Essential Emergency Medicine For the Healthcare Practitioner

1600 John F. Kennedy Blvd.Suite 1800Philadelphia, PA 191032899

ESSENTIAL EMERGENCY MEDICINE: FOR THE ISBN: 9781416029717HEALTHCARE PRACTITIONERCopyright # 2007 by Saunders, an imprint of Elsevier Inc.

All rights reserved. No part of this publication may be reproduced or transmitted in any form or byany means, electronic or mechanical, including photocopying, recording, or any information storageand retrieval system, without permission in writing from the publisher.Permissions may be sought directly from Elsevier's Health Sciences Rights Department inPhiladelphia, PA, USA: phone: (1) 215 239 3804, fax: (1) 215 239 3805, e-mail:[email protected]. You may also complete your request on-line via the Elsevierhomepage (http://www.elsevier.com), by selecting Customer Support and then ObtainingPermissions.

Notice

Knowledge and best practice in this field are constantly changing. As new research andexperience broaden our knowledge, changes in practice, treatment and drug therapy may becomenecessary or appropriate. Readers are advised to check the most current information provided (i)on procedures featured or (ii) by the manufacturer of each product to be administered, to verifythe recommended dose or formula, the method and duration of administration, andcontraindications. It is the responsibility of the practitioner, relying on their own experience andknowledge of the patient, to make diagnoses, to determine dosages and the best treatment for eachindividual patient, and to take all appropriate safety precautions. To the fullest extent of the law,neither the Publisher nor the Editor assumes any liability for any injury and/or damage to personsor property arising out or related to any use of the material contained in this book.

Library of Congress Cataloging-in-Publication DataEssential emergency medicine : for the healthcare practitioner / [edited by] Steven W. Salyer. 1st.p. ; cm.Includes bibliographical references.ISBN 1416029710

1. Emergency medicineHandbooks, manuals, etc.I. Salyer, Steven W.[DNLM: 1. EmergenciesHandbooks. 2. Emergency MedicineHandbooks.

WB 39 E768 2007]

RC86.7.E785 2007616.02'5dc22 2007000839

Acquisitions Editor: Rolla CouchmanDevelopmental Editor: Mary Beth MurphyProject Manager: Bryan HaywardDesign Direction: Steven Stave

Printed in the United States of America

Last digit is the print number: 9 8 7 6 5 4 3 2 1

To my wife Sally, my daughter Laura Emilie, and my son Zachary whogave up so much daddy time while I wrote and edited this second book.And to all those Physician Assistants and physicians who have chosen theprofession of EmergencyMedicine and who still go to work everyday stillcaring about the lives, hearts, and souls of their patients. And a specialprayer for all those men and women on the frontiers of freedom whoeveryday defend our way of life and keep us all free. God bless allof you!

Dedication

Contributors

GREG A. ABRAHAMIAN,MDAssistant Professor of Surgery, Transplant Center, University of Texas HealthScience Center at San Antonio, San Antonio, TexasChapter 20.Renal Transplantation

JONATHON ALLEN,MDDepartment of Emergency Medicine, Medical College of Georgia, Augusta,GeorgiaChapters 08.Diabetic Ketoacidosis; HyperglycemicHypersmolar Nonketotic Coma;

19. AcuteRenal Failure

CULLEN ARCHER,MDDepartment of Obstetrics and Gynecology, University of Texas Health ScienceCenter at San Antonio, San Antonio, TexasChapter10.Ectopic Pregnancy; HypertensiveDisorders of Pregnancy (Preeclampsia

andEclampsia)

MICHAEL A. AROCHO,MD,CPT,USAFUnited States Air Force

Chapter17.Lead; Mercury

SIMEONW. ASHWORTH,DO,CPT,MC,USAMadigan Army Medical Center, Tacoma, Washington

Chapter 03.ToxicodendronDermatitis

DAVE BARRY,MD,MAJ,MC,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapter17.Barbituates; Hallucinogens

CHARLES R.BAUER,MD,CPE,FACS,FACPE,FACEPDirector, Center for Public Health Preparedness & Biomedical Research,Professor of Surgery & Emergency Medicine, The University of Texas HealthScience Center at San Antonio, San Antonio, TexasChapter18. Abdominal Trauma; PelvicTrauma; ThoracicTrauma; Trauma in the

Pregnant Patient

ROGERMATTHEWBAUTISTA,MD,CPT,MC,USABrooke Army Medical Center, Fort Sam Houston, Texas

Chapters 07.Tetanus; 10.OvarianCysts

MARYANNBROWNING, FNPFamily Nurse Practitioner, Oregon Health & Sciences University, Instructor,Department of Emergency Medicine, Portland, OregonChapters 04. Jaundice andHepatitis; 13.Dehydration in Children; 19.UrinaryTract

