04% of all deliver-ies.4 However, in the last 50 years, the inci-dence has increased 10-fold, likely fromincreased CS rates.3,4,5 It occurs in nearly 10%of pregnancies where placenta previa is pres-ent, compared to 0.005% when it is not pres-ent.4 The incidence increases with the numberof CS and may reach as high as 24-67% withconcurrent previa and a history of two or moreprevious CS.4,9 Serial US, color-flow Doppler,

and MRI are the most useful diagnostic tools,however, definitive diagnosis cannot be madeuntil the uterus can be visualized duringcesarean section and the placenta cannot beeasily separated from the uterus.3,7

The greatest risk of placenta previa and pla-centa accreta is massive uterine hemorrhagewith resulting maternal and/or fetal demise,especially if placental separation occurs out-side of the hospital setting. If the placenta istightly adhered to the uterus and cannot beseparated easily, immediate and even emer-gent hysterectomy may be required to preventcatastrophic hemorrhage. Statistically, bloodloss exceeds two liters in over half of all surgi-cal cases.4 It is important to inform the motherof this risk and that hysterectomy may be nec-essary, as well as the possibility of blood prod-uct transfusion. Autologous blood collectionand storage may be an option as well.5

Anesthetic choice for the patient with placenta previa-placenta accreta is controver-sial. While many believe that a conservativeapproach of general anesthesia (GA) for CSshould be used for placenta previa, at least twostudies have shown that regional anesthesia(RA) can be used safely resulting in more sta-ble intraoperative blood pressures, reducedblood loss, and decreased postoperative trans-fusion rates when compared to GA.2,10

Additionally, use of RA allows the mother tobe conscious and aware during the birth whichis usually desired, and can allow for spousalpresence as well. The anesthesia practitionerhas the option to cautiously convert to GAafter the birth if needed or desired for CH.

Although few studies have been published onthe subject, balloon occlusion catheters placedpreoperatively in the internal iliac arteries, andinflated to minimize blood flow to the utero-placenta complex during CH have been foundto result in a remarkable decrease in blood lossintraoperatively.5,6,7 Catheters can remain

73

deflated during CS, and then inflated anddeflated during the CH portion to occludeblood flow and evaluate bleeding. Thecatheters can be discontinued at a later timewith a low risk of complications.

Upon evaluating the patient for anesthesia, wetook into consideration the uncomplicated andstable pregnancy course, with no evidence ofinternal or external bleeding confirmed byphysical exam, ultrasonography, and MRI.Additionally, the patient had no contraindica-tions to neuraxial anesthesia, and desired to beaware and conscious during the birth. Thepatient had an adequate preoperative hemo-globin level, we planned IV hydration with 1-2 liters of crystalloid fluid prior to incision,and the surgical team was thoroughly preparedfor substantial blood loss. We felt placement ofan epidural catheter and dosing it accordinglyfor surgical purposes and leaving it in place forpostoperative pain control was appropriate.

While regional anesthesia may not be the bestchoice for every placenta previa/accreta case,after thorough assessment of this patient, wefelt it was the best choice in our situation. Inretrospect, we are unsure of why there wassome sacral sparing during the hysterectomythat obliged us to supplement IV analgesics,sedatives and then general inhalational anes-thetics. Due to the risk of aspiration, this mustbe done with a protected airway in place.Perhaps spinal anesthesia or combined spinalepidural anesthesia would have provided adenser block, and would have covered sacraldermatomes more adequately.

References

1. Wong DL, Perry SE. Maternal Child Nursing Care. 1st ed. St. Louis: Mosby;

| 1998:224-539.

2. Parekh N, Husaini SWU, Russell IF. Caesarean section for placenta praevia: aretrospective study of anaesthetic management. Br J Anaesth. 2000; 84:725-730.

3. Resnik R. Diagnosis and management of placenta accreta. ACOG Clinical Review. 1999;4(2):8-9.

4. Miller DA, Chollet JA, Goodwin TM. Clinical risk factors for placenta previa-placenta accreta. Am J Obstet Gynecol 1997;177:210–214.

5. Benumof JL. Anesthesia and Uncommon Diseases. 4th ed. Philadelphia: W.B. Saunders Company; 1998:465-467.

6. Dubois JD, Garel L, Grignon A, Lemay M, Leduc L. Placenta percreta: balloon occlusion and embolization of the internal iliac arteries to reduce intraoperative blood losses. Am J Obstet Gynecol.1997;176:723-726.

7. Oyelese Y, Smulian JC. Placenta previa,placenta accreta, and vasa previa. Obstet Gynecol 2006;107:927-941.

8. Iyasu S, Saftlas AK, Rowley DL,Koonin LM, Lawson HW, Atrash HK. The epidemiology of placenta previa in the United States, 1979 through 1987. Am J Obstet Gynecol. 1993;168:1424-1429.

9. Clark SL, Koonings PP, Phelan JP. Placenta previa/accreta and prior cesarean section. Obstet Gynecol. 1985;66: 89-92.

10. Hong J-Y, Jee Y-S, Yoon H-J, Kim SM. Comparison of general and epidural anesthesia in elective cesarean section for placenta previa totalis: maternal hemodynamics, blood loss and neonatal outcome. Int J Obstet Anesth. 2003;12:12-16.

Mentor: Sharon Hadenfeldt, CRNA, PhD

74

Keywords: Dexmedetomidine, alpha-2agonist, controlled hypotension, neuropro-tection, anesthesia

Dexmedetomidine is an alpha-2 agonist. Itsselective alpha-2 agonism is 1620:1 alpha-2 to alpha-1, and compared to clonidine hasa faster onset and shorter half life.1 Itsnumerous uses in anesthesia include:analgesia, sedation and anxiolysis,decreased blood pressure and heart rate,and inhibition of the sympathetic nervoussystem.1 Other effects of dexmedetomidineinclude antisialogogue, suppression ofantidiuretic hormone secretion, and neuro-protection.2 Clinically, dexmedetomidine isuseful in the operating room for reasonspreviously stated and useful in the intensivecare unit for sedation. Although it is notavailable in all operative settings, its use is more widely accepted and gaining popularity in the anesthesia community.

Case Report

A 72 year old female was scheduled for anorbitotomy, sphenoidectomy, and maxillec-tomy with possible craniotomy. The patientpresented to clinic with a recurring adenoidcystic carcinoma of the left maxillary sinus.In 2002 the patient underwent radiationtherapy with some shrinkage of the mass.The current CAT scan of paranasal sinusesand the brain revealed a large mass of theleft maxillary sinus extending through themaxillary sinus walls invading the orbit, thesphenoid sinus, the sella turcica and leftmiddle cranial fossa, as well as the palateand left nasal fossa. The borders of thetumor were not fully defined on CAT scan.The patient’s past medical history included

hypertension, hypercholesterolemia, andrecurrent adenoid cystic carcinoma. The past surgical history was significant fortonsillectomy as a child with no complica-tions from anesthesia. The medication profile included diovan, fexofenodine,and pravachol.

The patient weighed 88 kg and was 5 feet 6inches. Preoperative blood pressure was145/82 mmHg, heart rate of 73 beats perminute, respiratory rate of 20 breaths perminute, and room air oxygen saturation was97%. Her physical status was classified asASA II and the airway assessment revealedMallampati class II with normal cervicalrange of motion, atlanto-occipital jointextension, and thyromental distance. Thepatient could also move all extremities withequal strength, and her mental status wasalert and oriented times three. There wereno apparent neurological deficits.

The patient’s preoperative medicationincluded midazolam 2 milligrams,dexmedetomidine 20 micrograms, dexam-ethasone 10 milligrams, and cefazolin 1gram. The patient was taken to the operat-ing room and preoxygenated with 12 litersof oxygen via the anesthesia machine cir-cuit, and standard monitors were applied. A14 gauge intravenous catheter and 20g radi-al arterial line were inserted into the rightarm. Intravenous induction was then per-formed with fentanyl 150 micrograms(mcg), propofol 120 milligrams (mg), andsuccinylcholine 100 mg. The trachea wasintubated with a 7.5 centimeter anode tubeand secured on the right side of the face.The arms were tucked and eyes lubed andtaped shut. Mechanical ventilation was

Dexmedetomidine: Use as an Analgesic and Hemodynamic StabilizerKirsten H. Meister, B.S.N.University of Pennsylvania

75

initiated and anesthesia was maintainedwith sevoflurane end tidal concentrations of0.6-1.1%, and 1.5 liters flow of both oxygen and air. Throughout the case, thepatient received a total of dexmedetomidine240 mcg, fentanyl 250 mcg, hydromor-phone 2.8 mg, and vecuronium 30 mg. Thepatient’s systolic blood pressure was keptbetween 90-110 mmHg throughout the case.

The patient underwent decompressionorbitotomy, left medial maxillectomy, infratemporal fossa excision, and total sphe-noidectomy. Total blood loss was 600 milli-liters. The surgery lasted 7 hours, and at theend of the case the patient was extubated,placed on 50% oxygen face tent, and trans-ported to the intensive care unit. The patientwas able to answer questions appropriately,maintain oxygenation with face tent, anddid not complain of any pain. Postoperativeblood pressure was 107/62 with heart rateof 69.

Discussion

Patients undergoing facial or cranial sur-gery frequently require large dose narcoticsto decrease pain and maintain controlledhypotension to decrease blood lossthroughout the case. Anesthetic considera-tions related to large dose narcotic adminis-tration for this patient included: thepatient’s age, history of hypertension, and apossible craniotomy with surgery. It is pos-sible that large doses of narcotic woulddelay wakeup and cause respiratory depres-sion, which are unwanted side effects forthe elderly and for patients undergoingcraniotomy. The delay in wakeup couldlead the surgical team to believe there is apotential neurological deficit. Secondary tothe possible effects of large amounts of nar-cotics, and given the patients history ofhypertension, our anesthesia team decidedto use dexmedetomidine for analgesia and

to facilitate stability of hemodynamics bymaintaining controlled hypotension.

Alpha-2 receptor sites are found inside andoutside the central nervous system and inthe periphery. In the brain, they are foundprimarily in the pons and medulla whichtransmit sympathetic activation from higherbrain centers to the periphery. This signaltransduction acts on presynaptic alpha-2receptors inhibiting release of norepineph-rine and on postsynaptic alpha-2 receptorsdecreasing sympathetic activity.3 The over-all effect is a decrease in blood pressure andheart rate. In the spinal cord, alpha-2 ago-nism inhibits nocioceptive signal transduc-tion providing analgesia, and in the periph-ery induces vasoconstriction.3

Dexmedetomidine is a potent alpha-2 agonist and provides analgesia viasupraspinal and spinal sites without respira-tory depression, decreases plasma cate-cholamine release, produces centrallymediated hypotension and bradycardia,produces dose dependent sedation and anx-iolysis, causes diuresis due to inhibition ofanti-diuretic(ADH) hormone release andantagonism of ADH tubular effects, andmay produce decongestant and antisialo-gogue effects.3 Its use as an analgesic mayhelp to reduce narcotic requirement,although the exact mechanism of action isnot known.3,4 In regards to hemodynamics,the initial response may be a transienthypertension secondary to its effects in theperiphery, but the overall effect is adecrease in the sympathetic outflow of thecentral nervous system with resultingincrease in parasympathetic outflow.3

This results in decreased circulating catecholamines, blood pressure, and heart rate.

Activation of the alpha-2 receptors locatedin the locus ceruleus in the brain produce

Desflurane vs. Isoflurane: Early Recovery Parameters

Extra weight shouldn’t mean

extra wait1

REFERENCES1. Data on file. Baxter Healthcare Corporation, New Providence, NJ. 2. National Center for Health Statistics, Health, United States, 2006, With ChartbookTrends in the Health of Americans, Hyattsville, MD: 2006 3. Rose DK, Cohen MM. The airway: problems and predictions in 18,500 patients. Can J Anaesth1994;41:372-83. 4. Meininger D, Zwissler B, Byhahn C, et al. Impact of overweight and pneumoperitoneum on hemodynamics and oxygenation duringprolonged laparoscopic surgery. World J Surg 2006;30:520-6. 5. Zerah F, Harf A, Perlemuter L, et al. Effects of obesity on respiratory resistance. Chest1993;103:1470-6. 6. Shinohara E, Kihara S, Yamashita S, et al. Visceral fat accumulation as an important risk facter for obstructive sleep apnoeasyndrome in obese subjects. Journal of Internal Medicine. 1997;241:11-18. 7. Adams JP, Murphy PG. Obesity in anesthesia and intensive care.Br J Anaesth. 2000;85:91-108.

Baxter Healthcare Corporation, 95 Spring Street, New Providence, NJ 07974 1-800-ANA-DRUG (1-800-262-3784) www.suprane.com Baxter and Suprane are trademarks of Baxter International Inc.US Patent No 4,762,856 742724 04/07

Please see brief summary of Prescribing Information on the next page.

D

Desflurane vs. Isoflurane in Overweight Subjects: Early Recovery Parameters1

* BMI > 25 † Age < 65‡ Desflurane significantly faster than isoflurane for all parameters, p<0.05; mean (min.) ± standard deviation

Early Recovery Parameters Desflurane‡

n=136*†Isoflurane‡

n=102*† p-value

Cessation of anesthesia to eye opening 9.0±6.5n=134

12.0±11.5n=98 0.0220

Response to command:

Squeeze my fingers 9.6±6.7n=135

13.3±10.7n=98 0.0029

Tell me your date of birth 12.9±9.9n=117

16.4±9.3n=87 0.0129

Tell me your name 12.2±9.3n=117

15.7±9.3n=87 0.0094

The most recent data available show that 67% of the adult U.S. populationis overweight (BMI >25).2 Extra weight has been associated with difficultyin tracheal intubation,3 hypoxemia,4 decreased functional residual capacity,5

increased airway resistance,5 sleep apnea 6 and aspiration.7

One of the main goals following general anesthesia is to optimize recovery.With Suprane (desflurane, USP), overweight patients experienced fasterearly recovery from anesthesia compared with isoflurane (see table). Inaddition, adverse events were comparable for overweight patientscompared to normal weight patients.1

So if you’re not considering Suprane (desflurane, USP) in your overweightpatients, what are you waiting for?

IInnddiiccaattiioonnss aanndd UUssaaggee::Suprane (desflurane, USP) is indicated as an inhalation agent for induction and/or maintenance of general anesthesia for inpatient & outpatient surgery in adults.

Suprane is not recommended for induction of anesthesia in pediatric patientsbecause of a high incidence of moderate to severe upper airway adverseevents. After induction of anesthesia with agents other than Suprane , andtracheal intubation, Suprane is indicated for maintenance of anesthesia ininfants and children.

Suprane should be administered only by persons trained in the administration of general anesthesia, using a vaporizer specifically designed and designated for use with desflurane. Facilities for maintenance of a patent airway, artificial ventilation, oxygen enrichment, and circulatory resuscitation must be immediately available. Hypotension and respiratory depressionincrease as anesthesia is deepened.

IImmppoorrttaanntt SSaaffeettyy IInnffoorrmmaattiioonn::Suprane should not be used in patients with a known or suspected geneticsusceptibility to malignant hyperthermia, or known sensitivity to Suprane orto other halogenated agents.

Use of inhaled anesthetic agents has been associated with rare increases in serumpotassium levels that have resulted in cardiac arrhythmias and death in pediatricpatients during the postoperative period. Patients with latent as well as overtneuromuscular disease, particularly Duchenne muscular dystrophy, appear to bemost vulnerable. Concomitant use of succinylcholine has been associated withmost, but not all of these cases. Despite the similarity in presentation to malignanthyperthermia, none of these patients exhibited signs or symptoms of muscle rigidityor hypermetabolic state. Suprane is not recommended for induction of generalanesthesia via mask in infants or children because of the high incidence ofmoderate to severe laryngospasm in 50% of patients, coughing 72%, breathholding68%, increase in secretions 21% and oxyhemoglobin desaturation 26%.

Concentrations of desflurane exceeding 1 MAC may increase heart rate.Thus an increased heart rate may not be a sign of inadequate anesthesia.

Suprane should not be used as the sole agent for anesthetic induction in patientswith coronary artery disease or patients where increases in heart rate or bloodpressure are undesirable. It should be used with other medications, preferablyintravenous opioids and hypnotics. Suprane , like some other inhalationalanesthetics, can react with desiccated carbon dioxide (CO2) absorbents toproduce carbon monoxide which may result in elevated levels ofcarboxyhemoglobin in some patients. Case reports suggest that bariumhydroxide lime and soda lime become desiccated when fresh gases are passedthrough the CO2 absorber canister at high flow rates over many hours or days.

As with other halogenated anesthetic agents, Suprane (desflurane, USP) maycause sensitivity hepatitis in patients who have been sensitized by previousexposure to halogenated anesthetics. The average MAC for Suprane in a70 year old patient is two-thirds the MAC for a 20 year old patient.

R

SUPRANE(desflurane, USP)Volatile Liquid for InhalationBrief Summary. See Product Insert for Full Prescribing Information.

INDICATIONS AND USAGESUPRANE (desflurane, USP) is indicated as an inhalation agent for inductionand/or maintenance of anesthesia for inpatient and outpatient surgery in adults(see PRECAUTIONS).SUPRANE (desflurane, USP) is not recommended for induction of anesthesiain pediatric patients because of a high incidence of moderate to severe upperairway adverse events (see WARNINGS). After induction of anesthesia withagents other than SUPRANE, and tracheal intubation, SUPRANE is indicated formaintenance of anesthesia in infants and children.

CONTRAINDICATIONSSUPRANE (desflurane, USP) should not be used in patients with a known orsuspected genetic susceptibility to malignant hyperthermia.Known sensitivity to SUPRANE (desflurane, USP) or to other halogenated agents.

WARNINGSPerioperative HyperkalemiaUse of inhaled anesthetic agents has been associated with rare increases inserum potassium levels that have resulted in cardiac arrhythmias and death inpediatric patients during the postoperative period. Patients with latent as wellas neuromuscular disease, particularly Duchenne muscular dystrophy, appearto be most vulnerable. Concomitant use of succinylcholine has been associatedwith most, but not all, of these cases. These patients also experiencedsignificant elevations in serum creatinine kinase levels and, in some cases,changes in urine consistent with myoglobinuria. Despite the similarity inpresentation to malignant hyperthermia, none of these patients exhibited signsor symptoms of muscle rigidity or hypermetabolic state. Early and aggressiveintervention to treat the hyperkalemia and resistant arrhythmias isrecommended, as is subsequent evaluation for latent neuromuscular disease.Malignant HyperthermiaIn susceptible individuals, potent inhalation anesthetic agents may trigger askeletal muscle hypermetabolic state leading to high oxygen demand and theclinical syndrome known as malignant hyperthermia. In genetically susceptiblepigs, desflurane induced malignant hyperthermia. The clinical syndrome issignalled by hypercapnia, and may include muscle rigidity, tachycardia,tachypnea, cyanosis, arrhythmias, and/or unstable blood pressure. Some ofthese nonspecific signs may also appear during light anesthesia: acutehypoxia, hypercapnia, and hypovolemia.Treatment of malignant hyperthermia includes discontinuation of triggeringagents, administration of intravenous dantrolene sodium, and application ofsupportive therapy. (Consult prescribing information for dantrolene sodiumintravenous for additional information on patient management.) Renal failuremay appear later, and urine flow should be monitored and sustained if possible.Pediatric UseSUPRANE (desflurane, USP) is not recommended for induction of generalanesthesia via mask in infants or children because of the high incidence ofmoderate to severe laryngospasm in 50% of patients, coughing 72%,breathholding 68%, increase in secretions 21% and oxyhemoglobindesaturation 26%.SUPRANE (desflurane, USP) should be administered only by persons trained inthe administration of general anesthesia, using a vaporizer specifically designedand designated for use with desflurane. Facilities for maintenance of a patentairway, artificial ventilation, oxygen enrichment, and circulatory resuscitationmust be immediately available. Hypotension and respiratory depressionincrease as anesthesia is deepened.