Infections in Adults

vii

viii CONTRIBUTORS

JOHNH.CALHOON,MDProfessor, Department of Surgery, Chief, Division of Cardiothoracic Surgery,University of Texas Health Science Center, San Antonio, TexasChapter 20.Cardiac andLung Transplantation

JASON CAPRA,MDUnited States Air Force, Medical Corps

Chapter17.Cyanide

BARBARA A.CARR,MD,CPT,MC,USABrooke Army Medical Center, Fort Sam Houston, Texas

Chapters 06.Spider Bites and Scorpion Stings; 12. Acute Ankle Injuries

ROBERT L.CLOUTIER,MDOregon Health and Sciences University, Department of Emergency Medicine,Portland, OregonChapter13.Electrolyte andFluidManagement in Pediatric Patients

JIMMY COOPER,MD CAPT,MC,USAMadigan Army Medical Center, Tacoma, Washington

Chapter 02.Permanent Pacemakers

STEPHEN A.CRANDALL,MDDivision of Emergency Medicine, University of Washington, Madigan ArmyMedical Center, Tacoma, WashingtonChapter13. Asthma

CHRISTOPHERB.CROWELL,MDUniversity of Washington, Emergency Medicine Residency, Madigan ArmyMedical Center, Tacoma, WashingtonChapter13. Abdominal Pain

RICHARD L.DAGROSA,MDU.S. Air Force, Medical Corps

Chapter 07.Herpes Virus

CHARLES P.DAVIS,MD,PHDProfessor, Department of Surgery, Division of Emergency Medicine, Universityof Texas Health Science Center at San Antonio, San Antonio, TexasChapter19.CommonDisorders of the Penis

MOHAMUD DAYA,MDAssociate Professor of Emergency Medicine, Oregon Health and ScienceUniversity, Portland, OregonChapter17.Clonidine; Phenytoin

MARC L.DAYMUDE,MD,FACEPUnited States Army, Brooke Army Medical Center, Fort Sam Houston, Texas

Chapter 01. Abdominal Aortic Aneurysm (AAA); Appendicitis; Hernias; IntestinalObstruction; Thoracic Aortic Dissection

Contributors ix

JOHN T.DEEL,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20.Cardiac andLung Transplantation

CARRY DEPOLD, PA-CPhysician Assistant, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapters12.Elbow Injuries; 17. IronToxicity

GERALD D.DEPOLD,PA-C,MPASCaptain, Army Medical Specialist Corps

Chapters 06.Thermal Burns; 12.Elbow Injuries

DIANE DEVITA,MD,FACEPStaff Physician, DEM MAMC, Assistant Clinical Professor, University ofWashingtonChapter13. Asthma

AMY K.DITZEL, PA-CFamily Practice Physician Assistant

Chapters 07, Influenza; 10.Emergent Pelvic and Abdominal Pain; Genital Herpes

MARTIN A.DOCHERTY,MD,MAJOR,USARClinical Instructor, Division of Emergency Medicine, Washington UniversitySchool of Medicine, Attending Physician, Barnes-Jewish Hospital,St. Louis, MissouriChapters 02.CongestiveHeart Failure; Hypertensive Emergencies; 07.HIV Infections;

08.Geriatric Emergencies

GARY W.DUFRESNE,DO,CPT,MC,USABrooke Army Medical Center, Fort Sam Houston, Texas

Chapter 09. Seizures and Status Epilepticus

JENNY E.DUNLAVY,MD,CPT,USAFWilford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas

Chapters 06.Snakebite Injuries; 12.Foot Injuries

STEVE DURNING,MD,FACPDirector, Department of Medicine, Uniformed Services University of the HealthSciences, Bethesda, MarylandChapter 02.Mitral Valve Prolapse

TERRY EMANUEL,PA-C,MPASFaculty Associate, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters 08.Lactic Acidosis; 19.End-StageRenal Disease

x CONTRIBUTORS

ALFREDO ESPINOZA,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20.LiverTransplantation

ROBERT M.ESTERL,MDProfessor of Surgery, Transplant Center, University of Texas Health ScienceCenter at San Antonio, San Antonio, TexasChapter 20.Renal Transplantation

BARBARAM.FISHMAN,MDAssociate Professor, Department of Medicine, Department of EmergencyMedicine, University of Texas Health Science Center at San Antonio, SanAntonio, TexasChapters 08. Acid^Base Problems; Fluid andElectrolyte Emergencies; 17.Cocaine

JEFF FOXWORTH,PA-CDivision of Plastic Surgery, Department of Surgery, University of Texas HealthScience Center at San Antonio, San Antonio, TexasChapter18.TraumaOverview