PRECAUTIONSDuring the maintenance of anesthesia, increasing concentrations of SUPRANE(desflurane, USP) produce dose-dependent decreases in blood pressure.Excessive decreases in blood pressure may be related to depth of anesthesia andin such instances may be corrected by decreasing the inspired concentration ofSUPRANE.Concentrations of desflurane exceeding 1 MAC may increase heart rate. Thusan increased heart rate may not be a sign of inadequate anesthesia.In patients with intracranial space occupying lesions, SUPRANE (desflurane,USP) should be administered at 0.8 MAC or less, in conjunction with abarbiturate induction and hyperventilation (hypocapnia). Appropriate measuresshould be taken to maintain cerebral perfusion pressure (see CLINICALSTUDIES, Neurosurgery in full prescribing information).In patients with coronary artery disease, maintenance of normalhemodynamics is important to the avoidance of myocardial ischemia.Desflurane should not be used as the sole agent for anesthetic induction inpatients with coronary artery disease or patients where increases in heart rateor blood pressure are undesirable. It should be used with other medications,preferably intravenous opioids and hypnotics (see CLINICAL STUDIES,Cardiovascular Surgery in full prescribing information).Inspired concentrations of SUPRANE (desflurane, USP) greater than 12% havebeen safely administered to patients, particularly during induction ofanesthesia. Such concentrations will proportionately dilute the concentration ofoxygen; therefore, maintenance of an adequate concentration of oxygen mayrequire a reduction of nitrous oxide or air if these gases are used concurrently.The recovery from general anesthesia should be assessed carefully beforepatients are discharged from the post anesthesia care unit (PACU).SUPRANE (desflurane, USP), like some other inhalational anesthetics, canreact with desiccated carbon dioxide (CO2) absorbents to produce carbonmonoxide which may result in elevated levels of carboxyhemoglobin in somepatients. Case reports suggest that barium hydroxide lime and soda limebecome desiccated when fresh gases are passed through the CO2 absorbercannister at high flow rates over many hours or days. When a cliniciansuspects that CO2 absorbent may be desiccated, it should be replaced beforethe administration of SUPRANE (desflurane, USP).As with other halogenated anesthetic agents, SUPRANE (desflurane, USP) maycause sensitivity hepatitis in patients who have been sensitized by previousexposure to halogenated anesthetics (see CONTRAINDICATIONS).Drug InteractionsNo clinically significant adverse interactions with commonly used preanestheticdrugs, or drugs used during anesthesia (muscle relaxants, intravenous agents,and local anesthetic agents) were reported in clinical trials. The effect ofdesflurane on the disposition of other drugs has not been determined.Like isoflurane, desflurane does not predispose to premature ventriculararrhythmias in the presence of exogenously infused epinephrine in swine.

BENZODIAZEPINES AND OPIOIDS (MAC REDUCTION)Benzodiazepines (midazolam 25-50 µg/kg) decrease the MAC of desflurane by16% as do the opioids (fentanyl 3-6 µg/kg) by 50% (see DOSAGE ANDADMINISTRATION in full prescribing information).NEUROMUSCULAR BLOCKING AGENTSAnesthetic concentrations of desflurane at equilibrium (administered for 15 ormore minutes before testing) reduced the ED95 of succinylcholine byapproximately 30% and that of atracurium and pancuronium by approximately50% compared to N2O/opioid anesthesia. The effect of desflurane on durationof nondepolarizing neuromuscular blockade has not been studied.

DOSAGE OF MUSCLE RELAXANT CAUSING 95% DEPRESSIONIN NEUROMUSCULAR BLOCKADE

Mean ED95 (µg/kg)Desflurane Concentration Pancuronium Atracurium Succinylcholine0.65 MAC 60% N2O/O2 26 123 -1.25 MAC 60% N2O/O2 18 91 -1.25 MAC O2 22 120 362————————————————————––––––———––—––——Dosage reduction of neuromuscular blocking agents during induction ofanesthesia may result in delayed onset of conditions suitable for endotrachealintubation or inadequate muscle relaxation, because potentiation ofneuromuscular blocking agents requires equilibration of muscle with thedelivered partial pressure of desflurane.Among nondepolarizing drugs, only pancuronium and atracurium interactionshave been studied. In the absence of specific guidelines:1. For endotracheal intubation, do not reduce the dose of nondepolarizing

muscle relaxants or succinylcholine.2. During maintenance of anesthesia, the dose of nondepolarizing muscle

relaxants is likely to be reduced compared to that during N2O/opioidanesthesia. Administration of supplemental doses of muscle relaxantsshould be guided by the response to nerve stimulation.

Renal or Hepatic InsufficiencyNine patients receiving SUPRANE (desflurane, USP) (N=9) were compared to9 patients receiving isoflurane, all with chronic renal insufficiency (serumcreatinine 1.5-6.9 mg/dL). No differences in hematological or biochemicaltests, including renal function evaluation, were seen between the two groups.Similarly, no differences were found in a comparison of patients receivingeither SUPRANE (desflurane, USP) (N=28) or isoflurane (N=30) undergoingrenal transplant.Eight patients receiving SUPRANE (desflurane, USP) were compared to sixpatients receiving isoflurane, all with chronic hepatic disease (viral hepatitis,alcoholic hepatitis, or cirrhosis). No differences in hematological orbiochemical tests, including hepatic enzymes and hepatic function evaluation,were seen.Carcinogenesis, Mutagenesis, Impairment of FertilityAnimal carcinogenicity studies have not been performed with SUPRANE(desflurane, USP). In vitro and in vivo genotoxicity studies did not demonstratemutagenicity or chromosomal damage by SUPRANE. Tests for genotoxicityincluded the Ames mutation assay, the metaphase analysis of humanlymphocytes, and the mouse micronucleus assay.Fertility was not affected after 1 MAC-Hour per day exposure (cumulative 63and 14 MAC-Hours for males and females, respectively). At higher doses,parental toxicity (mortalities and reduced weight gain) was observed whichcould affect fertility.PregnancyTERATOGENIC EFFECTSNo teratogenic effect was observed at approximately 10 and 13 cumulativeMAC-Hour exposures at 1 MAC-Hour per day during organogenesis in rats orrabbits. At higher doses increased incidences of post-implantation loss andmaternal toxicity were observed. However, at 10 MAC-Hours cumulativeexposure in rats, about 6% decrease in the weight of male pups was observedat preterm caesarean delivery.PREGNANCY CATEGORY BThere are no adequate and well-controlled studies in pregnant women.SUPRANE (desflurane, USP) should be used during pregnancy only if thepotential benefit justifies the potential risk to the fetus.Rats exposed to desflurane at 1 MAC-Hour per day from gestation day 15 tolactation day 21, did not show signs of dystocia. Body weight of pups deliveredby these dams at birth and during lactation were comparable to that of controlpups. No treatment related behavioral changes were reported in these pupsduring lactation.Labor and DeliveryThe safety of desflurane during labor or delivery has not been demonstrated.Nursing MothersThe concentrations of desflurane in milk are probably of no clinical importance24 hours after anesthesia. Because of rapid washout, desfluraneconcentrations in milk are predicted to be below those found with other volatilepotent anesthetics.Pediatric UseSUPRANE (desflurane, USP) is not recommended for induction of generalanesthesia via mask in pediatric patients because of the high incidence ofmoderate to severe laryngospasm, coughing, breathholding and increase insecretions and oxyhemoglobin desaturation (see WARNINGS).Geriatric UseThe average MAC for SUPRANE (desflurane, USP) in a 70 year old patient istwo-thirds the MAC for a 20 year old patient (see DOSAGE ANDADMINISTRATION in full prescribing information).Neurosurgical UseSUPRANE (desflurane, USP) may produce a dose-dependent increase incerebrospinal fluid pressure (CSFP) when administered to patients withintracranial space occupying lesions. Desflurane should be administered at0.8 MAC or less, and in conjunction with a barbiturate induction andhyperventilation (hypocapnia) until cerebral decompression in patients withknown or suspected increases in CSFP. Appropriate attention must be paid tomaintain cerebral perfusion pressure (see CLINICAL STUDIES, Neurosurgeryin full prescribing information).

ADVERSE REACTIONSAdverse event information is derived from controlled clinical trials, the majorityof which were conducted in the United States. The studies were conductedusing a variety of premedications, other anesthetics, and surgical procedures ofvarying length. Most adverse events reported were mild and transient, and mayreflect the surgical procedures, patient characteristics (including disease)and/or medications administered.Of the 1,843 patients exposed to SUPRANE (desflurane, USP) in clinical trials,370 adults and 152 children were induced with desflurane alone and 687patients were maintained principally with desflurane. The frequencies givenreflect the percent of patients with the event. Each patient was counted oncefor each type of adverse event. They are presented in alphabetical orderaccording to body system.

PROBABLY CAUSALLY RELATED: Incidence greater than 1%.Induction (use as a mask inhalation agent)

ADULT PATIENTS (N=370): Coughing 34%, breathholding 30%,apnea 15%, increased secretions*,laryngospasm*, oxyhemoglobindesaturation (SpO2 < 90%)*,pharyngitis*.

PEDIATRIC PATIENTS (N=152): Coughing 72%, breathholding 68%,laryngospasm 50%, oxyhemoglobindesaturation (SpO2< 90%) 26%,increased secretions 21%,bronchospasm*.(See WARNINGS)

Maintenance or RecoveryADULT AND PEDIATRIC PATIENTS (N=687):

Body as a Whole HeadacheCardiovascular Bradycardia, hypertension, nodal

arrhythmia, tachycardiaDigestive Nausea 27%, vomiting 16%Nervous system Increased SalivationRespiratory Apnea*, breathholding, cough

increased*, laryngospasm*,pharyngitis

Special Senses Conjunctivitis (conjunctivalhyperemia)

* Incidence of events: 3% - 10%PROBABLY CAUSALLY RELATED: Incidence less than 1%

Reported in 3 or more patients, regardless of severity (N=1,843)Adverse reactions reported only from postmarketing experience or in theliterature, not seen in clinical trials, are considered rare and are italicized.Cardiovascular Arrhythmia, bigeminy, abnormal

electrocardiogram, myocardialischemia, vasodilation

Digestive HepatitisNervous System Agitation, dizzinessRespiratory Asthma, dyspnea, hypoxia

CAUSAL RELATIONSHIP UNKNOWN: Incidence less than 1%Reported in 3 or more patients, regardless of severity (N=1,843)

Body as a Whole FeverCardiovascular Hemorrhage, myocardial infarctMetabolic and Nutrition Increased creatinine phosphokinaseMusculoskeletal System MyalgiaSkin and Appendages PruritusSee WARNINGS for information regarding pediatric use and malignanthyperthermia.SUPRANE (desflurane, USP) has been associated with perioperativehyperkalemia (see WARNINGS).There have been rare post-marketing reports of hepatic failure and hepaticnecrosis associated with the use of potent volatile anesthetic agents, includingSUPRANE (desflurane, USP). Due to the spontaneous nature of these reports,the actual incidence and relationship of SUPRANE (desflurane, USP) to theseevents cannot be established with certainty.Laboratory FindingsTransient elevations in glucose and white blood cell count may occur as withuse of other anesthetic agents.

HOW SUPPLIEDSUPRANE (desflurane, USP), NDC 10019-641-24, is packaged in amber-colored bottles containing 240 mL desflurane.Safety and HandlingOCCUPATIONAL CAUTIONThere is no specific work exposure limit established for SUPRANE (desflurane, USP).However, the National Institute for Occupational Safety and Health Administration(NIOSH) recommends that no worker should be exposed at ceiling concentrationsgreater than 2 ppm of any halogenated anesthetic agent over a sampling period notto exceed one hour.The predicted effects of acute overexposure by inhalation of SUPRANE (desflurane, USP)include headache, dizziness or (in extreme cases) unconsciousness.There are no documented adverse effects of chronic exposure to halogenatedanesthetic vapors (Waste Anesthetic Gases or WAGs) in the workplace.Although results of some epidemiological studies suggest a link betweenexposure to halogenated anesthetics and increased health problems(particularly spontaneous abortion), the relationship is not conclusive. Sinceexposure to WAGs is one possible factor in the findings for these studies,operating room personnel, and pregnant women in particular, should minimizeexposure. Precautions include adequate general ventilation in the operatingroom, the use of a well-designed and well-maintained scavenging system,work practices to minimize leaks and spills while the anesthetic agent is in use,and routine equipment maintenance to minimize leaks.StorageStore at room temperature, 15°- 30°C (59°- 86°F). SUPRANE (desflurane, USP)has been demonstrated to be stable for the period defined by the expiration datingon the label. The bottle cap should be replaced after each use of SUPRANE.Baxter and SUPRANE are trademarks of Baxter International Inc.

Manufactured forBaxter Healthcare CorporationDeerfield, IL 60015 USA

For Product Inquiry 1 800 ANA DRUG (1-800-262-3784)

MLT-00070/7.0

Revised: July 2006

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anxiolysis and sedation. The locus ceruleusis a key modulator for critical brain func-tions including arousal, sleep, and anxiety.3

Dexmedetomidine effects are not depend-ent on gamma-aminobutyric acid (GABA)system, and seem to produce a cooperativeform of sedation where patients are easilyaroused when stimulated and back to sleepwhen left alone. Cognitive function mayalso be better preserved when comparedwith other anxiolytics or hypnotics.3

Dexmedetomidine also offers neuroprotec-tion. It helps to inhibit ischemia inducedrelease of norepinephrine, and reduces glutamate release as well as facilitating glu-tamate disposal by oxidative metabolism.3

Dexmedetomidine seems to have no directeffect on intracranial pressure (ICP) but itreduces cerebral metabolic rate of oxygen,decreases cerebral blood flow therebydecreasing ICP, and has minimal effects onevoked potential latency or amplitude.

Despite all the benefits of dexmedetomi-dine, it is not without side effects. Commonside effects include hypotension, transienthypertension, dry mouth, bradycardia,reduction in the cerebral blood flow/ cere-bral metabolic rate of oxygen ratio, andexcessive sedation.2,3 Some of these sideeffects may be reduced by using a slowbolus for the initial loading dose, and care-ful titration of subsequent doses. It is sug-gested that a loading dose of 1 mcg/kg begiven over a period of 10 minutes as the ini-tial dose, and that this dose not be bolused.

In the case presented, dexmedetomidineproved useful by helping to reduce narcoticand inhalational agent requirement, and bymaintaining slight hypotension. We wereable to maintain the patient’s systolic bloodpressure within a tight range without theuse of other antihypertensives. The patientdid develop transient hypertension in the

beginning with our loading dose secondaryto rapid infusion. Given the recommenda-tions of administration of dexmedetomi-dine, this side effect could have been poten-tially prevented with a slow bolus as the ini-tial dose. Overall, the patient did notrequire large doses of narcotics or inhala-tional agents which facilitated rapid emer-gence at the end of the case. The patientalso did not require the use of other antihy-pertensives to maintain controlled hypoten-sion to help decrease blood loss. Moreover,the patient was comfortable, arousable, andpain free after major surgery.

References

1. Lawson NW, Johnson J. Autonomic nervous system: physiology and pharmacology. In: Barash, PG, ed. Clinical Anesthesia. 5th ed.Philadelphia: Lippincott Williams & Wilkins; 2006:315-316.

2. Golembiewski J. Dexmedetomidine-does it have a role in the perioperative setting? J PeriAnesth Nurs. 2005; 20(4): 289-291.

3. Bekker A, Sturaitis MK. Dexmedetomidine for neurological surgery. Neurosurgery. 2005;57 (1 suppl): 1-10.

4. Unlegenc H, Gunduz M, Guler T,Yagmur O, Isik G. The effect of pre-anesthetic administration of intravenous dexmedetomidine on post-operative pain in patients receiving patient controlled morphine. Eur J Anaesthesiol. 2005; 22: 386-391.

Mentor: Russ Lynn CRNA, MSN

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Keywords: brain dead, organ donor,organ procurements, anesthesia

Brain dead organ donor patients presentchallenging issues in anesthetic manage-ment. Brain death is declared when cerebraland brainstem function has irreversiblyceased1. This complex process involveshemodynamic instability with endocrineand metabolic regulation disruption ifuntreated. Salvaging viable organs is possi-ble when homeostasis is closely regulated.Anesthetic management includes adminis-tration of vasopressors to maintain a meanarterial pressure (MAP) of 70 mmHg,aggressive fluid resuscitation for hypov-olemia, thermoregulation, management ofdiabetes insipidus, correction of electrolyteabnormalities, maintaining adequate oxy-genation, management of cardiac arrhyth-mias, pulmonary toilet, and > 30% hemat-ocrit (Hct) values3. This case report discuss-es one case of liver and kidney donationfrom a brain dead donor.

Case Report

A 35 year-old male was admitted to thehospital for an intracranial subarachnoidhemorrhage. He was transferred to theintensive care unit (ICU) and declared braindead after the completion of an apnea testand confirmation of the absence of brainstem reflexes. He was classified an ASA VI.History and consent for organ donation wasreceived from immediate family members.No prior surgical history was noted.Medical history included hypertension anddextrocardia. The patient’s heart and spleenwere on the right side of his body and hisliver was on the left side. According to fam-

ily history and chart review, the patient didnot have any noted issues due to hisreversed anatomy. He was healthy andfunctioned normally. After brain death dec-laration, all medications were discontinuedexcept for a phenylephrine infusion tomaintain a MAP between 70-100 mmHg. Avasopressin infusion was administered fordiabetes insipidus that developed during thepatient’s ICU course. Once serum and urineosmolality were within normal limits, thisinfusion was discontinued in the ICU. Labvalues preoperatively: Na – 152 mEq/L, K– 4.1 mEq/L, Glucose 167 mg/dL, Hct –34%, PT – 12 sec, PTT – 45 sec, INR 1.0.Ejection fraction of 70%, normal left ventricular and valvular function werereported in the preoperative echocardio-gram, and the ECG showed normal sinusrhythm with a heart rate of 92 bpm. Thepatient’s trachea was intubated upon admis-sion to the emergency room and respira-tions were mechanically controlled withventilator settings of assist control, TV 700,and Rate 12, FiO2 100% in the ICU.Preoperative arterial blood gas (ABG) val-ues were normal (ph – 7.39, PaCO2 – 39mmHg, PaO2 – 200 mmHg) and monitoredhourly intraoperatively. Intra-arterial andcentral venous pressure monitoring wereutilized in the ICU and continued intraoper-atively. The patient was receiving NS solution intravenously at 100 ml/hr. Heartsounds heard on the right side were normaland lungs sounds were clear, though dimin-ished in the lower lobes.

The United Network for Organ Sharing(UNOS) was perioperatively involved inthe management of the patient. A guideline

Multiorgan Procurement ManagementBhavika Patel, B.S.N.Northeastern University

81

was provided by UNOS to aid with theintraoperative management.6 The anestheticplan focused on maintaining hemodynamicstability that supported organ function. Thepatient was placed on portable monitors,10 L/min oxygen administered by manualventilation with ambu bag and transferredto the operating room by anesthesia practi-tioners and UNOS personnel. Upon enter-ing the operating room, the patient’s respi-rations were controlled by mechanical ventilation and ICU ventilator settings weremaintained. Hemodynamic stability wasmaintained with a phenylephrine infusionat 25 mcg/min titrated as needed to main-tain MAP of 70-100 mmHg, NS at 100ml/hr was continued. Inhalation or neuro-muscular blockade agents were not utilizedduring the surgical procedure. Anesophageal stethoscope and temperatureprobe was placed. Intra-arterial blood pressure and central venous monitoringwere continued. Heparin 30,000 units andMannitol 25 grams were administeredintravenously immediately before crossclamping of the aorta. When the aorta wascross-clamped, NS and phenylephrine solutions and ventilatory support were dis-continued. Tissue biopsies of the procuredorgans were sent to pathology. The endotra-cheal tube (ETT), all invasive monitoringdevices and intravenous catheters were leftin place, and the patient was declaredexpired. Anesthesia management was notrequired for the post procurement closure.After the organs were removed, the sur-geons transported the liver and kidneys totheir respective facilities for organ trans-plantation (after pathology reportsreceived). UNOS remained in the operatingroom for incision closure and removal ofinvasive monitoring devices, intravenouscatheters, Foley, and ETT. The body wasplaced in a body bag and taken to the

morgue accompanied by transport person-nel and an operating room RN.

Discussion

Preoperative management and assessmentare as important as intraoperative manage-ment in this case scenario. Measures uti-lized preoperatively to maintain hemody-namic stability, optimum oxygenation, andendocrine regulation needed to be contin-ued until organs had been procured.Communication with the ICU team manag-ing the patient was invaluable. Inhalationagents are not necessary during organ pro-curement after the declaration of braindeath, but spinal reflexes and some move-ment may be present so neuromuscularblockade with a nondepolarizing agent isrecommended2. Per surgeon request, neuro-muscular blockade was avoided in thiscase. Oxygen 2 l/min was administered viaETT to prevent ischemia and promote max-imum oxygenation to all tissues. ICU venti-lator settings were continued. Esophagealstethoscope probe was utilized to monitortemperature and heart and lung sounds.Fluid warmer and Bair hugger were used toprevent hypothermia. Phenylephrine wasneeded to maintain MAP greater than 70mmHg to preserve tissue perfusion.Maintaining this patient’s blood pressurewas a challenge. The patient was very sen-sitive to the titration adjustments ofphenylephrine. Excessive vasoconstrictionthat would compromise tissue perfusionwas a concern when the patient’s bloodpressure would increase above a systolicblood pressure (SBP) of 160 mmHg. Whenthe infusion was titrated down in smallincrements, the SBP would decrease to 80mmHg. Constant titration of the infusionwas necessary to maintain optimum perfu-sion pressures. This instability may havereflected loss of feedback modulation

82

reflexes. Dopamine and epinephrine infu-sions were immediately available if thephenylephrine infusion did not prove suffi-cient to maintain the desired MAP.According to current literature, a vaso-pressin infusion is an excellent choice forhypotension management. Exogenouslyadministered vasopressin can produce aprolonged increase in arterial blood pres-sure within one minute4. In this case, circu-lating vasopressin was lower due to thepatient’s presurgical diagnosis of diabetesinsipidus from endocrine disruption due tobrain death. Hemodynamic instability maybe due to the lack of endogenous circulat-ing vasopressin. Perhaps, if the vasopressininfusion was continued intraoperatively inconjunction with the phenylephrine infu-sion, fluctuations in the patient’s bloodpressure would not have occurred.

In addition to the phenylephrine infusion,NS intravenous solution was used to pre-vent hypotension due to hypovolemia andsurgical fluid loss. The NS solution wasalso chosen as the intravenous fluid for thispatient because of hypernatremia at 152mEq/L preoperatively and a subsequentrecorded value of at 149 mEq/L one hourinto the operation. Measures to correcthypernatremia and hypovolemia seemedsuccessful. Urine output was monitoredhourly by Foley catheter to assure renal per-fusion. ABGs were drawn hourly to moni-tor electrolyte imbalances/corrections andpresence of acidbase derangement. ABGvalues remained within normal limitsthroughout the procedure. Mannitol wasadministered immediately before cross-clamping of the aorta to prevent reperfusioninjury from oxygen-free radicals. Mannitolfunctions as a hydroxyl free radical scavenger.2 Total anticoagulating dose ofheparin was administered intravenously toprevent increases in clotting factor activity

or thrombus formation in response to crossclamping2. These measures allowed maxi-mum blood flow and tissue profusion need-ed for the procurement of the liver and kid-neys. Intravenous fluid total was 1600 mland urine output total was 560 ml for theduration of the case.

Organ donation over the last decade hasincrease by 3.7% while the recipient wait-ing list has grown by 19%. According toUNOS, the current number of people onorgan transplant waiting lists is 94,299. Thenumber of transplanted organs fromJanuary 2006 to September 2006 was22,010, and 11,188 organ donations weremade during this time.5 With these statis-tics, the most realistic option to increaseorgan donation is to maximize organ usefrom brain dead patients.1 The anesthesiapractitioner has the responsibility to main-tain tissue perfusion, adequate volume sta-tus, and oxygenation without injuring anypotential donated organs. In this particularcase, management techniques and medica-tions were adequate. Due to the lack of ran-domized controlled trials conducted onbrain dead organ donors, evidence basedguidelines for anesthetic management arenot available. Management is gearedtowards the needs of the harvesting sur-geons and organ procurement personnelsuch as UNOS, while maintaining donordignity. The guidelines provided by UNOSare the major resources for the managementin this type of case.5 Further research thatincludes evidenced outcomes needs to beconducted in order to develop harvest spe-cific guidelines for anesthetic management.

References

1. Csete M, Glas K. Anesthesia for organ transplantation. In: Barash PG, Cullen BF, Stoelting RK. eds. Clinical

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Keywords: Depodur, epidural, morphine,anesthesia

Depodur® is indicated for epidural adminis-tration, at the lumbar level, for the treat-ment of pain following major surgery.Depodur® is an extended release formula-tion of morphine in a lyposomal carrier. Asingle injection into the epidural space ofconventional morphine lasts 24 hours,which is clearly not long enough in patientsrecovering from lower abdominal surgery.Although one of the main concerns with theadministration of Depodur® is respiratorydepression, this side-effect is also seen withother opioids. One advantage of Depodur®

is that it does not require an indwellingcatheter which can limit patients’ mobilityand anticoagulation treatment options following surgery. It can also augment thepain control provided by patient controlledintravenous analgesia (PCA).1-4

Case Report

An 85-year-old ASA II male presented for alow anterior open colon resection for coloncancer. His past medical history includedcontrolled hypertension treated withnifedipine daily. The patient was a formerpipe smoker and reported drinking twoalcoholic drinks per week. His exercise tol-erance was good and included daily swim-ming, weight lifting, tennis, and racquet-ball. The patient was allergic to penicillinwhich caused urticaria. Past surgical histo-ry included two colonoscopies, carpal tun-nel release, and a hydrocele repair at birth.There were no anesthetic complicationswith any of his prior procedures.

On the morning of surgery he weighed82.2kg; vital signs were unremarkable withexception of mild hypertension (140/62).Laboratory results were within normal lim-

Single-Shot Epidural for Post-Operative Pain Management in Colon ResectionJessica D. Sherman, B.S.N.

Northeastern University

Anesthesia, 5th ed. Philadelphia:Lippincott Williams & Wilkins:2006:1358-1360.

2. Ellis JE, Roizen MF, Mantha S,Schwarze ML, Lubarsky DA, Kenaa CA. Anesthesia for vascular surgery. In: Barash PG, Cullen BF, Stoelting RK. eds. Clinical Anesthesia, 5th ed. Philadelphia: Lippincott Williams & Wilkins: 2006:957-958.

3. Salim A, Velmahos, GC, Brown C,Belzberg H, Demitriades D. Aggressive organ donor management significantly increases the number of organs available for transplantation. J Trauma. 2005; 58:991-994.

4. Waltier DC. The vasopressin system:physiology and clinical strategies. Anesthesiology. 2006; 105:599-612.

5. United Network for Organ Sharing. Available at http://www.unos.org/. Accessed November 12, 2006.

6. Critical Pathway for the Organ Donor. Available at http://www.unos.org/resources/pdfs/Cri t icalPathwayPoster.pdf. Accessed November, 12,2006.

Mentor: Janet A. Dewan, MS, CRNA

84

its and an EKG showed normal sinusrhythm and a rate of 62. His transthoracicechocardiogram showed mild concentricleft ventricular hypertrophy with an ejec-tion fraction of 60%. He had a MallampatiII airway with full range of motion of hisneck. The patient was premedicated withmidazolam 1 mg in the preoperative hold-ing area.

The patient was brought to the OR wherehe assumed a sitting position on the ORtable. Once positioned, an additional 1mgof midazolam was administered. Routinemonitors were placed and a total of 750 ccof LR had been infused by this time.Landmarks were confirmed, appropriatesterile skin preparation and draping wereperformed, and local anesthetic was infil-trated at the L3-4 interspace. An epiduralneedle was placed into this interspace and aloss of resistance was confirmed througheasy injection of normal saline. Following anegative aspiration test, a test dose of 2%lidocaine with epinephrine, 2 cc, wasadministered with no changes in heart rateor blood pressure noted. Depodur® 10 mgwas then administered into the epiduralspace and the needle was withdrawn. Thepatient tolerated the procedure well andwas assisted to the supine position on theOR table.

General endotracheal anesthesia wasinduced with lidocaine 80 mg, propofol 200mg, vecuronium 7 mg, and fentanyl 50 mg.Ertapenum 1G was administered over 10minutes for antibiotic prophylaxis.Anesthesia was maintained with isoflurane0.8-1.2% with air and oxygen at 1.5L/minflows each. A heated air blanket was placedover the patient’s upper extremities and anesophageal temperature probe was placedinto the esophagus. Fentanyl was adminis-tered over the course of next two hours to a

total of 200 mcg. Neuromuscular blockadewas maintained with additional vecuroni-um. The total amount of vecuronium usedduring the case was 15 mg.

Approximately 2 hours into the case, thepatient became hypertensive with bloodpressures reaching 190/96 while thepatient’s heart rate remained between 45-65bpm. An additional 300 mg of Fentanyl wasgiven over 30 minutes. Blood pressuresremained unchanged. The fraction ofinspired isoflurane was also increased buthad little effect on the patient’s blood pres-sure or heart rate. Hydralazine, 20 mg, wasgiven in 5 mg increments over 1.5 hours.The patient’s blood pressure returned tobaseline and his heart rate remained at 50-60 bpm.

A total of 4200 cc of LR was infused overthe case. Blood loss was 100 cc and urineoutput was 250 cc. A total of 500 mcg of fen-tanyl was given over the course of the case.Ondansetron, 4 mg, was given at closing.Bupivacaine was injected to the incision bythe surgeon. Full muscle relaxant reversalwith neostigmine and glycopyrrolate wasadministered with a return of four twitchesand sustained tetany after seven minutes.Upon emergence, the patient was breathingspontaneously, opened his eyes, and fol-lowed verbal commands. His oropharynxwas suctioned and endotracheal extubationwas completed under positive pressure.

The patient was transported to PACU withoxygen administered via face mask. Thepatient remained comfortable in PACU andrequired small amounts (50 mcg/per admin-istration) of fentanyl for the first few hoursof his postoperative period. He was trans-ferred to the floor where he reported mildpain over the next 48 hours and requiredminimal amount of additional narcotics.After a two week hospital stay complicated

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by hematuria, suspicions of an anastomoticleak, delay in starting nutrition,hypokalemia, atrial flutter, and eventualTPN bridging to a regular diet, the patientwas discharged to a rehabilitation facility.

Discussion

Epidural anesthesia and peripheral nerveblockade are widely used in the UnitedStates to achieve the goal of regional anes-thesia and analgesia. In a prospective studyof 5969 surgical patients over 7 years, ahigh mean score of 8.5 out of 10 wasreported when patients were questionedabout satisfaction with neuraxial opioidanalgesia.3

Epidural morphine has long been adminis-tered by single and intermittent bolus injec-tion, continuous infusions, and PCA for themanagement of postoperative pain.Although single dose injection of conven-tional morphine affords up to 24 hours ofpain relief, this can sometimes prove insuf-ficient for patients having major surgery. Astudy found a 7-fold decrease in IV PCAfentanyl use in patients treated with epidur-al Depodur® when compared to convention-al epidural morphine.1,2 Epidural PCAsrequire an indwelling catheter that can limitmobility, carry the risk of infection, andlimit the use of anticoagulants for fear ofpossible epidural hematoma formation.1

Preoperative administration of Depodur®

provides up to 48 hours of pain controlpostoperatively suggesting that patientscould essentially be transitioned directly tooral analgesics; thus leading to reduction incosts stemming from drug cost, infusionsets and devices, and pain service time.2

Depodur® consists of microscopic liposo-mal particles containing chambers thatencapsulate preservative-free morphine.Following injection, under physiological

conditions, the liposomes break down byerosion of the lipid membranes and slowlyrelease the morphine over 48 hours.Morphine then slowly crosses the dura anddiffuses to the cerebrospinal fluid produc-ing high regional and low systemic drugconcentrations.1-3,5 A one time dose of 10 mg for Depodur® results in lower sys-temic concentrations of the drug, resultingin decreased severity of systemic adverseeffects such as nausea, sedation, and consti-pation.1,53,4

Recommendations for dosages of Depodur®

epidural injection include 10 mg for cesare-an delivery, 10-15 mg for lower abdominalor pelvic surgery, and 15 mg for majororthopedic surgery of lower extremities.1

Generally, elderly and debilitated patientsshould be given dosages on the lower endof recommendations.2

It is important to note that Depodur® is indi-cated for postoperative pain management,so the patient must have adequate narcoticgiven throughout the initial hours afterinjection and during surgery. Careful attention must be given to avoid long actingnarcotics, such as additional morphine orhydromorphone, as the peak plasma con-centration may coincide with the start ofDepodur® breakdown possibly leading toundue sedation, respiratory depression, orhypotension. The time to first request foradditional analgesics varies widelythroughout the research with median timesof approximately 3-21 hours. The mostcommon adverse affects include pruritisand nausea.1-4

In conclusion, single dose epidural injection of Depodur® can provide clini-cians a valuable new option in the manage-ment of patients with pain after majorabdominal surgery.2 It can provide painrelief for up to 48 hours following surgery,

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Keywords: obstruction, airway, pul-monary edema, postoperative, anesthesia

Tonsillectomy and adenoidectomy (T&A)surgery is performed an estimated 750,000times a year in the United States for sever-al conditions including airway obstruction,sleep apnea, and persistent abscesses orthroat infections.1 Approximately 70% ofthese surgeries are performed on children.2

There exists a potentially serious complica-tion termed postobstructive pulmonaryedema (POPE), which is acute and severein onset. POPE can follow an acute airwayobstruction (commonly known as negativepressure pulmonary edema) or the surgicalrelief of a chronic airway obstruction in

otherwise healthy patients.3 The followingcase report describes the anesthetic care, postoperative course and clinical considerations for an adult patient undergo-ing T&A with the potential for develop-ment of POPE.

Case Report

A 26 year old female with a BMI of 42.5(weight 102 kg and height 152.5 cm) and arecent history of obstructive adenotonsillarhypertrophy presented for partial inferiorturbinectomy with T&A. Her recent com-plaints included shortness of breath onexertion, snoring, recent weight gain andconstant daytime fatigue. A sleep study to

Potential for Postobstructive Pulmonary EdemaAngela D. Ewers, B.S.N.Texas Christian University

although supplemental narcotics are oftenrequired in the immediate post operativeperiod. The need for rescue medication isminimal, analgesic gaps are few, and a one-time injection avoids the need for cathetersand pumps.3 A single epidural injection canlower opioid requirements and possiblyshorten the postoperative hospital stay bydecreasing complications and side effectsof high dose parenteral opioid therapy orepidural PCA with indwelling catheters.2,3

References

1. Pasero C, McCaffery M. Extended-release epidural morphine (Depodur). JPeriAnesthesia Nursing. 2005; 20:345-350.

2. Gambling D, Hughes T, Martin G, et al. A comparison of Depodur, a novel,single-dose extended-release epidural

morphine, with standard epidural morphine for pain relief after lower abdominal surgery. Anesth Analg. 2005; 100: 1065-1074.

3. Viscusi E. Emerging techniques in the management of acute pain: epidural analgesia. Anesth Analg. 2005; 101: S23-S29.

4. Viscusi E, Martin G, Hartrick C, et al. Forty-eight hours of postoperative pain relief after total hip arthroplasty with a novel, extended-release epidural morphine formulation. Anesthesiology. 2005; 102: 1014-1022.

5. Viscusi E, Kopacz D, Hartrick C, et al. Single-dose extended-release epidural morphine for pain following hip arthroplasty. Am J Ther. 2006; 13:423-431.

Mentor: Janet A. Dewan, MS, CRNA

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evaluate for obstructive sleep apnea (OSA)had not been performed Significant historyincluded 1/2 pack/day smoking for tenyears and untreated gastro-esophagealreflux disease. An ASA physical status of 3was assigned, and her airway classificationwas Mallampati class 3 with normal neckrange of motion and thyromental distanceof three fingerbreadths. Examination of theoropharynx revealed enlarged and inflamedtonsils. The patient received famotidine 20mg and metoclopramide 10 mg by mouthpreoperatively. Pre-induction vital signs:blood pressure of 134/67 mmHg, sinusrhythm 89 beats/min, and room air oxygensaturation of 97%.

Upon arrival to the operating room (OR),the patient was positioned on the OR tablewith her head, neck and shoulders alignedin the sniffing position. The table wasplaced in reverse Trendelenburg, standardmonitors were applied, oxygen was admin-istered via mask at 10 liters/minute for 5minutes and fentanyl 100 mcg was admin-istered. A rapid sequence induction tech-nique with cricoid pressure was then per-formed using rocuronium 3 mg, lidocaine60 mg, propofol 180 mg, and succinyl-choline 100 mg. Oral tracheal intubationwas accomplished with ease, end-tidal CO2

and bilateral breath sounds were confirmed.Anesthesia was maintained with an end-tidal sevoflurane of 2.2-2.4 % while thepatient maintained spontaneous respira-tions with tidal volumes of 0.4-0.55 liters ata rate of 16-18 breaths/min. 1500 milliliterslactated ringers solution was infused and anestimated blood loss of less than 10 milli-liters was noted.

At the conclusion of surgery, the patientwas breathing spontaneously but not yetresponding to commands. She was trans-ported to the post anesthesia care unit(PACU) with the endotracheal tube in place

connected to flow-by oxygen. Vital signswere: blood pressure 128/77 mmHg, sinusrhythm 69 beats/min, respiratory rate 16breaths/min, oxygen saturation 91%, andtemperature 36.7 degrees Celsius. Uponarrival in the PACU lidocaine 100 mg andfentanyl 50 mcg were administered intra-venously. Approximately ten minutes afterarrival, the patient was noted to be calm,alert and responding to verbal commands.Oxygen saturation was 96% and breathsounds were clear to auscultation and equalbilaterally. The trachea was extubateduneventfully with no significant change invital signs. She maintained a stable respira-tory pattern with no coughing. The patientwas discharged home four hours later with-out complications.

Discussion

Anesthesia professionals are acutely awareof negative pressure pulmonary edemawhich is described in the literature as Type1 (POPE 1), while the less commonlyknown post-surgical relief pulmonaryedema is known as Type 2 (POPE 2).3

Presenting signs and symptoms for both arethe same: pink frothy sputum, tachypnea,tachycardia, rales, oxygen desaturation, andpossibly alveolar infiltrates appearing as“whited out” areas on a chest radiograph. 3,4

POPE 1 occurs from 60 minutes after theobstructive event up to six hours later.POPE 2 develops soon after the relief of achronic airway obstruction and can occurwith tracheal intubation as well as surgicalintervention.3 One report describes a 5 yearold, healthy female admitted for T&A totreat chronic airway obstruction that developed acute pulmonary edema immedi-ately following intubation and precedingthe start of surgery.5 Surgery was cancelledand the patient transferred to pediatricintensive care for mechanical ventilationand treatment.5

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The pathophysiology of POPE 2 is associ-ated with changes in respiratory mechanicscaused by a chronic airway obstruction.Chronic obstruction creates a “compensat-ed” state where inspiratory and expiratorypressures are elevated; this is termed“intrinsic positive-end-expiratory-pressure(PEEP).”5,6 Higher negative intrathoracicpressure on inspiration increases venousreturn and ultimately, pulmonary blood vol-ume.5 This is counter balanced by higherexpiratory pressure. This induces positivepleural and alveolar pressures that subse-quently decrease the pulmonary blood vol-ume. This is termed the “expiratory gruntmechanism.”5 With relief of the airwayobstruction, the “grunt” is removed andintrathoracic pressures suddenly drop, fol-lowed by an abrupt increase in venousreturn.6 The consequence of increasedvenous return and pulmonary blood volumeis increased hydrostatic pressure, whichleads to pulmonary edema as transudationof fluid occurs from capillaries to alveoli.

The goals of anesthetic management forpatients undergoing T&A for chronic air-way obstruction are early recognition andprompt treatment of POPE 2. The clinicalpicture of POPE 2 can be mistaken forother postoperative respiratory problems. Ahelpful, though not necessarily preventivemeasure is careful management of fluidbalance during the intraoperative period toavoid over-hydration.6 If signs and symp-toms of POPE 2 develop shortly after reliefof a chronic obstruction, treatment includesoxygen, ventilatory support, and possiblydiuretics.3,6 Positive pressure ventilation isprovided in the form of continuous positiveairway pressure or mechanical ventilationwith PEEP, whichever accomplishes ade-quate oxygenation.6 Careful assessment ofairway patency is vital if the trachea hasbeen extubated; re-intubation may be nec-

essary. With prompt treatment, POPE 2 isgenerally resolved without complications.

The patient in this report was closely monitored for symptoms of pulmonaryedema after intubation and again at the con-clusion of surgery with no development ofuntoward effects. Anesthetic timing andinterventions were directed at providing asmooth emergence and a safe extubation.T&A surgery is commonly performed onadults and children for chronic airwayobstruction and the incidence of POPE 2 isdifficult to ascertain. Studies of pediatricpatients undergoing T&A have shown anincidence ranging from 9.4 to 44%.3 Thefrequency at which this procedure is per-formed dictates a need for anesthesia pro-fessionals to be prepared to identify andrespond to POPE 2. Awareness facilitatesprompt recognition and treatment.

References

1. Nekhendzy V. Tonsillectomy and/or adenoidectomy. In: Jaffe RA, Samuels SI. eds. Anesthesiologist’s Manual of Surgical Procedures. 3rd ed. Philadelphia: Lippincott Williams & Wilkins; 2004: 143-146.

2. Encyclopedia of surgery: tonsillectomy. Available at: www.answers.com/topic/tonsillectomy. Accessed Oct 1, 2006.

3. Van Kooy MA, Gargiulo RF. Postobstructive pulmonary edema. Am Fam Physician. 2000;62:401-404.

4. Thomas CL, Palmer TJ, Shipley P. Negative pressure pulmonary edema after a tonsillectomy and adenoidectomy in a pediatric patient:case report and review. AANA J.1999;67:425-430.

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Keywords: transurethral resection,prostate, hyponatremia, anesthesia

Transurethral resection of the prostate(TURP) is the most effective endoscopicsurgical procedure for treatment of benignprostatic hyperplasia (BPH) and is per-formed approximately 100,000 times ayear.1 BPH is the most common benigntumor in men. The prostate is positionedsuch that hypertrophy of the gland cancompress the urethra and cause urinaryretention. BPH is responsible for the major-ity of urinary symptoms in men over theage of 50 and results in the need for prosta-tectomy in approximately one-third of allmen who live to age 80.2

Case Report

A 64 year-old male, ASA class II, height180 cm, weighing 66.5 kilograms, present-ed for a TURP. The patient’s past medicalhistory revealed a history of BPH and uri-nary retention despite medical treatment.The patient reported taking dutasteride andtamsulosin for treatment of BPH with noallergies to medications. Lab work revealedhemoglobin 14.3 g/dL, hematocrit 43.0%and sodium 141 mEq/L. Surgical historyincluded cystoscopy and bladder biopsytwo months prior. The patient arrived from

the pre-operative holding area with a 20 gIV in the right hand with lactated Ringer’sinfusing. Standard monitors were applied inthe operating room. Baseline vital signswere blood pressure 120/49 mmHg, pulse68 bpm, temperature 35.7o C and room air oxygen saturation of 100%. After 5 minutesof preoxygenation with 100% O2, thepatient was induced with fentanyl 100 mcg,lidocaine 40 mg, propofol 150 mg androcuronium 40mg intravenously (IV).Atraumatic endotracheal intubation wassuccessful on the first attempt.Endotracheal tube placement was con-firmed by chest rise and fall, the presenceof CO2 waveform and auscultation of breathsounds bilaterally. A warming blanket wasapplied at 43o C. Mechanical ventilationwas initiated with tidal volume 550 ml andrate of 8 per minute. Peak inspiratory pres-sures ranged from 16 to 22 mmHg.Anesthesia was maintained with > 1 MACsevoflurane and oxygen delivered at 2L/min. Pulse oximetry remained at 100%.

During the procedure the surgeon com-plained of continued blood loss and a largeprostate weighing approximately 50 Gm.Blood loss was immeasurable due to theuse of a floor drain for blood and irrigationevacuation. Approximately 2 hours follow-ing induction the circulating nurse reported

Hyponatremia Associated with Transurethral Resection of the Prostate (TURP)Brandi L Lane, B.S.N.

Texas Christian University

5. Feinberg AN, Shabino CL. Acute pulmonary edema complicating tonsillectomy and adenoidectomy. Pediatrics. 1985;75:112-114.

6. Motamed M, Djazaeri B, Marks R. Acute pulmonary oedema complicating adenotonsillectomy for obstructive sleep apnoea. Int J Clin Pract. 1999;53:230-231.

Mentor: Nelson L. Strother, CRNA, BS

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that 3-liter bags number 13 and 14 ofglycine had been brought into the room.Temperature was 33.0o C. Blood was drawnand sent to the lab for a sodium level. Labresults revealed a sodium level of 104mEq/L. An 18g intravenous catheter wasinitiated in the left forearm and additionalblood was drawn and sent to lab for hemo-globin, hematocrit and a repeat sodiumlevel. Lab results were hemoglobin 10.7mg/dL, hematocrit 33.1% and hyponatrem-ia was confirmed with a sodium level of106 mEq/L. Furosemide 80 mg IV wasgiven. Lactated Ringer’s was discontinuedand 3% NaCl was initiated at 106 ml/hr inthe operating room. The surgery was com-pleted; midazolam 2.5 mg and rocuronium30 mg IV were given. The patient remainedintubated and was transported to the postanesthesia care unit (PACU) with ambu bagand 100% supplemental oxygen. Thepatient was placed on a ventilator with settidal volume 600 ml, rate 8 per minute, and50% FiO2. Post anesthesia care unit(PACU) temperature was 34.1o C. A fullbody bear hugger was applied and 3% NaClwas placed on a pump at 105 mL/hr. Threehours postoperatively the sodium level was112 mEq/L and urine output was greaterthan 2 liters. 3% NaCl was discontinuedand furosemide 40 mg IV was administeredand the patient was extubated. Neurologicalassessment revealed a patient that wasawake, alert and oriented x 3 followingextubation. The patient was admitted to theintensive care unit (ICU) for further 3%NaCl and observation. Six hours postopera-tively the patient received 200 mL of 3%NaCl and furosemide 40 mg IV. 10 hourspost operative the sodium level was 118.The 3% NaCl was discontinued andfurosemide 40 mg IV was administered.The sodium level 22 hours post operativelywas 126 mEq/L. The patient was trans-ferred to the urology unit for additional labs

where he made a full recovery.

Discussion

Hyponatremia during TURP is commonwith serum sodium concentration decreasesof 6 to 54 mEq/L having an incidence rang-ing from 7% to 26%.3 Hyponatremia duringTURP occurs due to the absorption ofhypotonic irrigation solution. Absorptionhappens as surgical resection opens the pro-static venous plexus allowing irrigationfluid to be absorbed into the systemic circu-lation or it is absorbed from the retroperi-toneal space.3 The amount of fluid that isabsorbed depends on the length of the sur-gical resection time, the height of the irriga-tion bag above the patient, the vascularityof the prostate and amount of irrigationfluid used. It has been estimated that 10 to30 mL of fluid is absorbed per minute ofresection time.4 Gravenstein recommendslimiting the height of the irrigation bag to40 cm above the prostate to minimize theabsorption of irrigation fluid.3

Some anesthesia professionals believe thatregional anesthesia is advantageous forpatients undergoing TURP to allow assess-ment of mental status as an indicator ofearly sodium changes.5 Patients undergoinggeneral anesthesia are unable to show thecentral nervous system (CNS) signs ofhyponatremia such as confusion, nauseaand convulsions. After a risk and benefitdiscussion of general versus regional anes-thesia the patient in this case decided ongeneral anesthesia for this procedure. Inthis case regional anesthesia may haverevealed early CNS changes prompting anassessment of serum sodium.

It has been proposed that hypoosmolarity,not hyponatremia is the primary physiolog-ical cause of CNS dysfunction associatedwith TURP. The blood-brain barrier is not

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permeable to sodium, but is freely perme-able to water. Studies on hippocampalslices in rats have revealed that neuronswith low sodium concentrations and normalosmolality have normal neuronal excitabil-ity.3 Regardless of the physiological causeof symptoms; treatment goals are to nor-malize the serum sodium and osmolality.Management includes the use of diureticsto decrease the fluid volume, fluid restric-tion and initiation of 3% NaCl for rapidcorrection of hyponatremia. Care must betaken to prevent central pontine myelinoly-sis (CPM), which results from rapid correc-tion of hyponatremia leading to brain dehy-dration and separation of the myelin sheathfrom axons in the brain.3 In symptomaticpatients it is recommend to correct hypona-tremia at a rate of 1.5-2.0 mEq/L per hourfor 3 to 4 hours or for the duration of symp-toms, but not to exceed 8-10 mEq/L in thefirst 24 hours. Asymptomatic patientsshould be corrected at a rate of less than 0.5mEq/L per hour not to exceed 8-10 mEq/Lin the first 24 hours.6 Treatment is alsoaimed at controlling seizure activity withbenzodiazepines. In this case administra-tion of diuretics and 3% saline were initiat-ed to normalize serum sodium and midazo-lam was chosen for sedation to raise thethreshold for seizure activity. The patient inthis case was at high risk for altered mentalstatus and seizure activity, leading to thedecision to keep the patient sedated, intu-bated and on a ventilator to correct serumsodium prior to extubation.

Hyponatremia is a rare but life threateningcomplication of TURP that requires a highindex of suspicion, early recognition andprompt treatment. Treatment should be ini-tiated quickly whether it is hypertonicsaline or diuresis. Anesthesia practitionersmust be aware of the high-risk situation andbe vigilant about observing the patient forsigns and symptoms of hyponatremia.

References

1. Issa MM, Young MR, Bullock AR,Bouet R, Petros JA. Dilutional hyponatremia of TURP syndrome: A historical event in the 21st century. Urology. 2004;64:298-301.

2. O’Hara JF, Cywinski, JB, Monk TG. The renal system and anesthesia for urological surgery. In: Barash PG,Cullen BF, Stoelting RK. eds. Clinical Anesthesia. 5th ed. Philadelphia:Lippincott Williams and Wilkins; 2006:1026-1029.

3. Gravenstein D. Transurethral resection of the prostate (TURP) syndrome: A review of the pathophysiology and management. Anesth Analg.1997;84:438-446.

4. Porter M, McCormick B. Anesthesia for transurethral resection of the prostate (TURP). World Anesthesia. [serial on the Internet]. 2003;16(8):2 . Available at: http://www.nda.ox.ac.uk/w f s a / h t m l / u 1 6 / u 1 6 0 8 _ 0 1 . h t m . Accessed Oct. 16, 2006.

5. Lynch M, Anson K. Time to rebrand transurethral resection of the prostate? Curr Opin Urol. 2006;16:20-24.

6. Green SM. Tarascon Pocket Phamacopoeia. 7th ed. Lompoc, CA:Tarascon; 2005.

Mentor: Kristy Beaver, CRNA, MSN

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General Anesthesia in a Patient with History of Acute Intermittent PorphyriaChad A. Hinton, B.S.N.

University North Carolina, Greensboro

Keywords: anesthesia, porphyria, stress,trigger

Acute intermittent porphyria is a rareinborn error of metabolism that can be lifethreatening.1 Acute intermittent porphyriaoccurs in about 1 in 10,000 in the generalpopulation.2 Acute intermittent porphyriaproduces serious symptoms such as sys-temic hypertension and renal dysfunction.1

Hypertension and renal failure are the mostcommon causes of death in the patient withporphyria.3 There is a possibility of trigger-ing an attack of acute intermittent porphyr-ia, with the use of enzyme-inducing drugsthat are often used in anesthesia. Therefore,it is essential to select drugs that are safe foruse in the presence of acute porphyria. Thefollowing case report discusses the care of apatient with acute intermittent porphyriaundergoing an anterior and posterior lum-bar fusion.

Case Report

A 52 year old, 61 inch tall, 92 kg. male pre-sented for an anterior and posterior L4-5,L5-S1 spinal fusion. He had a history sig-nificant for acute intermittent porphyriawith acute episodes in 1998 and 2005.Although the triggering events for the acuteepisodes were unknown he had had previ-ous surgery with no complications. He hadan allergy to cefadroxil which includedgeneralized swelling and throat closure.Preoperative vital signs were blood pres-sure 119/72 mmHg, heart rate 70 bpm, res-pirations 18, oxygen saturation 96%, andtemperature 98.6°F. His bilateral breathsounds were clear. He had had previousposterior lumbar surgery with no anesthesia

complications. The anesthesia airway eval-uation revealed a Mallampati Class II air-way with normal, 3 finger- breadths mouthopening, atlanto-occipital range of motion,and a thyromental distance of greater thanthree finger- breadths.

He was given midazolam 2 mg IV andtaken to the operating room. In the operat-ing room, he was given additional midazo-lam 1 mg and fentanyl 200 mcg in 100 mcgdoses IV. He was preoxygenated with 100%oxygen by face mask and standard monitorswere applied. Rocuronium 5 mg IV wasgiven for defasciculation. General anesthe-sia was induced with lidocaine 80 mg andpropofol 150 mg IV. Mask ventilation wasconfirmed and succinylcholine 140 mg IVwas given followed by an atraumatic endo-tracheal intubation with an 8.0 mmID endo-tracheal tube under direct laryngoscopy. Aright radial arterial line and additional 14gauge peripheral IV were then started.

General anesthesia was maintained withone liter per minute (L/m) oxygen, 1 L/mair, and 1% isoflurane. Neuromuscularblockade was maintained throughout theprocedure using vecuronium. Bispectralindex monitoring was used with readingsbetween 37 and 55 during the procedure.The patient received an additional 200 mcgfentanyl in 100 mcg doses prior to incision.After incision the heart rate increased to 90bpm and blood pressure rose to 160/90mmHg. Additional doses of fentanyl wereadministered during the procedure to a totalof 2250 mcg. His heart rate was maintainedat approximately 70 bpm and blood pres-sure in the 100-120/50-70 mmHg range.Urine output was monitored continuously

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via Foley catheter with the urine remainingclear yellow and the minimum hourly out-put being 0.86 ml/kg.

At the end of the procedure muscle relax-ation was antagonized with neostigmineand glycopyrrolate and the trachea wasextubated. Upon extubation, the patient’sheart rate was approximately 90 bpm andhis blood pressure was 140/80 mmHg. Hewas given 10 mg of morphine in 2 mgincrements. The heart rate and blood pres-sure remained elevated, and he was given atotal dose of esmolol 30 mg followed bylabetalol 10 mg. His heart rate decreasedinto the 70's and blood pressure to 140/80mmHg. He was then taken to the recoveryroom and was subsequently discharged tohome on postoperative day six.

Discussion

Porphyria usually remains subclinical untilan endogenous or exogenous stress triggersa porphyria crisis.2 Surgery is a stressfulevent that can trigger a porphyria crisis. Thedegree of stress associated with surgery isassociated with the amount of painful stimuli imposed during the procedure suchthat a larger, more painful surgery gener-ates/induces a greater stress response than asmaller minor surgery. Fentanyl was usedthroughout this procedure in order controlpain and reduce the stress response whichcould have triggered a porphyria crisis.Additionally, some medications used in thepractice of anesthesia such as barbiturates,etomidate, and glucocorticoids can triggeran attack. If a triggering agent is adminis-tered, and an attack occurs, the mortalityrate is 10-40%.4 The anesthetic plan for thispatient was developed with the goal of pre-venting an attack by avoidance of triggeringmedications.

In order to avoid triggering an acute attack,the plan was developed using recommenda-tions for use of drugs in the presence ofacute porphyrias reported by Stoelting.1

Fentanyl, lidocaine, propofol, and succinyl-choline are all listed as safe drugs to admin-ister to a patient with acute porphyria.Midazolam, rocuronium, isoflurane, andvecuronium are all listed as probably safeand unlikely to provoke acute porphyria.

The two leading signs and symptoms of anacute attack of porphyria are abdominalpain and dark urine. This patient, havingbeen under general anesthesia, was unableto indicate the presence of abdominal pain.After emergence, if he had an attack, itwould have been difficult to differentiatethis from incisional pain due to the anteriorapproach used for the lumbar fusion. Thispatient's urine flow remained greater than0.5 ml/kg throughout the case and was clearyellow. Additional signs and symptoms ofan acute attack of porphyria include vomiting, anxiety, confusion, autonomicinstability manifested by hypertension andtachycardia, dehydration and electrolytedisturbances such as hyponatremia,hypokalemia, and hypocalcemia.5 Thispatient’s sodium, potassium, and calciumwere checked twice during the course of thesurgery with normal values maintainedthroughout.

If this patient had developed an acuteepisode of porphyria there are severalimportant steps involved in treating a crisis.First, any known porphyria triggers must beremoved. Second, symptoms such as tachy-cardia, hypertension and electrolyte imbal-ances must be treated, adequate hydrationmust also be maintained. It is important tonote that if seizures occur they must betreated with benzodiazepines as other anti-convulsants are unsafe to use with porphyr-

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ia.1 Last, in an effort to suppress ALA syn-thetase activity hematin 3 to 4 mg/kg IVover 20 minutes can be administered.1

This case report illustrates the importanceof a thorough preoperative evaluation.Knowing that this patient had a history ofacute intermittent porphyria, it was possibleto develop an individual anesthetic plan tosafely perform anesthesia without trigger-ing an acute attack. If this patient needsadditional surgery in the future, anesthesiacan be safely administered if the anesthesiapractitioner is informed of the history ofporphyria during the preoperative evalua-tion and an appropriate anesthesia plan isthen followed.

References

1. Stoelting RK, Dierdorf SF. Anesthesia and Coexisting Diseases. 4th ed. New York: Churchill Livingstone; 2002:455-460.

2. Miller RD. Miller’s Anesthesia. 6th ed. New York: Churchill Livingstone; 2005:749.

3. James MFM, Hift RJ. Porphyrias. Br J Anaesth. 2000;85:143-153.

4. Kouppinen R. Porphyrias. Lancet. 2005;365:241-252.

5. Jenson NF, Fiddler DS, Striepe VM. Anesthetic Considerations in Porphyrias. Anesth Analg. 1995; Mar.80:591-599.

Mentor: Nancy Bruton-Maree, CRNA,MS

Uterine Rupture in the Unscarred UterusAlison Daly, B.S.N.

University of Pennsylvania

Keywords: anesthesia, uterus, rupture,pregnancy, complication

Severe postpartum hemorrhage remains aleading cause of maternal morbidity andmortality.1,2 Uterine rupture reportedlyoccurs in 1 in 2500 to 5000 deliveries.3 Theleading cause of uterine rupture is a previ-ous uterine scar. The incidence of uterinerupture in a previously unscarred uterus is 1in 15,000 to 20,000.2,4 High parity, induc-tion of labor, and augmentation of uterinecontractions with oxytocin increase the riskof spontaneous uterine rupture in theunscarred uterus.2,4 A large amount of bloodis lost very quickly following uterine rup-ture. The patient is at increased risk for

many complications including hemorrhagicshock and myocardial ischemia.1

Case Report

A 31 year old female (gravida 7, para 7)presented to the operating room for emer-gency laparotomy and possible hysterecto-my. The patient had just vaginally deliveredher seventh child complicated by an esti-mated blood loss of 1500-2000 mL. Thebleeding was refractory to repeated dosesof hemabate, methergine, pitocin, andmisoprostol. The patient had no knowndrug allergies. Her medical history was sig-nificant for anemia; hemoglobin was 8.2g/dL on admission. All pervious deliverieshad been uncomplicated vaginal births and

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there was no history of uterine surgery. Therepeat hemoglobin reported on arrival to theoperating room was 1.7 g/dL, which wasrepeated to confirm.

The patient was awake and oriented onarrival to the operating room. Heart ratewas 85 bpm and blood pressure was110/60. The patient had two well function-ing 18 g peripheral IV’s for intravenousaccess. The second unit of PRBC’s wasinfusing. A rapid sequence induction withsuccinylcholine 100 mg, propofol 150 mg,and cricoid pressure was performed. A 7.0ETT was placed under direct laryngoscopyto secure the airway and allow for mechan-ical ventilation. The patient tolerated induc-tion remaining hemodynamically stable.Anesthesia was maintained with 6% desflu-rane, vecuronium and fentanyl. Six units ofplatelets were infused immediately follow-ing induction and additional blood productswere ordered. A Baer Hugger® and fluidwarmer were used to maintain normother-mia.

Visualization of the uterus revealed rupturewith possible dissection of the bladder cuff.Urology was consulted to evaluate bladderintegrity. The patient had an indwellingFoley catheter and at this time was anuric,further evaluation was needed to determineif the cause was bladder injury or hypov-olemia.

Vital signs remained stable. Ephedrine andphenylephrine were administered to main-tain a systolic blood pressure greater than100 mm Hg while maintaining a heart rateof 60-100. A third and forth unit of PRBC’sand two units of FFP were administered. A20 g left radial arterial line was inserted forcloser blood pressure measurement andblood gas analysis. After the fourth unit ofPRBC’s the repeated hemoglobin was 6.8g/dL with a hematocrit of 22%.

Urology found the bladder to be unharmed.After completion of a supracervical hys-terectomy, hemostasis was achieved andsurgical closure initiated. The total bloodloss including the preoperative hemorrhagewas estimated to be four liters. A total of sixunits of PRBC’s, four units of FFP, two six-packs of platelets, 250 ml of 5% albumin,and three liters of crystalloid were adminis-tered. The final intraoperative hemoglobinwas 9.0 g/dL. The patient was taken to thesurgical intensive care unit chemically par-alyzed and mechanically ventilated. APropofol infusion was initiated to maintainsedation and allow for continuation ofmechanical ventilation. The patient wasevaluated for disseminated intravascularcoagulation which was ruled out.

Discussion

On arrival in the surgical suite, the patientwas awake and oriented and did not showsigns of myocardial ischemia that wouldhave been expected with a hemoglobin of1.7 g/dL. Patients with such dramatic bloodloss, even without cardiac disease, are atrisk for myocardial ischemia. Hemorrhagicshock may also lead to circulatory collapse.Fortunately transfusion was initiated quick-ly and this did not occur.1 Careful manage-ment of hemodynamics are imperative tothe outcomes associated with hemorrhage.Karpati et al. found that parturients experi-encing postpartum hemorrhage, high heartrate, low blood pressure, and low hemoglo-bin were the greatest indicators of myocar-dial ischemia.1 Recognition of these find-ings is important because parturients areoften healthy and not considered to havecardiac risk factors. Close attention to EKGchanges, replacement of blood loss, andmaintaining hemodynamics can improvepatient outcomes.1

The patient’s high parity placed her at

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greater risk of uterine rupture. In a reviewof 5800 parturients, parity of seven andgreater increased the incidence of uterinerupture to twenty times that of lower paritywomen.2,4 Oxytocin even at low dosesshould be used very cautiously in the aug-mentation of labor in women of high parity,historically its use has been associated withuterine rupture.4 Rupture of the unscarreduterus is associated with a higher morbidityand mortality of the mother and child thanin rupture of a scarred uterus.2 In this case,fortunately, both the mother and child weretreated and discharged without any furthercomplications.

The patient delivered vaginally with anepidural for labor analgesia. Diagnosis ofuterine rupture may be delayed because ofthe absence of pain or because pain is asso-ciated with a patchy epidural. Extreme andsudden decelerations in fetal heart rate arethe most indicative sign of uterine rupture.4

Absence of fetal heart rate associated withthe sudden onset of severe abdominal painand excessive vaginal bleeding with cessa-tion of uterine contractions are also com-mon presentations of uterine rupture.4 Thecompletion of vaginal delivery before theonset of bleeding coupled with no historyof uterine surgery were deceptive.Diagnosis was not made until the uteruswas visualized.

Maternal mortality associated with uterinerupture is often accompanied by hemor-rhagic or septic shock, disseminatedintravascular coagulation, renal failure, andpulmonary embolism.4 Fortunately, earlysurgical intervention and transfusion main-tained hemodynamics, coagulation, andresulted in a positive outcome.Consideration should be given to the riskfactor associated with high parity womenreceiving oxytocin to augment uterine con-

tractions and the increased incidence ofuterine rupture.2 Breakthrough pain may bemasked or lessened by analgesic medica-tions administered during labor. An inade-quate epidural block may also be blamedfor the occurrence of abdominal pain asso-ciated with uterine rupture.4 Therefore theanesthetist must be vigilant to changes inthe mother and fetus during the labor anddelivery.

References

1. Karpati PCJ, Rossignol M, Pirot M, et al. High incidence of myocardial ischemia during postpartum hemorrhage. Anesthesiology. 2004; 100:30-36.

2. Ofir K, Sheiner E, Levy A, Katz M,Mazor M. Uterine rupture: differences between a scarred and an unscarred uterus. Am J Ob Gyn. 2004; 191:425-429.

3. Ofir K, Sheiner E, Levy A, Katz M,Mazor M. Uterine rupture: risk factors and pregnancy outcomes. Am J Ob Gyn. 2003; 189: 1042-1046.

4. Siddiqui MN, Ranasinghe, JS. Spontaneous rupture of uterus. J Clin Anesth. 2002; 368-370.

Mentor: Russ Lynn, MSN, CRNA

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Keywords: anesthesia, bougie, tracheo-malacia, larynx, damage

Prolonged mechanical ventilation can becomplicated by laryngeal damage.Although most injuries heal spontaneously,tracheomalacia (TM) is one of the potentiallong term complications.1 Tracheomalaciarefers to softening of the tracheal cartilageresulting in weakness of the tracheal walland premature airway closure during expiration; it can be classified as primary(congenital), or secondary (acquired).Secondary TM is most often a complicationof prolonged intubation, tracheostomy,chronic infection, or chronic inflammation.Symptoms include chronic cough, sputumproduction, and hemoptysis. Diagnosis isoften delayed because it is difficult to dis-tinguish symptoms of TM from those ofemphysema, chronic bronchitis, cigarettesmoking, and/or asthma.2

Case Report

A 44 year old female, 68" tall and 93 kg,presented for removal of a tracheal stent viarigid bronchoscopy. Significant medicalhistory included a previous gunshot woundto the abdomen, chronic renal failure withhemodialysis, hypertension, and tracheo-malacia. Prior surgical history includedtubal ligation, laparotomy, splenectomy,tracheostomy and tracheal silicone stentplacement. Her current medications wereacetylcysteine and amoxicillin. Her preop-erative vital signs were: blood pressure188/87 mmHg; pulse 85 beats per minute;respiratory rate 22 breaths per minute; andtemperature 36.5° C. Laboratory valueswere: hemoglobin 11.6 gm/dl; hematocrit

35%; platelet count 245,000; PT 11.2 sec-onds; PTT 29 seconds; serum potassium4.4 mEq/L; blood urea nitrogen 53 mg/dl;and serum creatinine 3.3 mg/dl. Shereceived hemodialysis the day before sur-gery. Pre-anesthetic physical evaluation ofthe patient was within normal limits exceptfor a chronic moist cough with no dyspneanoted. Airway assessment was within nor-mal limits and revealed a Mallampati IIclassification. She had no range of motionlimitations.

She was placed in the supine position onthe OR table. Standard monitors wereapplied and activated. Oxygen was administered at 100% via facemask. Aremifentanil infusion was initiated at 0.1µcg/kg/minute and propofol infused at 75µcg/kg/minute to a level of sedation sufficient to allow airway instrumentation.Respiration was supported with positivepressure mask ventilation, as needed tomaintain oxygen saturation greater than90%. The OR table was turned 90° to thesurgical field. A nasal cannula was placedto entrain oxygen during bronchoscopy.Remifentanil was titrated up to a maximumof 0.3 µcg/kg/minute, and the propofol wastitrated up to 180 µcg/kg/min. Sevofluranewas added for a short period to provideadditional anesthesia. The surgeon made multiple attempts to instrument thetrachea with the rigid bronchoscope without success.

The surgeon asked to have a laryngealmask airway (LMA) placed to serve as aconduit for a flexible bronchoscope.However, the standard size bronchoscopewould not fit through the LMA. Direct

Use of An Elastic Gum Bougie During Silicone Stent RetrievalSerena Ackerman, B.S.NUniversity of Pennsylvania

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laryngoscopy was then used to place a gumelastic bougie which facilitated instrumen-tation of the trachea with the rigid broncho-scope. The stent was easily retrieved andthe bronchoscope was removed.

Anesthetics were discontinued and an LMAwas placed to maintain adequate ventilationuntil the patient was spontaneously breath-ing and fully awake. The LMA wasremoved and oxygen was delivered bynasal cannula for transport to the post anes-thesia care unit (PACU). Upon arrival to thePACU, the patient was given 30% oxygenvia mist mask. She exhibited signs of air-way irritation and was treated with a lido-caine and albuterol nebulizer treatment andgiven intravenous fentanyl for airway irrita-tion. She was also given ondansetron fornausea and hydralazine for hypertension.The patient’s recovery included lidocainenebulizer treatments at night, saline nebu-lizers during the day, also steroids andantibiotics for 72 hours. She encounteredno episodes of respiratory distress or desat-uration postoperatively and was dischargedfrom the hospital four days later.

Discussion

A gum elastic bougie, also called anEschman stylet or a Sun Med bougie, is atool that is helpful when encountering a dif-ficult airway.3 A gum elastic bougie is along flexible stylet, over which an endotra-cheal tube can be threaded. The bougie’seffectiveness is related to its' angled tip,which can be advanced blindly past theoropharynx and into the trachea. As thebougie's angled tip passes through the rimaglottis, the tip will “bump” along the tra-cheal rings as an additional clue to properplacement.2

Tracheomalacia treatment is directed tosupportive techniques initially. Patients

with premature large airway (tracheal) clo-sure may benefit from stent placement.Stents support the airway wall against col-lapse or external compression.4 Siliconestents are most favored because of theirease of deployment and removal. A rigidbronchoscope is necessary to place andremove silicone stents.2 The rigid broncho-scope is used to instrument the airway bylifting the epiglottis and advancing thebronchoscope through the vocal cords.5

Stent removal is indicated when there is acomplication such as stent migration,chronic infection, marked tissue hyperpla-sia, or when no longer needed.6

Tracheomalacia is not usually associatedwith a ‘difficult airway’ or problems inintubating. In addition, this patient did notpresent with any common conditions pre-dictive of a difficult airway, such as: thyro-mental distance of less than 7 cm, ster-nomental distance less than 12.5 cm, facialdeformity, limited neck extension, or aclass III or IV Mallampati score. In thiscase, the gum elastic bougie was a practicalalternative in the management of an unan-ticipated difficult airway instrumentationwith a rigid bronchoscope. The gum elasticbougie has a reputation for being a usefuland efficient aid in managing an anticipatedor unanticipated difficult airway.8 A gumelastic bougie is listed in the ASA PracticeGuidelines for the Management of theDifficult Airway as a useful strategy toimprove intubation success and diminishairway-related adverse outcomes.9 It canalso be used in reverse order, as describedby Nekhendzy & Simmons, as a exchangedevice from a bronchoscope to an endotra-cheal tube.3 Anesthesia professionals couldbetter serve their patients if they are awareof the usefulness of the gum elastic bougiefor individuals in whom airway instrumen-tation is difficult.

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References

1. Stone DJ, Bogdonoff DL. Airway considerations in the management of patients requiring long-term endotracheal intubation. Anesth Analg. 1992; 2:276-287.

2. Noguchi T, Koga K, Shiga Y,Shigematsu A. The gum elastic bougie eases tracheal intubation while applying cricoid pressure compared to a stylet. Can J Anaesth. 2003; 50:712-717.

3. Nekhendzy V, Simmonds PK. Rigid bronchoscope-assisted endotracheal intubation: Yet another use of the gum elastic bougie. Anesth Analg. 2004; 98:545-547.

4. Puma F, Ragusa M, Avenia N. The role of silicone stents in the treatment of cicatricial tracheal stenosis. J Thorac Cardiovasc Surg. 2002; 120:1064–1069.

5. Jaffe, RA & Samuels, SI. Anesthesiologist’s Manual of Surgical Procedures. 3rd ed. Philadelphia, Pa:Lippincott; 2004:147.

6. Shin, JH, Song, HY, Ko, GY, et al. JVasc Interv Radiol. 2006; 17(4):657-63.

7. Morgan, G, Mikhail, M Murray, M. Clinical Anesthesiology. 3rd ed. New York, NY: Lange; 2002:80-82.

8. Combes X, LeRoux B, Suen P, et al. Unanticipated difficult airway in anesthetized patients: Prospective validation of a management algorithm. Anesthesiology. 2004; 100(5):1146-50.

9. Caplan, RA, Benumof, JL, Berry, FA,et al. 2002. Practice Guidelines for the Management of the Difficult Airway. Developed by the American Society of Anesthesiologists Task Force on Difficult Airway Management.

Mentor: Maria Magro, CRNA, MSN, MS

Pediatric Awake Craniotomy for Pallidal Deep Brain Stimulator (DBS) PlacementPaul A. Gregor, B.S.N.

Columbia University

Keywords: anesthesia, pediatric, cranioto-my, awake, brain stimulator

Dystonia produces slow, twisting, involun-tary muscle movements, affecting both pas-sive and active muscle groups. The patho-physiology is not well understood and mayarise from multiple cerebral structuresincluding the basal ganglia, cerebellum,thalamus, and cortex.1,2 Treatment optionshave included biofeedback, application ofrestrictive braces, injection of acetylcholinereceptor inhibitors such as botulinum toxintype A, or administration of anticholinergic

agents such as trihexyphenidyl. Surgicalintervention involving selective denervationor thalamotomy has also been utilized.Placement of deep brain stimulators fortreatment of dystonia remains under inves-tigation, with approximately 50 implanta-tions completed by 2002.3

Case Report

A 127cm, 41kg 10 year old female present-ed for elective placement of a deep brainstimulator. The procedure was scheduled totreat increasing manifestations of dystonia,

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specifically dysarthria, balance and gaitproblems, and dystonic movements of herextremities. The patient demonstrated significant mobility issues and relatedbeing held back a year at her public schoolsecondary to difficulties with writing. Nocongenital abnormalities were noted andher disorder was not elucidated until several years after birth.

Preoperative examination revealed involuntary muscular contraction of bothupper extremities. The patient’s vital signsand laboratory studies were within normalparameters, and a type and screen wasordered prior to arrival in the OR. Airwayevaluation revealed a Mallampati class IIairway, with full cervical range of motion.Mouth opening was approximately 4cm.Her only medical history was of familialhypercholesterolemia, which was wellcontrolled with simvastatin 10 mg daily.She had no previous surgical history andknown allergies.

The parents consented for anesthesia fol-lowing a significant risk/benefit discussionand formulation of an anesthetic plan. A20G peripheral IV was inserted and 0.9%NS infusion was started in the MRI suite.Standard ASA monitors were placed andO2 via nasal cannula was started at 3L/min.Fentanyl 25 mcg and propofol 30 mg IVwere administered for sedation along withlocal anesthetic to headpin sites during theplacement of a stereotactic head frame. AnMRI study was performed and the patientwas transported to the operating room fullyawake.

In the operating room the patient wasplaced in a sitting position and a transtho-racic Doppler was employed for additionalsafety during the procedure. O2 remainedat 3L/min via nasal cannula. Intraoperativedeep brain neurological monitoringrequired isolation of all electrical circuitry

and the standard anesthesia monitors weredetermined to cause significant electricalinterference, therefore a transport monitorwas used to document patient vital signs.

A dexmedetomidine infusion was initiatedand a loading dose of 0.5mcg/kg IV wasinfused over one hour. Subsequently it wasdecreased to 0.2mcg/kg per hour and utilized to maintain sedation throughout thesurgical procedure. Bupivacaine 0.25% wasinfiltrated in the incisional area and anadditional 50mg of propofol was adminis-tered during creation of the bone flap. Thepatient remained conscious but sedatedthroughout the procedure, and retained theability to follow verbal commands andcomplete tasks as requested. The patient’svital signs were stable throughout the pro-cedure. Following successful mapping andplacement of DBS leads the craniotomywas closed. Bupivacaine local anestheticinfiltration provided additional anesthesiafor the flap and skin incision closure. Thedexmedetomidine infusion was terminated,and the patient was transported to the PICUfor postoperative care. The procedure lasted4 hours and 20 minutes. EBL was 200 mlwith approximately 1300 ml of crystalloidadministered throughout the procedure.Postoperative recovery was uneventful.

Discussion

Deep brain stimulator implantation is a rel-atively new treatment for dystonia whichrequires an awake patient to perform select-ed tasks throughout the pallidal mappingprocedure. Use of neurological monitoringin combination with operative stereotaxisminimizes damage to normal brain tissuewhile identifying target structures.Significant risks include intraoperativeintracerebral hemorrhage in 1-3% of cases,and postoperative infection in approximate-ly 4-5% of patients.4

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Issues regarding pain, patient cooperation,and potential airway obstruction presentmajor impediments to awake craniotomyprocedures. In adults a range of anesthetictechniques usually combining an opioid,droperidol, or propofol, have been utilizedwith various rates of success.5 Few litera-ture references specifically address theanesthetic requirements and approaches toan awake craniotomy in the pediatric popu-lation. Anticipated complications mayinclude pain, vomiting, airway obstruction,respiratory depression and hemodynamicinstability.

Developing a safe and effective anesthesiaplan for a pediatric awake craniotomy pres-ents a significant challenge for the CRNA.Requirements for analgesia, anxiolysis, andsedation must be addressed, yet leave thepatient able to perform crucial neurologicaltesting. Adequate protection of airwayreflexes must be preserved, and depressionof ventilation must be avoided. In addition,the patient must be able to tolerate 4-5hours of an awake procedure.

Patient selection is critical to the success ofplanned anesthesia care for pediatric awakecraniotomy patients. Preoperative patientassessment is of vital importance, and afrank discussion with both the parents andchild regarding the entire operative processis essential.6 All phases should be dis-cussed, emphasizing the need to cooperate,understand, and follow instructions.Distractions and diversions, such as a selec-tion of the patient’s favorite books orvideos, should be explored at this time andprepared before arrival on the day of sur-gery. A patient representative from the hos-pital’s Child Services Department met withthe child on a preoperative visit, then stayedwith the child intraoperatively and read sev-eral stories as a diversion during the longprocedure. Additionally, several back-up

anesthesia plans that afford awake neuro-logical monitoring should be formulatedshould the patient not tolerate the selectedprimary mode of anesthesia.

Dexmedetomidine is a highly selective·adrenoceptor agonist which reliably produces analgesic, sedative, and anesthet-ic-sparing effects.5 It does not directly suppress ventilation, although it may produce obstruction subsequent to relaxation of pharyngeal muscles.Dexmedetomidine’s primary action is aCNS mediated reduction of sympathetictone. Inhibited release of norepinephrinedirectly attenuates excitation within thecentral nervous system, which may in turnproduce both hypotension and bradycardia.However, both receptors remain unaffectedand are able to be activated to treat theseside effects as required.

Dexmedetomidine was selected as the primary anesthetic for this procedure as itprovided the essential elements of analgesiaand sedation, with minimal potential forside effects. Its lack of respiratory depres-sion offered a distinct advantage in dealingwith a pediatric patient. Additionally, itsunique pharmacological profile allowedtitration of a delicate balance between seda-tion and wakefulness that could be rapidlyadjusted as needed. Dexmedetomidine hasbeen shown to produce a sleepy, comfort-able patient that arouses easily to a “calmand alert” state.7 Stimulating portions of theprocedure required administration ofpropofol, a field block by the surgeon, andfentanyl was on hand should additional nar-cotic coverage be required. Additional air-way monitoring was required as additionalsedation was administered. Propofol wasimmediately available, and a #3 LMA wasprepared should the urgent need to convertto a general anesthetic arise.

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Augmentation of the dexmedetomidinewith an opioid infusion was considered,however concern was expressed regarding apotential decrease in patient responsivenesssecondary to fentanyl or remifentaniladministration. A remifentanil/propofolinfusion technique, with its quick metabo-lism and rapid reawakening, was selectedas a back-up anesthetic agent should thedexmedetomidine infusion not be tolerated.

Dexmedetomidine provides an excellentchoice for patient sedation, individually orin combination with a remifentanil infu-sion. Further experience with dexmedeto-midine in pediatric awake craniotomypatients is needed to gain additional data,knowledge, and familiarity with the drug’sutilization and individual’s response.

References

1. McCance K, Huether S. Pathophysiology. 4th ed. St.Louis:Mosby; 2002:472-473.

2. Periut, P. Dystonia. Available at:h t t p : / / w w w . e m e d i c i n e . c o m /Med/topic620.htm. Accessed June 01,2006.

3. Okun MS, Fernandez HH, Foote KD. Am I a Candidate for Deep Brain Stimulation? Available at:http://mdc.mbi.ufl.edu/candidate/candidate-intro.htm. Accessed June 01,2006.

4. Starr PA, Marks W, Clay H. FAQ for Patients: Deep Brain stimulation for Dystonia. Available at:h t tp : / /neurosurgery.medschool .ucsf .edu/patient_care/movement_patientFAQ_dys.html. Accessed June 01, 2006.

5. Ard JL, Bekker AY, Doyle WK. Dexmedetomidine in awake craniotomy: a technical note. Surg Neurol. 2005;63:114-117.

6. Ard JL, Doyle WK, Bekker AY. Awake craniotomy with dexmedetomidine in pediatric patients. J NeurosurgAnesthesiol. 2003;15:263-266.

7. Mack PF, Perrine K, Kobylarz E,Schwartz TH, Lien CA. Dexmedetomidine and neurocognitive testing in awake craniotomy. JNeurosurg Anesthesiol. 2004:20-25.

Mentor: Maribeth Massie, CRNA, MS

Unanticipated Difficult IntubationErika Murphey, B.S.N.

University of Pennsylvania

Keywords: anesthesia, difficult intuba-tion, difficult airway, unanticipated

Unanticipated difficult intubations are asource of significant morbidity and mortal-ity in anesthesia. The incidence of a diffi-cult intubation is 1%-18%, whereas, theincidence of cannot ventilate and cannotintubate is estimated to occur 0.0001%-

0.02%.1 Difficult intubation is defined bythe American Society of Anesthesiologistsas when “proper insertion of the endotra-cheal tube by an individual skilled in air-way management with conventional laryn-goscopy requires more than three attempts,or more than ten minutes.”2 This case reportevaluates an unanticipated difficult intuba-tion and implementation of the difficult air-

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way algorithm to establish endotrachealintubation.

Case Report

A 59 year-old female, ASA II, 5 feet talland weighing 65 kg presented for electivetotal abdominal hysterectomy. Medical his-tory was insignificant. The patient took noprescription medication and all preopera-tive labs were within normal limits.Electrocardiogram revealed normal sinusrhythm. On preoperative examination, thepatient was a Mallampati class II with gooddentition and adequate neck flexion andextension. An 18 gauge peripheral intra-venous catheter was placed and midazolamwas administered.

In the operating room, standard monitorswere placed on the patient. The patient wasdenitrogenated with 100% oxygen. Uponinduction, lidocaine 100 mg, propofol 150mg, fentanyl 100 mcg, and rocuronium 7mg were administered intravenously. Maskventilation was easy with a 9 cm oral air-way in place. Direct laryngoscopy (DL)was performed with a Miller 2 blade by thestudent registered nurse anesthetist(SRNA). A grade 2 airway was visualizedand a 7.0 mmID oral endotracheal tube(ETT) was attempted to be placed withoutsuccess. The patient was then mask venti-lated with 100% oxygen and 2% sevoflu-rane; the pulse oximeter remained 100%. Asecond DL was performed with the head-rest removed, revealing a grade 1 view. Thesecond attempt of ETT placement was alsounsuccessful. The patient was again handmask ventilated with 100% oxygen and 2%sevoflurane. A third and fourth attempt atDL by the CRNA was performed with aMacintosh 3 blade, both with unsuccessfulplacement of the ETT. The patient’s oxygensaturation dropped to 65%, now requiringtwo person mask ventilation. The patient’s

pulse oximeter increased to >90% satura-tion, and a laryngeal mask airway (LMA)size 4 was inserted with ease and the diffi-cult airway cart was called to the operatingroom.

Ventilation and general anesthesia weremaintained with the LMA, 100% oxygenand 2% sevoflurane. Glycopyrrolate 0.2 mgwas administered and the fiberoptic bron-choscope prepared. The LMA was removedand an asleep laryngeal fiberoptic broncho-scope intubation was attempted.Supraglottic edema was evident and thevocal cords were not visualized. Two per-son mask ventilation with a 9 cm oral air-way resumed while a Fast-Trach LMATM

size 4 was prepared. The Fast-Trash LMATM

was inserted followed by successful intuba-tion with a 6.0 mm Fast-TrachEndotracheal Tube TM. Placement was veri-fied with the fiberoptic bronchoscope, bilat-eral breaths sounds, and end tidal carbondioxide. The remainder of the case wasuneventful. General anesthesia was main-tained with 1% isoflurane. A total of 350mcg of fentanyl was administered, as wellas rocuronium 12 mg; decadron 10 mg andkytril 0.1 mg. Neuromuscular blockade wasreversed with neostigmine 4 mg and gly-copyrrolate 0.6 mg at the end of the surgi-cal procedure. The patient met standardextubation criteria and was extubated with-out incidence. On post operative day onethe patient was examined. The patientreported a sore throat, but denied recall ofthe event. The patient was notified of beinga difficult intubation and given a letter forfuture anesthesia reference.

Discussion

The unanticipated difficult intubation canbe managed by understanding and applica-tion of the difficult airway algorithm. Theunanticipated difficult airway can be of

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great consequence as the anesthesia professional would not take the same conservative approach as compared to theobvious difficult airway. Through knowl-edge of the published practice guidelines ondifficult airway management and prepara-tion by practicing airway managementtechniques, the anesthesia professional isable to manage life threatening situationsand the unanticipated difficult airway.

Prevention and preparation for difficult airway management has led to the develop-ment of ASA Practice Guidelines.2 Theguidelines suggest a thorough airwayexamination preoperatively with considera-tion for the possibility for the patient to bedifficult to ventilate, difficult to intubate,difficult with patient cooperation or con-sent, and a difficult tracheostomy. Withconsideration of preoperative examinationfindings, the anesthesia professional deter-mines the appropriate approach to place anendotracheal tube choosing between: 1)awake intubation versus intubation afterinduction of general anesthesia, 2) use ofnoninvasive techniques for the initialapproach to intubation versus the use ofinvasive techniques (surgical or percuta-neous tracheostomy or cricothyrotomy) and3) preservation of spontaneous ventilationduring intubation attempts versus ablationof spontaneous ventilation during intuba-tion attempts.2 The anesthesia professionalfurther determines the preferred manage-ment on a case by case basis for the follow-ing situations: awake intubation, adequateventilation but difficult intubation, and thelife threatening situation in which you can-not ventilate or intubate.2 The ASA guide-lines suggest having a portable storage unitspecifically for difficult airway manage-ment that has: rigid laryngoscopy blades ofvarious sizes with possibly a rigid fiberop-tic laryngoscope, tracheal tubes of assorted

sizes, tracheal tube guides including semi-rigid stylets, ventilating tube changer, lightwands, and forceps, exhaled carbon dioxidedetector, LMAs of assorted sizes, intubat-ing LMAs, flexible fiberoptic intubationequipment, retrograde intubation equip-ment, a device suitable for an emergencynoninvasive airway such as a Combitube(Kendall-Sheridan Catheter Corp., Argyle,NY) a hollow jet ventilation stylet, atranstracheal jet ventilator and equipmentsuitable for emergency invasive airwayaccess (cricothyrotomy).2

The difficult airway algorithm focuses ondeveloping a primary and alternative strate-gy to managing the airway. After inductionof general anesthesia and the initial intuba-tion attempt is unsuccessful, it is pivotal todetermine if face mask ventilation is ade-quate. If hand mask ventilation is adequatethe non-emergent pathway of the algorithmis followed. At this point the anesthesia pro-fessional should consider: calling for help,returning to spontaneous ventilation, andawakening the patient.2 After instrumenta-tion of an airway with rigid laryngoscopyduring multiple attempts to manage an air-way, supraglottic structures become edema-tous and visualization is further compro-mised by soft tissue edema, bleeding andsaliva. Hand mask ventilation also becomesincreasingly difficult. At this point whenventilation is inadequate and intubationattempts are unsuccessful a life threateningemergency ensues. Call for help andattempt placement of a non-invasive emer-gency airway. If ventilation is inadequatewith this approach, emergency invasive air-way must be attempted.2

Our case study followed the ASA guide-lines on difficult airway management. Afterinduction of general anesthesia, hand maskventilation was established with an oral air-

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way in place. After multiple unsuccessfulintubation attempts utilizing traditional DLand fiberoptic bronchoscope, hand maskventilation became increasingly difficult.The airway was established with the intu-bating Fast-Trach LMATM. Correct place-ment was verified with the fiberoptic bron-choscope, bilateral breath sounds and endtidal carbon dioxide.

References

1. Naguib M, Scamman FL, O’Sullivan C, Aker J, Ross AF, Kosmach S. Predictive performance of three multivariate difficult tracheal intubation models: a double blind, case controlled study. Anesth Analg. 2006; 102:818-24.

2. American Society of Anesthesiologists. Practice guidelines for management of the difficult airway: an updated report by the American Society of Anesthesiologists Task Force on management of the difficult airway. Anesthesiology. 2003; 98:1269-77.

Mentor: Maria Magro, CRNA, MSN, MS

Acute Post-Operative LaryngospasmWith Negative Pressure Pulmonary Edema

Adam J. Durant AS, B.S.N.University of Pennsylvania

Keywords: negative pressure pulmonaryedema, acute laryngospasm, respiratorydistress, inspiratory pressure, stridor,anesthesia

Acute laryngospasm is a known complica-tion in anesthesia care. Although attributedto significant mortality if unrecognized, itcan usually be resolved if treated quicklyresulting in a good patient outcome.1 Thefollowing is a case report of negative pres-sure pulmonary edema in a healthy femalefollowing an acute laryngospasm that wasquickly recognized and remedied.

Case Report

A 48-year-old woman was admitted to thehospital for same-day surgical repair of aleft shoulder sub-acromian decompression

via arthroscopy. A pre-operative assessmentwas significant for obesity (64”, 89 kg,Body Mass Index-BMI 33.7) and uterinefibroids. She was taking no prescriptionmedications. An airway assessmentrevealed a Mallampati II, a thyromental dis-tance of 3 finger breadths, intact teeth andfull neck range of motion. A general anes-thetic was determined to be most appropri-ate for this ASA II patient.

The patient was premedicated with midazo-lam 2 mg and glycopyrrolate 0.2 mg. Aftera routine intravenous induction with propo-fol 200 mg, vecuronium 10mg and fentanyl150 mcg, direct laryngoscopy was per-formed and a 7.0 endotracheal tube (ETT)was inserted without difficulty. Positive

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pressure ventilation was initiated at a rate of10 breaths per minute (BPM) with tidal vol-umes of 650 ml. Sevoflurane was chosen asthe inhalational anesthetic agent.

The arthroscopy proceeded uneventfullyfor the next 140 minutes. No further neuro-muscular blockade was administered. Anadditional 200 mcg of fentanyl was givenfor a total of 350 mcg of fentanyl (4mcg/kg). Total crystalloids were 1700 cc,estimated blood loss was <25 cc. Near theend of the case the anesthetic agent wasturned off and the oxygen flow wasincreased to 8 L/min. A train-of-four wasperformed and the patient was noted tohave four strong twitches. Neostigmine 4 mg and glycopyrrolate 0.6 mg were givento antagonize any residual neuromuscularblockade. The patient began breathingspontaneously however her respiratory ratewas slow and with decreased tidal volumes.She was also slow to respond to commands.After approximately 15 minutes her respi-ratory rate increased to 12-14 breaths perminute with spontaneous tidal volumes300-400 ml. She responded to voice com-mand and was able to perform a sustainedhead lift for five seconds. Once these extu-bation criteria were met, the ETT wasremoved. The patient was given 4 L/min ofsupplemental oxygen via nasal cannula andtransported to the Post Anesthesia CareUnit (PACU).

Immediately upon entering the PACU thepatient was noted to be in respiratory dis-tress with obvious stridor. An initial pulseoximetry reading was 78%, BPM 6, heartrate 58, blood pressure 102/52. The patientwas obtunded and did not respond torepeated verbal commands. Anesthesiaproviders were immediately available andbegan to give positive pressure ventilationsvia bag-valve mask with 100% oxygen. Anasal pharyngeal airway was inserted and

the oxygen saturation quickly rose to 99%.Naloxone (Narcan) 120 mcg was adminis-tered to antagonize any residual narcoticthat may have been causing the patient’sunresponsiveness. A few minutes after theadministration of naloxone the patient’srespiratory rate was 14 and she no longerrequired bag-valve mask assistance. A non-rebreathing mask with 15 L/min of oxygenwas placed on the patient. Auscultation oflung sounds revealed wheezing in the upperbronchi. A nebulized albuterol breathingtreatment was ordered along with a chestX-ray and an arterial blood gas. Cardiacenzymes were drawn and a bedside 12-leadECG was preformed.

After the breathing treatment, the patientbegan to cough and expectorate smallamounts of bloody, frothy sputum. Bloodgas results were as follows: pH-7.33,paCO2-51, paO2-264, HCO3 -27.3, O2Sat %-100, Base Excess (+1). Re-intubation wasdiscussed, however, it was felt that thepatient was responding to therapy andwould not immediately require this. Thebedside chest X-ray revealed diffuse patchyalveolar infiltrates consistent with flashpulmonary edema. A bedside 12-lead elec-trocardiogram (EKG) revealed no evidenceof cardiac ischemia and cardiac enzymeswere: creatine phosphokinase (CPK) -341,myoglobin (MB) -3.2 and troponin (TnT) I<0.1. A Foley catheter was inserted andfurosemide 10 mg was administered. Afterseveral hours of observation in the PACU,the patient was much more alert and with-out signs of respiratory distress. Pulseoximetry was 97% on 8 L O2 via face mask,BP 116/72, HR 98, BPM 20. Lungs soundswere noted to be coarse with faint expirato-ry wheeze. A total of 1600 cc of urine out-put had been recorded. The patient wasadmitted to the Intensive Care Unit (ICU)for further observation.

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The patient’s progress was followed closelyby the medical house staff as well as theanesthesia staff. A cardiologist was alsoconsulted. On post operative day (POD) #1the patient was without any signs or symp-toms of respiratory distress and was trans-ferred from the ICU to a medical/surgicalunit. Serial cardiac enzymes and EKGscontinued to reveal no evidence of amyocardial infarction. A chest X-ray onPOD #2 showed no pulmonary edema andwas greatly improved from the originalPACU film. The patient’s room air oxygensaturation was now 99%; however a persist-ent non-productive cough was still noted.Lung sounds revealed some rhonchi and nowheezing. The patient was discharged witha diagnosis of acute laryngospasm, result-ing in negative pressure pulmonary edema(NPPE).

Discussion

Laryngospasm is a forceful involuntaryspasm of the laryngeal musculature result-ing in closure of the vocal cords and theinability to ventilate. This spasm is causedby sensory stimulation of the superiorlaryngeal nerve.1 It is most commonlycaused by an irritating stimulus to the air-way typically occurring during induction oremergence.1,2 Common noxious stimuli thatmay induce this reflex include secretions,vomitus, blood, volatile anesthetics, artifi-cial airway placement, laryngoscopy,painful stimuli, and peritoneal traction dur-ing light anesthesia.1 It occurs more fre-quently in children, and patients with a his-tory of asthma, bronchitis, smoking,bronchiectasis and chronic obstructive lungdisease.1,5

Negative pressure pulmonary edema(NPPE) has been reported in 11% ofhealthy young patients who experiencelaryngospasm.5 The incidence of NPPE has

been reported to be as high as 1 in 1,000anesthetic cases.1,5 Inspiration against aclosed glottis creates an exaggerated nega-tive intrathoracic pressure. This may reacha level of -100 cm H20 or as much as fivetimes more negative then normal.1,4,5

Negative intrapleural pressure induces theformation of pulmonary edema by increas-ing venous blood return to the right heartand pulmonary artery. This results in a significant increase in volume and pressurewithin the microvasculature in the pul-monary bed. The physiologic response tohypoxia is a massive catecholamine releaseresulting in increased systemic vascularresistance. This augments venous bloodreturning to the right heart and pulmonarycirculation, further increasing pulmonarymicrovascular pressures.1,4,5 The elevationof blood volume into pulmonary circulationincreases the hydrostatic pressure withinthe pulmonary capillaries. Simultaneously,the interstitial pressure within the lungs willdecrease, as a result of the transmission ofthe negative intrathoracic pressures. Thisresults in the gross production of intra-alve-olar transudative edema. The negative pres-sures can also result in rupture of the capil-laries leading to the formation of interstitialedema and bleeding leading to the appear-ance of pink frothy sputum.1,3,4,5

This patient likely experienced an acuteupper airway obstruction secondary toredundant pharyngeal soft tissue and loss ofmuscle tone related to the combined effectsof residual narcotics, benzodiazepines andanesthetic agent. This state was enough totrigger laryngospasm, which resolved withpositive pressure ventilation. Inspiratoryefforts against an obstructed upper airwayled to the development of negative pressurepulmonary edema. Supportive treatmentincluded 100% oxygen administration, neb-ulized beta 2 agonists, appropriate monitor-

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ing and laboratory studies to evaluate theextent of this episode. A chest X-ray takenshortly after the respiratory distress beganin the PACU revealed diffuse patchy alveo-lar infiltrates consistent with flash pulmonary edema. Treatment of the pulmonary edema then became the mainfocus of therapy.

Traditionally, acute pulmonary edema istreated with endotracheal intubation, oxy-gen therapy and positive end-expiratorypressure (PEEP) via a ventilator.1,5 Themajor effect of PEEP is to increase func-tional reserve capacity (FRC). It also acts toincrease lung volume, improve lung com-pliance, increase oxygen delivery andreverse ventilation/perfusion mismatching.At the alveolar level, PEEP helps to stabi-lize and expand partially collapsed alveoli;this is often referred to as recruitment.1

While diuretics will help to reduce pul-monary capillary pressure, PEEP may helpto reduce intra-alveolar permeability andact to redistribute or slow edema “leaking”.In patients with persistent hypoxemia, othermaneuvers to improve oxygenation mayinclude the use of inhaled nitric oxide,inhaled prostacyclin (PGE) or ventilation inthe prone position.1

The patient was admitted to the intensivecare unit overnight and for further treat-ment with oxygen, diuretic and nebulizedBeta adrenergic medication (albuterol).Serial cardiac enzymes and electrocardio-grams failed to show signs of myocardialinfarction and this was ruled out as a possi-ble cause of the pulmonary edema. Thepatient's oxygen requirement decreasedprogressively over the ensuing 48 hours andshe was discharged from the hospital tohome. Despite the quick recognition andtreatment of this patient’s acute laryn-gospasm, negative pressure pulmonary

edema can manifest minutes or even hoursafter the initial emergency is over.

References

1. Morgan G, Mikhail M, Murray M. Clinical Anesthesiology. 4th ed. New York, New York: McGraw-Hill Medical Publishing 2002:78-80,942-943, 968-973.

2. Hurford W. et al. Clinical Anesthesia Procedures of the Massachusetts General Hospital. 6th ed. Philadelphia,PA: Lippincott-Williams and Wilkins. 2002:217, 288.

3. Oswalt CE, Gates GA, Holmstrom,FMG (1977) Pulmonary edema as a complication of acute airwayobstruction. JAMA. 238:1833-1835.

4. Pertrou, A., et al. (2003) Negative pressure pulmonary oedema in a patient ventilated with a laryngeal mask. The Greek E-Journal of Perioperative Medicine 1:69-73.

5. Dolinski SY, MacGregor DA, Scunderi PE. (2000) Pulmonary hemorrhage associated with negative-pressure pulmonary edema. Anesthesiology 93:888-890.

Mentor: Russ Lynn, CRNA, MSN

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Keywords: pulmonary artery catheter,criteria, aneurysm, anesthesia

Pulmonary artery catheters (PAC) can pro-vide clinically useful information in cardiacand major vascular surgery by allowing thedirect measurement of cardiac output andpressures on both the right side of the heartand in the pulmonary vasculature. Makingan appropriate decision regarding the use ofa PAC is imperative because of the com-plexity of its use, inherent risks, and thelevel of expertise required placing, moni-toring, and interpreting data from thecatheter. Major risk factors associated withPAC insertion include pulmonary arteryrupture, pneumothorax, arrhythmias andinfection.

Consideration for PAC use should also takeinto account the cost-benefit ratio. The costof a PAC includes equipment and person-nel. Published estimates range from $300 to$1,649 with one study documenting PACcost to be $667 on the initial day of place-ment and $541 each additional day.1 Eachyear in the United States approximately220,000 new cases of abdominal aorticaneurysms (AAA) are diagnosed withabout 45,000 undergoing surgical repair.2 Itis critical for anesthesia practitioners tohave the ability to determine a safe andeffective anesthetic plan for each patient.This report will describe a case for whichPAC monitoring was not utilized for therepair of an AAA.

Case Report

A 69 year old female weighing 68 kg and168 cm tall presented with an infrarenal

AAA for elective surgical repair. Thepatient noted a pulsating mass in herabdomen two years prior and had sincebeen followed by her primary care physi-cian. The aneurysm measured 5.2 cm bycomputed tomography scan with a probable0.4 cm enlargement in the past year. Shepresented on the day of surgery without ahistory of chest pain, dizziness or shortnessof breath. A stress echocardiogram revealedan ejection fraction of 68%. The patient’smedications for depression and hypercho-lesterolemia included atorvastatin calcium,escitalopram oxalate, lamotrigine and que-tiapine fumarate as needed. Additionally,she quit smoking 18 months prior to sur-gery. She had no known drug allergies. Herpre-operative laboratory values were unre-markable. The hematocrit was 39.8%. Herpre-operative blood pressure was 133/64mmHg with a heart rate of 73 beats perminute. Cefazolin one gram was given viaan 18 gauge peripheral intravenous line thatwas started in the pre-operative area.

In the operating room she was given mida-zolam two mg and fentanyl 50 mcg intra-venously. A T-8 thoracic epidural wasplaced while in the sitting position. A 20gauge left radial artery catheter was placedwhich revealed a blood pressure of 112/69mmHg. Standard monitors were appliedand general anesthesia was induced withfentanyl 150 mcg, propofol 100 mg andvecuronium seven mg. Her trachea wasintubated with a 7.0 mmID endotrachealtube. Isoflurane was titrated between 0.8-1.2% in a mix of one liter of air and oneliter of oxygen. After induction, a 7-Frenchcatheter was inserted into her right internal

Pulmonary Artery Catheter Criteria in Abdominal Aortic Aneurysm RepairsStacey Freda, B.S.N.

Northeastern University

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jugular vein using ultrasound guidance.Parameters for acceptable vital signs werediscussed with the surgeon and anesthesiapractitioners. Phenylephrine 90 mcg totalwas administered through the central line tomaintain the mean arterial pressurebetween 70-90 mmHg. An upper bodywarmer was set at 44 degrees and a fluidHot Line was used at 41 degrees to main-tain normothermia. A 14-French oral gas-tric tube was placed to suction, and anesophageal temperature/stethoscope wasinserted. A Foley catheter was placed. Theaneurysm was surgically identified andheparin 3,500 units was administered intra-venously before the aorta was clamped justbelow the renal arteries. The aneurysm wasdissected and the aorta was anastomosed.Aortic cross clamp time was 26 minutesand the patient tolerated it well. Blood losswas 850 ml and urine output was 350 ml.Normovolemia was maintained with theinfusions of two units of salvaged red cellsand 2200 ml of lactated Ringer’s solution.

An epidural infusion of 100 ml of normalsaline with bupivicaine one mg/ml and fen-tanyl 2.5mcg/ml was started at six ml anhour 20 minutes before completion of theprocedure. Three milliliters of two percentlidocaine were given epidurally just prior toextubation. Neuromuscular blockade wasantagonized upon completion of the sur-gery. The trachea was extubated afterappropriate criteria were met. The patientwas transported with an oxygen mask to theintensive care unit. She was discharged onthe seventh post-operative day following anuncomplicated recovery.

Discussion

An aortic aneurysm is a "permanent local-ized dilation of the aorta that is at least 50%larger than the normal or expected diame-ter.”3 The etiology may be degenerative,

atherosclerotic or non-specific. Risk factorsinclude hypertension, atherosclerotic dis-ease, dyslipidemia, infection, smoking andtrauma. The vessel wall is predisposed todilation from internal pressure with con-comitant increase in wall tension resultingin an expanded radius. The risk of aneurys-mal rupture correlates with luminal diame-ter and surgery is considered as theaneurysm approaches 4.5-5.0 cm in diame-ter.2

The anesthetic goal in an AAA repair is tomaintain major organ perfusion and oxy-genation while minimizing the risk of rup-ture in relation to blood pressure and bloodvolume.4 Choosing the appropriate devicesfor invasive pressure monitoring is individ-ualized based on assessment of the patient’shistory, co-morbidities and anticipatedextent of surgery and cross clamp time.Identifying high risk patients such as thosewith a recent myocardial infarction, con-gestive heart failure, unstable angina,suprarenal aneurysms, or an emergent AAArupture would guide monitoring decisions.4

A central venous pressure (CVP) line maybe sufficient in patients such as the onedescribed in this report with unimpairedventricular function and exercise toleranceof a flight of stairs or more.4 A PAC was notplaced in this case because of the patient’sunderlying good health and the infrarenallevel of the aneurysm. Conventional moni-tors with a CVP and arterial line providedadequate information to manage her hemo-dynamics intra-operatively. Even with herabsence of co-morbidities, a PAC wouldhave been considered if the aneurysm hadextended suprarenally. A suprarenalaneurysm would have put her at a higherrisk of end organ hypoxia and decreasedsystemic perfusion because of the intra-operative aortic clamping and unclamping.2

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The PAC is a valuable monitoring devicefor measuring cardiac output. The use of aPAC may be reserved for patients who areat risk for significant blood loss or pul-monary and cardiovascular complications.Because of the complexity and associatedco-morbidities of major vascular surgery,these patients are more likely to have alonger recovery period resulting in higherhospital costs. The increased cost of a PACshould not deter the anesthesia practitionerin correctly identifying patients who wouldbenefit from its use. A PAC, however, maynot benefit a patient who is not at a highrisk, such as the one whose case isdescribed above. In this case report theCVP and arterial line provided adequatehemodynamic monitoring for surgery. Thischoice of invasive monitors was the bestanesthetic plan for this patient and mayhave decreased the length of stay, risk ofcomplications and hospital costs comparedto recovery with a PAC. If a PAC was usedduring this case, assuming an estimatedthree day indwelling time, the projectedcosts may have been an additional $1750.

Technology in healthcare is progressing.Surgical and anesthetic techniques haveadvanced and diminish the risks associatedwith routine AAA repairs. In 1998Valentine et al. concluded that routine useof PACs for routine use and might have ahigher rate of intraoperative complicationsduring low risk vascular repairs.5 Manymedical institutions are utilizing trans-esophageal echocardiography (TEE)probes to evaluate cardiac output and ven-tricular function where a PAC may havepreviously been used. With the recentadvancement of endoluminal aneurysmrepairs, CVP and PAC monitoring are nolonger the standard of care.6

The benefit of any monitoring device willbe optimized when the anesthetist has thor-

ough knowledge of its use, benefits andrisks. Our patient who had normal ventric-ular function, an infrarenal aneurysm andno other co-morbidities had a successfuloutcome without the added risks and costsof a PAC. The use of a PAC should be evidence based and therefore used selec-tively for AAA repairs.

References

1. American Society of Anesthesiologists. Practice guidelines for pulmonary artery catheterization. Anesthesiology. 2003:99:988-1010.

2. Ellis JE, Roizen MF, Mantha S,Schwarze ML, Lubarsky DA, Kennan CA. Anesthesia for vascular surgery. In: PG Barash Clinical Anesthesia. 5th ed. Philadelphia: Lippincott Williams & Wilkins; 2006:954-971.

3. Anderson LA. Abdominal aortic aneurysm. J Cardiovasc Nurs. 2001; 15(4):1-14.

4. Jacka MK, Cohen MM, To T, Devitt JG, Byrick R. The use of and preferences for the transesophageal echocardiogram and pulmonary artery catheter among cardiovascular anesthesiologists. Anesth Analg.2002;94:1065-1071.

5. Valentine RJ, Duke ML, Inman ML, et al. Effectiveness of pulmonary artery catheters in aortic surgery: a randomized trial. J Vasc Surg. 1998; 27:203-212.

6. Swan HJ. The pulmonary artery catheter in anesthesia practice.Anesthesiology. 2005:103:890-893.

Mentors: Paul Sawler, CRNA, LanaLeinbach Yaney, CRNA, MS

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Keywords: mid-cavity ballooning, leftventricular apical ballooning, Takotsubocardiomyopathy, anesthesia

Mid-cavity ballooning syndrome refers to avariant of transient left ventricular apicalballooning syndrome.1 Also known asTakotsubo cardiomyopathy, this syndromewas initially identified in Japan in the early1990’s. Typically, it presents in post-menopausal women following emotionalstress and results in temporary akinesis ofthe left ventricle. Because it is difficult todistinguish this cardiomyopathy from anacute myocardial infarction, a recent histo-ry of emotional stress should prompt anes-thesia professionals to consider this diagno-sis when faced with a female patient whoexhibits chest pain, elevated cardiacenzymes, electrocardiographic changes,mid-ventricular hypokinesis and lack ofcoronary artery disease on angiography.2

Case Report

A 46-year old, 72 kg female (BMI 27.5)presented to the OR for outpatient electiveexcision of redundant right breast/axillarytissue (non-malignant). Past medical histo-ry included non-specific muscle pain, lowback pain, chondromalacia patella, arthritisand gastrointestinal reflux disease. She didnot have a history of coronary artery dis-ease. She denied recent tobacco, ETOH orillicit drug use. Current medications includ-ed methocarbamol, omeprazole, ranitidine,calcium acetate and celecoxib. Shedescribed an allergy to ampicillin. Pre-operative laboratory values were withinnormal limits. An ASA 2 and Mallampaticlass III airway were determined. PONV

prophylaxis included diphenhydramine12.5 mg IV and ondansetron 4 mg IV.Approximately two minutes after adminis-tration of ondansetron, the patient com-plained of pain at the IV site and bilateralparesthesia of the upper extremities, dizzi-ness, throat discomfort and chest tightness.Cool, clammy skin and bilateral hand andwrist rigidity were noted. Her heart rate was40 beats per minute (bpm) and respirationswere 32 breaths per minute. Cardiac moni-tors were applied and oxygen was adminis-tered. Atropine 0.5 mg IV and diphenhy-dramine 25 mg IV were administered. Herheart rate increased to 130 bpm. She contin-ued to complain of chest tightness, throatpain and extremity tingling. Bilateral breathsounds were clear and equal. Erythemamultiforme was noted proximal to the IVsite. An additional dose of diphenhy-dramine 25 mg IV was administered. Herblood pressure and heart rate measured120/72 mmHg and 117 bpm, respectively.Esmolol 50 mg IV was administered. Herheart rate decreased to 90 bpm. The patientwas monitored for an additional forty-fiveminutes when she complained of chestpain. Systolic blood pressure measured80/63 mmHg and heart rate 100 bpm. Thesurgery was cancelled and a cardiac consultwas requested. An EKG revealed normalsinus rhythm and blood analysis revealed atroponin level of 2.55 ng/ml. After admis-sion to the coronary care unit, a 2-Dechocardiogram revealed global hypokine-sis with an ejection fraction (EF) of 35-40%. An emergency cardiac catheterizationrevealed normal coronary arteries withmid-cavity akinesis. The cardiologist madea diagnosis of mid-cavity ballooning syn-

Mid-cavity Ballooning Syndrome Following OndansetronJeanne M. Antolchick, B.S.N.

Barry University

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drome, a variant of transient left ventricularapical ballooning syndrome. An intra-aorticballoon pump (IABP) and a Swan Ganz®

catheter were placed. Overnight, the patientremained stable and IABP was discontin-ued after approximately 48 hours. A follow-up 2-D echocardiogram revealed normalleft ventricular systolic function with an EFof 55-60%. On the sixth day following theinitial presentation, the patient was discharged to home.

Discussion

A patient scheduled for outpatient, electiveexcision of redundant right breast/axillarytissue (non-malignant) presents with symp-toms suggesting extrapyramidal dysfunc-tion following administration ofondansetron for prophylactic treatment ofpost-operative nausea and vomiting(PONV). Despite pharmacologic interven-tion, additional signs and symptoms,including elevated troponin levels and chestpain, result in cancellation of the surgeryand further medical evaluation.Echocardiogram and cardiac catheteriza-tion reveal left ventricular akinesis support-ing a diagnosis of mid-cavity ballooningsyndrome. The stress response associatedwith a presumed adverse reaction toondansetron may have contributed to thedevelopment of this transient cardiomyopa-thy, which mimics an acute myocardialinfarction.

Ondansetron, a selective serotonin receptorantagonist, is a popular medication used toprevent and treat PONV. As a class, the 5-hydroxytryptamine (5-HT)3 antagonists areconsidered safe and are usually well tolerat-ed by most patients. Although typicallyinsignificant, in some patients, minor elec-trocardiographic changes associated withondansetron administration have been iden-tified.3 The first case of ondansetron-

induced extrapyramidal side effects wasdocumented in 1991 and additional caseshave subsequently been described.4

Although rarely life threatening, dystonicreactions can produce significant anxiety.While extrapyramidal side effects are typi-cally associated with dopamine antagonists- most notably neuroleptic agents - researchdata suggest that the dopaminergic andserotonergic systems may overlap. Thistheory may explain how the antagonism ofserotonergic receptors can initiate dystonicreactions, traditionally thought to be associ-ated only with the dopaminergic system.4

Ritter describes “a regulatory role of sero-tonergic innervation to the basal ganglia inthe limbic system on the central dopaminer-gic motor inhibitory activity.”4 Even thoughondansetron does not demonstrate an affin-ity for dopamine receptors, Ritter reportsevidence that ondansetron may indirectlystimulate dopamine receptors in a smallnumber of patients.4 Additional research isneeded to thoroughly understand this rela-tionship.

While the exact etiology of transient leftventricular apical ballooning syndrome, orTakotsubo cardiomyopathy,” is unknown, itis considered a “non-ischemic, metabolicsyndrome caused by stress-induced activa-tion of the cardiac adrenoceptors,” whichresults in a stunned portion of themyocardium.5 The “tako-tsubo-like” leftventricular dysfunction received its namefrom a short-necked, round fishing pot usedto trap octopi because of the similarity inappearance to the left ventricle on left ven-triculography. Mid-cavity ballooning syn-drome is described as a variant of transientleft ventricular apical ballooning syn-drome.1

Research data indicate that a relationshipexists between stress-induced cate-

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cholamine surges and the adrenergic inner-vation of the heart.1 Emotional stress pre-cipitates transient cardiomyopathies, whichmimic acute myocardial infarctions.2 Thesetransient syndromes are associated withchest pain, EKG changes, and elevation ofcardiac enzymes. Typically, there is no evi-dence of sustained myocardial ischemia orinjury. The pathological mechanism ofthese transient, catecholamine-associated,cardiac dysfunctions is not well under-stood.1 Multiple explanations have beenproposed including “multi-vessel epicardialspasm, coronary microvascular spasm,acute coronary syndrome with reperfusion,impaired fatty acid metabolism, myocardi-tis, transient obstruction to left ventricularoutflow and catecholamine-mediatedmyocardial dysfunction.”1 Since its identifi-cation, the syndrome has been recognizedworldwide. Patients exhibit an acute onsetof chest pain with minor myocardialenzyme release, transient wall motionabnormalities and ST-segment elevation.2

The mortality rate and risk for recurrenceappear to be low, although additionalresearch is required to substantiate thishypothesis. Typically, the left ventriculardysfunction resolves in three to fourteendays. In a meta-analysis, Donohue reportedmost patients were female (173 of 185cases) with Asians and Caucasians com-prising the majority of the reported races.6

Further investigation is required to deter-mine whether this is an inherited disorder.

This patient presented a challenging puzzleto the anesthesia care team. The differentialdiagnosis was symptomatic bradycardiaversus adverse reaction to ondansetron sug-gested by extrapyramidal symptoms toinclude limb dystonia, tremors and rigidity.Resolution of the skeletal muscle rigidity inthe patient’s upper extremities followingadministration of diphenhydramine pointed

to dystonic reaction to ondansetron. Theemotional stress stemming from a pre-sumed adverse reaction to ondansetron mayhave masked the presentation of thisuncommon, underlying cardiomyopathy.Chest pain, slightly elevated cardiacenzymes, mid-ventricular hypokinesis andlack of coronary artery disease on angiogra-phy support a diagnosis of mid-cavity bal-looning syndrome, a variant of transient leftventricular apical ballooning syndrome.

References

1. Hurst R, Askew J, Reuss C, et al. Transient midventricular ballooning syndrome: A new variant. J Am Coll Cardiol. 2006;48:579-583.

2. Bybee K, Kara T, Prasas A, et al. Systematic review: Transient left ventricular apical ballooning: A syndrome that mimics ST-segment elevation myocardial infarction. Ann Intern Med. 2004;141:858-865.

3. Pasricha PJ. Treatment of disorders of bowel motility and water flux; antiemetics; agents used in biliary and pancreatic disease. In: Brunton L, Lazo J, Parker K, ed. Goodman & Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. New York:McGraw-Hill; 2006: 983-1008.

4. Ritter M, Goodman B, Sprung J,Wijdicks E. Ondansetron-induced multifocal encephalopathy. Mayo Clin Proc. 2003;78:1150 – 1152. Available at http://www.mayoclinicproceedings.com/inside.asp?AID=408&UID= Accessed September 1, 2006.

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5. Lee W, Miao L, Chan H, Chen M. Takotsubo syndrome with transient complete atrioventricular block. Chin Med J (Engl). 2006;119:73-76. Available at http://www.cmj.org/Periodical/PDF/2006/2006173.pdf. Accessed September 1, 2006.

6. Donohue D, Movahed M. Meta-analysis of transient left ventricular apical ballooning syndrome based on gender and race. Chest. 2005; 128:279S. Available at ht tp: / /meet ing.chest journal .org/cgi/reprint/128/4/279S. Accessed September 1, 2006.

Mentor: Paul J. Safara, CRNA, MSNA

Continuous Femoral Nerve Block for Total Knee ArthroplastyAmber Libby, B.S.N.Midwestern University

Keywords: anesthesia, femoral nerveblock, knee arthroplasty

Postoperative pain has been reported asbeing severe in 60% of patients and moder-ate in 30% of patients after total kneearthroplasty (TKA).1 The most influentialfactor in postoperative rehabilitation ispostoperative mobilization and physiother-apy. Postoperative pain may hinder thesefactors and prolong rehabilitation.2

Intravenous (IV) opioids are the mainstayof effective pain relief immediately follow-ing total knee arthroplasty (TKA).However, nausea, pruritis, constipation, andrespiratory depression associated with IVopioids are often unpleasant and disablingto both the patient and the postoperativecare team.3 A continuous femoral nerveblock is an alternative to the traditionalmethods of postoperative pain managementafter TKA. It has been shown to reduce theamount of intravenous analgesics, promotemobilization, and decrease opioid inducedside effects thus providing patients with asuperior method of pain management.4

Case Report

A 73 year old male patient, height 6’1” andweight 110 kilograms presented for a left

TKA. Comorbidities included hyperten-sion, a history of atrial fibrillation, gastroe-sophageal reflux disease, arthritis, degener-ative joint disease, chronic renal insuffi-ciency, and a history of treated testicularcancer. The patient previously underwent aright TKA. His current medication regimeincluded hydrochlorothiazide, isosorbide,lisinopril, verapamil, amitriptyline, aspirin,baclofen, flunisolide, and lansoprazole.

Laboratory values were within normal lim-its and a recent radiographic chest examina-tion revealed no active disease process. A12-lead electrocardiograph (ECG) revealeda right bundle branch block, ST changes inleads V4-V6 and T wave inversion in leadV2. The patient denied ever having amyocardial infarction or chest pain.

A lactated Ringers (LR) infusion was start-ed and the patient was administered 100micrograms of fentanyl IV for placement ofthe peripheral nerve block. The patient wasgiven oxygen at 4L/m via nasal cannula andhe was then prepared for a femoral nerveblock and catheter placement. With a twoinch insulated 18 gauge Tuohy needle withintegrated wire, the femoral nerve wasstimulated and a patellar snap was

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achieved, with a loss of twitch at 0.35 mil-liamps. Thirty milliliters of 0.5% bupiva-caine with five micrograms per milliliter ofepinephrine was injected and a 20 gaugecatheter was then threaded into the femoralsheath to provide postoperative analgesia.The patient denied any signs of neuronaltoxicity (e.g. tinnitus, circumoral numb-ness, metallic taste in mouth) nor was thereany sign of intravascular injection. Afterapproximately twenty minutes the patientreported to have a decreased sensation ofpain in the operative leg and was also notedto have decrease quadricep strength to theoperative leg, revealing that the block wassuccessful.

In the operating room a pulse oximeter andblood pressure cuff were applied. The ini-tial cuff blood pressure of 158/71 millime-ters of mercury (mmHg) and heart rate of69 beats per minute (bpm) were recorded.The patient was given oxygen at 4 L/minutevia nasal cannula and was then positionedfor a sitting spinal anesthetic. Fifteen mil-ligrams of bupivacaine was injected in thesubarachnoid space after cerebrospinalfluid was seen in all four quadrants. Afterfive minutes the patient reported to have asensory blockade at thoracic level six and a10 mmHg decrease in the patient’s systolicblood pressure was noted. There were nosynergistic effects noted from the combina-tion of the femoral nerve block and the sub-arachnoid block.

After the patient was positioned supine, aFoley catheter was placed, the patient wasprepped for the surgical procedure and aleft leg tourniquet was then inflated at 350mmHg. A propofol infusion was then start-ed at 25 micrograms per kilogram perminute (mcg/kg/min) which was titrated tokeep the patient sedated and hemodynami-cally stable. The propofol infusion was

maintained at 10 mcg/kg/min for the dura-tion of the procedure. Despite the propofolinfusion, analgesia was assessed per thepatient’s denial of pain throughout the pro-cedure.

The patient’s blood pressure was supportedwith incremental 5 mg doses of ephedrine(total of 30 mg) and 0.1 mg doses ofphenylephrine (total of 0.5 mg) IV duringthe procedure. The patient required thisvasopressor support during the initial partof the case after the subarachnoid blockwas placed. The patient’s heart rate wasmaintained at a rate of 45 to 69 bpm andsystolic blood pressure was maintainedbetween 92 and 158 mmHg. There were nosignificant ST changes noted throughoutthe procedure. The patient received a totalof 2100 milliliters (ml) of LR for the casewith approximately 320 ml of urine output.The procedure lasted 130 minutes and therewas an estimated 250 ml of blood loss.

The patient was transferred to the postanesthesia care unit (PACU) where thepatient’s spinal blockade was noted to be ata thoracic level of 8 and the patient report-ed having no pain. A continuous infusion of0.125% bupivacaine was started at eight mlper hour via the femoral nerve catheter.After the patient’s spinal blockade hadreceded to a thoracic level of 10, the patientwas transferred to the surgical care ward.The patient required no additional IV opi-oids in the PACU. On postoperative day onethe patient reported adequate pain controlon the anterior and medial portion of theoperative knee, however, the patient wasreceiving morphine sulfate IV for posteriorpain (20 mg total). On postoperative dayfour the catheter was removed without inci-dent and the patient was discharged oneweek later after rehabilitation therapy.

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Discussion

When postoperative pain after TKA is inad-equately treated, it intensifies reflexresponses, which may lead to serious com-plications, such as pulmonary or urinaryproblems, thromboembolism, hyperdynam-ic circulation, and increased oxygen con-sumption. Moreover, it hinders early physi-cal therapy, which is the most influentialfactor for beneficial postoperative rehabili-tation.5 After knee surgery, poorly managedpain may inhibit the early ability to mobi-lize the knee joint. This, may result in adhe-sions, capsular contracture, and muscleatrophy, all of which may delay or perma-nently impair the ultimate functional out-come of the operative knee.5

The knee is innervated by the lumbosacralplexus nerve roots. The femoral and obtura-tor nerves innervate the anterior aspect ofthe knee, while the sciatic nerve innervatesthe posterior aspect of the knee. After TKA,postoperative pain relief can be achieved byvarious techniques, such as patient con-trolled analgesia (PCA) with IV opioids,epidural analgesia with local anestheticsand/or opioids, intrathecal opioids, and/or acontinuous or single-shot peripheral nerveblock.6

Epidural with opioid and/or local anesthet-ics is a well established analgesia regimenafter TKA, as it provides superior pain con-trol than PCA with opioids. However, fre-quent side effects such as urinary retention,dizziness, sedation, pruritis, nausea, vomit-ing, catheter displacement, or the spread ofanalgesia to the non-operative limb mayinterfere with the patient’s postoperativerecovery.4

Chelly et. al. observed that continuousfemoral infusion decreased morphinerequirements by 75%, while continuous

epidural infusion decreased requirementsby 35%. Chelly et. al. found a number ofadvantages to continuous peripheral nerveblockade: better recovery and a 90%decrease in serious cardiovascular and pul-monary complications.7 Long et al reportedthat those subjects who had received afemoral catheter, consumed less IV mor-phine on postoperative day one comparedto the epidural group (p<0.05).3 In compar-ison to traditional analgesia approaches, theuse of continuous femoral nerve block pro-vides prolonged duration and superior anal-gesia. Continuous femoral nerve block notonly provides a similar high quality of anal-gesia in comparison with continuousepidural analgesia but also provides lessmotor blockade because of the unilateraleffect of the block.8

Single-injection femoral nerve blocks havealso been shown to significantly improvepostoperative analgesia compared with sys-temic opioid therapy, which may reduce thelength of hospital stay after TKA.Placement of a femoral nerve catheter pro-vides patients with prolonged site-specificanalgesia. This technique may be of benefit,because the duration of analgesic effectfrom a single-injection block typically lasts12-24 hours, depending on the local anes-thetic chosen and the proximity of thenerves to the needle tip upon injection.However, severe pain after TKA may per-sist beyond the duration of the single-injec-tion, often hindering the patient’s rehabili-tation.8

In a study conducted by Salinas et. al., theuse of a continuous femoral nerve blockresulted in lower pain scores than the sin-gle-injection femoral nerve block begin-ning on postoperative day one, despite asignificantly larger opioid consumption inthe single-injection group.8 However, the

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researchers found that the improved analge-sia did not improve long-term functionaloutcome or decrease the patient’s length ofstay in the hospital. While, Long et. al.found that the continuous femoral catheterprovided patients with a shorter hospitalstay which was attributed to the reducedincidence of opioid side effects.3 Thepatient in our report used a significantlyreduced amount of intravenous opioids, incomparison to those who do not receive acontinuous femoral nerve catheter at ourfacility. Additionally, his rehabilitation wasnot hindered due to postoperative pain man-agement allowing for unlimited participa-tion in the rehabilitation process.

Morin et. al. conducted a study to comparethe effectiveness of a psoas compartmentblock (continuous posterior lumbar plexusblock), a continuous femoral nerve block,and a combination of a continuous femoraland sciatic nerve block.9 They found thatadequate analgesia after TKA cannot beachieved with continuous femoral nerveblock alone and that the addition of a sciat-ic nerve block significantly improved theanalgesic effects to the patient.9 However,the researchers found that there were nodifferences between the groups when com-paring postoperative functional outcome. Ifavoidance of pain is the goal of the practi-tioner, the combined continuous femoraland sciatic nerve block was deemed thesuperior technique.9

Based upon a Medline review from 1966 to2006 there were no similar studies or casereports discussing the efficacy of the com-bined technique reported in this case report.

Placement of femoral nerve cathetersrequires additional skill, time, and postop-erative management. In addition, placementof catheters poses the potential for infectionand nerve damage.8 Thus, continuous

femoral nerve blocks are not ideal in everysetting or every patient; however, if they areused appropriately, they may efficientlyenhance a patient’s postoperative recoveryafter TKA.

References

1. Shoji H, Solomonow M, Yoshino S, et al. Factors affecting postoperative flexion in total knee arthroplasty. Orthopedics. 1990;34:643-649.

2. Capdevila X, Barthelet Y, Biboulet P, et al. Effects of perioperative analgesic technique on surgical outcomes and duration of rehabilitation after major knee surgery. Anesthesiology. 1999;91:8-15.

3. Long WT, Ward SR, Dorr LD, Raya J,Boutary M, Sirianni LE. Postoperative pain management following total knee arthroplasty: A randomized comparison of continuous epidural versus femoral nerve infusion. J Knee Surg. 2006;19:137-143.

4. Zaric D, Boysen K, Christiansen C,Christiansen J, Stephensen S,Christensen B. A comparison of epidural analgesia with combined continuous femoral-sciatic nerve blocks after total knee replacement. Anesth Analg. 2006;102:1240-1246.

5. Singelyn FJ, Deyaert M, Joris D,Pendeville E, Gouverneur JM. Effects of intravenous patient-controlled analgesia with morphine, continuous epidural analgesia, and continuous three-in-one block on postoperative pain and knee rehabilitation after unilateral total knee arthroplasty. Anesth Analg. 1998;87:88-92.

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6. Seet E, Leong WL, Yeo AS,Fook-Chong S. Effectiveness of 3-in-1 continuous femoral block of differing concentration compared to patient controlled intravenous morphine for post total knee arthroplasty analgesia and knee rehabilitation. Anaesth Intensive Care. 2006;34:25-30.

7. Chelly JE, Greger J, Gebhard R, et al. Continuous femoral nerve blocks improve recovery and outcome of patients undergoing total knee arthroplasty. J Arthroplasty. 2001;16:436-445.

8. Salinas FV, Liu SS, Mulroy MF. The effect of single-injection femoral nerve block versus continuous femoral nerve block after total knee arthroplasty on hospital length of stay and long-term functional recovery within an established clinical pathway. Anesth Analg. 2006;102:1234-1239.

9. Morin AM, Kratz CD, Eberhart LH,et al. Postoperative analgesia and functional recovery after total-knee replacement: Comparison of a continuous posterior lumbar plexus block, a continuous femoral nerve block, and the combination of a continuous femoral and sciatic nerve block. Reg Anesth Pain Med.2005;30:434-445.

Mentor: Mary Wojnakowski, CRNA, PhD

Intra-Operative Colloid Replacement TherapyHolly E. McGee, B.S.N., M.S.N.

Wake Forest UniversityBaptist Medical Center

Keywords: anesthesia, colloid, fluidreplacement, fluid balance, volume expansion

Infusion of crystalloid solutions remainsthe primary treatment to replace intra-oper-ative fluid loss.1 However, many situationsoccur where anesthesia providers mayimplement colloid replacement therapy.Practitioners may choose from syntheticcolloids, such as dextrans or starches, or thenonsynthetic colloid, albumin.2 Althoughresearch does not indicate a superior colloidfor use, there are factors to consider whenimplementing colloid replacement therapy,such as a patient’s current health status,medical history, allergies, religious beliefs,and costs to the patient and

institution. It is prudent to note that bloodproducts, also being colloids, should not beused for the sole purpose of volume expan-sion, but rather to improve oxygen carryingcapacity.1

Case Report

A 55 year old, ASA 3, 83 kg white male,presenting with peritoneal carcinomatosisand pseudomyxoma pertonei from anappendicial primary lesion, was to undergointraperitoneal hyperthermic chemothera-py. Medical history was significant forhypertension, noninsulin dependent dia-betes mellitus, malignant melanoma, andrecent onset of gastroesophageal reflux dis-ease. Pre-operative assessment and labs

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were within normal limits with the excep-tion of a hemoglobin of 10.9 g/dl and hema-tocrit of 32%. Current medications includ-ed olmesartan, amlodipine/benazepril,spironolactone, glimepiride, and iron.

The patient was transported to the operatingsuite at 6:51 a.m. Standard monitoring wasinitiated. After intravenous induction with150 mcg of fentanyl, 2 mg midazolam, and400 mg thiopental, 100 mg succinylcholinewas administered to rapidly secure airwayafter encountering unanticipated difficult 2-person manual ventilation. Direct visuallaryngoscopy was performed and a 7.5 mmID endotracheal tube secured after auscul-tation of bilateral breath sounds and visual-ization of an end tidal carbon dioxide trac-ing. Anesthesia and paralysis was main-tained with oxygen, air, isoflurane, andvecuronium. A nasogastric tube, radial arte-rial line, 16 gauge peripheral intravenouscatheter, and a right internal jugular triplelumen catheter were inserted.

The patient was placed in lithotomy posi-tion for cystoscopy, bilateral retrogradepyelogram, and stent placement. He wasthen returned to the supine position forresection of the colon, proximal rectum,spleen, distal pancreas, distal stomach, gall-bladder, omentum, and umbilicus. Aftersurgically entering the abdomen, 4.5 litersof serous and serosanguineous fluid wasevacuated. A sufentanil infusion was initiat-ed for intermittent elevations in blood pres-sure and titrated between 0.1 - 0.2mcg/kg/hr. An ionized calcium level of 0.89mmol/L was treated with 2 grams of calci-um chloride, with levels increasing to 0.97mmol/L. Metoprolol and phenylephrinewere used to maintain a heart rate of 80 anda systolic blood pressure greater than 100mmHg. Chemoperfusion channels wereplaced intra-abdominally and intraperi-

toneal hyperthermic chemotherapy was initiated after abdominal closure.

The patient received 1250 ml of 5% albumin, 4 units of packed red blood cells,4 liters of normal saline, thirteen liters ofplasmalyte, and 1 liter of hetastarch. Oneliter normal saline with 20 mEq potassiumchloride was infused to treat a potassiumlevel of 3.65 mEq/L. Urinary output was3.5 liters, and blood loss was estimated tobe 1200 ml.

At the conclusion of chemotherapy treat-ment, the abdomen was reopened, irrigated,and an ileostomy was created. The patientemerged from anesthesia, was extubated,and transported to the post-anesthesia careunit at 1930 hours. He was subsequentlytransferred to the intensive care unit after anuneventful recovery. On the second post-operative day, the patient was stable, alert andreporting no anesthetic complications.

Discussion

Colloid solutions are superior over crystal-loid solutions in their ability to increasecolloid osmotic pressure (COP), therebyincreasing intravascular fluid.2 While a per-centage of crystalloid solutions will leakinto the interstitial space, colloid solutionsnot only remain intravascularly, but createan osmotic gradient pulling additional fluidfrom the interstitial space into the intravas-cular space. In comparison, normal salinedecreases COP pressure by 12% whilealbumin increases COP by 11% andhydroxyethyl starch increases COP by 36%.4 Colloids continue to have this effectfor hours to days after administration,depending in the formulation used. Whenimplementing colloid therapy, anesthesiaproviders must consider certain adverseeffects.5 Practitioners should monitor forsigns of fluid overload, anaphylactic reac-

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tions, and induced coagulopathies.2 Centralvenous pressure monitoring may be indicated. In some clinical situations, suchas sepsis, venom poisoning, trauma, drugoverdose, or anaphylaxis, increased capillary permeability allows colloids toleak into the interstitial space. The displaced colloids would cause an osmoticgradient with the net movement of fluidfrom the intravascular space to the intersti-tial space resulting in third space fluid loss.During these situations, colloids should beavoided.4 In addition to these effects,providers must consider the cost benefitratio when considering colloid therapy.

Albumin remains the primary nonsyntheticcolloid, a natural protein derived fromdonated plasma.5 Most commonly usedintra-operatively is a 5% concentration ofalbumin, which is isotonic and iso-oncoticwith normal plasma.7 Initial doses shouldbegin at 12.5 – 25 grams (250 – 500 ml of5% solution). However, albumin can betitrated up to doses of 250 grams (5000 mlof 5% solution) over a 48 hour period.8

Dosing should be based on desired heartrate, blood pressure, central venous pres-sure, and urinary output.9 Desired intravas-cular effects may persist for 24-36 hours.4

However, the half life for synthetic albuminis around 24 hours, considerably differentfrom a half life of 22 days in naturally syn-thesized albumin.2,10 There are adverseeffects associated with albumin administra-tion. Albumin will bind to free calcium,possibly causing decreased cardiac contrac-tility or dysrhythmias.1 Albumin should betitrated carefully in patients with cardiac orrenal disease to prevent adverse sequelesuch as circulatory overload or pulmonaryedema.7 Practitioners should consider theeffect of albumin on the availability ofdrugs that are highly protein bound.5

Albumin does carry a minute risk for trans-

mission of blood borne pathogens includingHIV and hepatits.5 However, these risks areremote due to donor screening and steriliza-tion processes, including alcohol fractiona-tion and heat treatment.7

The synthetic compound, hydroxyethylstarch (HES), is equally effective to 5%albumin for intravascular volume replace-ment, but less expensive.1 HES compoundswill expand intravascular volume for 24 –36 hours after infusion, and they have a halflife of 17 – 48 days.4 The 6% solution iscommonly used and the recommended doseis 20 ml/kg, up to 1500 ml.8 Doses exceeding 30ml/kg will have greater anti-thrombotic effects on coagulation.4

This dose dependent effect results fromaccelerated conversion of fibrinogen to fib-rin, decreased activity of factor VIII, anddecreased platelet agglutination.4 Hextend®,a newer form of 6% hetastarch, is preparedin a solution with balanced electrolytes anda lactate buffer.5,6 The newer formulationhas a decreased incidence of adverse sideeffects (i.e. hyperchloremic metabolic aci-dosis) that were associated with Hespan®.5,8

Hextend is more commonly used than its6% hetastarch predecessor, Hespan®, whichwas prepared in a normal saline solution.5

HES compounds are relatively contraindi-cated in patients with renal disease becauseof their potential to exacerbate renal damage.8 The mechanism behind this contraindication is unclear. One theoryasserts that as starches are cleared renally,tubular inflammation and elevated creati-nine levels become evident.5 HES com-pounds cannot be eliminated withhemodialysis.8 Hetastarch solutions shouldalso be avoided in patients with an allergyto corn.4

Dextran, another synthetic colloid, can alsobe used to increase intravascular volume.

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However, due to its prominent anticoagula-tion effects, its use may be more limited.Dextran may be advantageous for patientswith an increased risk for thrombosis due toits ability to decrease blood viscosity.5

These effects could make Dextran an attrac-tive choice for vascular surgery.6 If admin-istered for its anticoagulation effects,Dextran 40 is the preferred formulation.Dextran 70, however, is favored for volumeexpansion.11 The recommended dose is 500– 1000 ml, or a maximum dose of 20 ml/kgover the first 24 hours. If therapy is neededbeyond 24 hours, the dose should bedecreased to 10 ml/kg over any subsequent24 hour period. Although onset may occurwithin minutes, its effect is not as pro-longed as other colloids, being excreted inthe urine within 24 hours.8 At doses greaterthan 1.5 ml/kg, a patient may have coagula-tion deficits which resemble VonWillebrand’s disease from decreased FactorVIII levels. This effect may be partiallyreversed with desmopressin.5 Dextran orHES compounds may be colloid alternatives for the Jehovah’s Witnesspatient, as they may object to the use ofalbumin.11 In addition, these synthetic compounds are less costly as compared to albumin.

There were many implications to considerduring this case. Of primary importancewas the consideration of fluid shifts froman open abdominal cavity, fluid deficits,and resuscitation requirements from bloodand insensible fluid loss. In order to facili-tate extubation at the conclusion of surgery,fluid administration had to be carefullymanaged. Regrettably, CVP monitoringwas not initiated until later in the case, afterconsiderable resuscitative efforts had beenmade. If initiated early, it would have pro-vided a baseline as well as given anotherparameter in which to measure fluid status.

Colloid therapy was initiated early due tothe large amount of serous fluid that wasevacuated upon entering the abdominalcavity. Different colloids were utilized toprevent adverse effects from over-adminis-tration of albumin, hextend, or crystalloids.Anesthesia professionals should be familiarwith various colloid solutions to bettermanage cases involving large fluid require-ments in order to achieve favorable out-comes.

References

1. Lighthall GK, Pearl RG. Volume resuscitation if the critically ill:Choosing the best solution. J Crit Illness, 2003;18:252-260.

2. American Thoracic Society. Evidence-based colloid use in the critically ill:American Thoracic Society consensus statement. Am J Resp Crit Care Med,2004;170:1247-1259.

3. Bunn F, Alderson P, Hawkins V. Colloid solutions for fluid resuscitation. The Cochrane Database of Systematic Review, 20 January 2003:1-39.

4. McIntosh LW. Essentials of Nurse Anesthesia. New York: McGraw-Hill; 1997:191-202.

5. Soni N. Electrolyte solutions and colloids. In: Evers AS, Maze M, eds. Anesthetic Pharmacology: Physiologic Principles and Clinical Practice. Philadelphia, PA: Churchill Livingstone; 2004:751-762.

6. Waters E. Fluids, electrolytes, and blood component therapy. In:Nagelhout JJ, Zaglaniczny KL, eds. Nurse Anesthesia. 3rd ed. St. Louis,MO: Elsevier Saunders; 2005:373-389.

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7. Albumin (Human) 5% Solution [package insert]. Kankakee, IL: ZLB Behring; 2005.

8. Donnelly AJ, Baughman VL, Gonzales JP, et al. Anesthesiology & Critical Care Drug Handbook. 6th ed. Hudson,OH: Lexi-Comp; 2005.

9. Copelin, C. Practical points in the use of albumin for hypovolemia. Journal of PeriAnesthesia Nursing, 1998;13:118-120.

10. Stoelting, RK, Hillier, SC. Pharmacology and Physiology in Anesthetic Practice. 4th ed. Philadelphia, PA: Lippincott, Williams,& Wilkins;2006:868.

11. Kalamas, AG. In Stoelting RK, Miller RD, eds. Basics of Anesthesia. 5th ed. Philadelphia, PA: Churchill Livingstone; 2007:347-353.

Mentor: Michael Rieker, DNP, CRNA

ABSTRACT: Projected CRNA Retirement in Michigan over the Next 20 YearsLaura Acosta B.S.N., Scott Spiridigliozzi B.S.

University of Michigan

Keywords: CRNA, retirement, Michigan

Introduction: The average age of thepracticing CRNA is 48 years old and anestimated 32% of practicing CRNAs willretire within the next decade. The retire-ment trends of CRNAs in Michigan havenot been studied in the past ten years.

Purpose: This research was designed tostudy retirement and exit from practice ofMichigan CRNAs over the next 20 years.

Hypotheses: The outflow from the work-force will be greater than the inflow ofanesthesia providers in Michigan.

Methodology: A single mailing of 1178surveys were sent to the Michigan CRNAsvia U.S. mail. They were asked about theirprimary place of work, years in practice asa CRNA, average hours worked per week,and anticipated future retirement.

Results: The response was 529 for a returnrate of 45%. Of the respondents, 37% weremale and 63% were female with the meanage of 50 years. Their primary employment

was at mid-size hospitals (101-499 beds) at51%. The average Michigan CRNA wasemployed in more than one setting with anaverage 8 hours per week of overtime. Themean age for anticipated retirement was61.7 years old with an expectation to work14.5 hours per week after retirement. Thestrongest reasons to continue working afterretirement were maintaining friends andsocial contact at 58% and maintain skills at35%. After retirement, 38.4% will relocateon seasonal basis, 14.6% permanently, and1.3% as locum tenums.

Conclusion: The current literature statesthere will be a 32% deficit in CRNA servic-es, yet the response to our survey predicts a42% deficit. The impact may be somewhatmodulated by the number of responses ofCRNAs planning to provide anesthesiaservices part time after retirement.

Funding: Grant from the Office ofResearch, University of Michigan

Mentors: Patricia Klask, CRNA, MS;Lulu Bender CRNA, MS

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