MARK S.FUNK,MDDepartment of Obstetric and Gynecology, University of Texas Health ScienceCenter at San Antonio, San Antonio, TexasChapter10. Sexual Assault

RYAN GARNER,MDUnited States Air Force, Medical Corps

Chapter13.Neonatal Emergencies; HirschsprungsDisease or Congenital AganglionicMegacolon; Pyloric Stenosis; The AbusedChild; Tetralogy of Fallot

DAVID GLENDENING,MDAssociate Professor, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapter15. Adult Bacterial Pneumonias

VINITA GOYAL,MDDepartment of Obstetrics and Gynecology, University of Texas Health Scienceat San Antonio, San Antonio, TexasChapter10.Miscarriage (Abortion)

ROBERT D.GRAYDON,PA-C,MPASFaculty Associate, Department of Surgery, Division of Emergency Medicine,The University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters 08. AcuteEthanolWithdrawal; 17.GeneralPrinciples of thePoisonedPatient;

Anticholinergics; Ethanol Intoxication; EthyleneGlycol; Opioids

Contributors xi

LEN GRUPPO,PA-C,CPT, SP,USABrooke Army Medical Center, Fort Sam Houston, Texas

Chapter 02. Acute Pericarditis; Cardiac Examination; Evaluation of Cardiac ChestPain

GLENNHALFF,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20. LiverTransplantation

BENJAMIN P.HARRISON,MD,FACEP,LTC,MC,USAMadigan Army Medical Center, Tacoma, Washington

Chapters 03.ToxicodendronDermatitis; 08. Adrenal Insufficiency; 12.Hand Injuries

KATHERINE ANNEHARRISON,MDAssistant Professor, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters10.Pelvic Inflammatory Disease; Toxic Shock Syndrome; Vulvovaginitis;

12. Shoulder Injuries

GUYON J.HILL,MD,CAPT,MC,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapters 03.Toxic EpidermalNecrolysis; 06.Lightning Injuries; 17.Hydrocarbons;

Isoproponal; Methanol

DAVID A.HNATOW,MDAssociate Professor, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters 04.Gastrointestinal Bleeding; Acute andChronic Pancreatitis; 06.Chemical

Burns

REX L.HOBBS, JR.,MPAS,PA-CAssistant Professor, UT Southwestern Medical Center-Dallas, Dallas, Texas

Chapters 07.Diphtheria; 09.Bells Palsy; Botulism; Multiple Sclerosis; MyastheniaGravis; Neurological Examination

JULIE HUSLEY,PA-CFaculty Associate, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science at San Antonio, San Antonio, TexasChapter13.Bronchiolitis; Constipation; Sudden Infant Death Syndrome and Apparent

Life-Threatening Event Syndrome

JENNIFER JAMUL,PA-CFaculty Associate, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapter 07.Foodborne andWaterborne Infections

xii CONTRIBUTORS

ROYJOHNSON III,MDUniformed Services University of the Health Sciences, Andrews Air Force Base

Chapters13.Pediatric AirwayManagement; Pediatric Analgesia and Sedation; 17.Cyanide; Theophylline

SCOTT B. JOHNSON,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20.Cardiac andLung Transplantation

MELISSA KAGARISE,MMS,PA-CDepartment of Physician Assistant Studies, Saint Francis University, Lorretto,PennsylvaniaChapter13.Pediatric Pneumonia; Pharyngotonsillitis; 15. Aspiration Pneumonia

SANDEEPJ.KHANDHAR,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20.Cardiac andLung Transplantation

C.GORDONKING,MDDepartment of Medicine, University of Texas Health Science Center at SanAntonio, San Antonio, TexasChapter 08.Fluid andElectrolyte Emergencies

JOHN T.KODOSKY,PA-C,MMSFaculty Associate, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center, San Antonio, TexasChapters 04.Peptic Ulcer Disease; 18.Head andBrainTrauma

ADAM CLAY KOERTNER,MD,CAPTUnited States Air Force, Medical Corps

Chapter 08.Hyperthyroidismand Thyroid Storm (Thyrotoxicosis); HypothyroidismandMyxedemaComa

CHRISTOPHERM.KREBS,MD,CPT,MC,USAUniformed Services University of the Health Sciences, Andrews Air Force Base,MarylandChapter17.Theophylline

DAVIDW.KUHNS,MD,FACEPDepartment of Emergency Medicine, Darnall Army Community Hospital, FortHood, TexasChapters 03.Urticaria; 13.Kawasaki Disease

KHIMK.LAM,MDDepartment of Obstetrics and Gynecology, University of Texas Health Scienceat San Antonio, San Antonio, TexasChapter10. Abruptio Placentae; Amniotic FluidEmbolism

Contributors xiii

LINDA L. LAWRENCE,MD,FACEP COL,USAF,MCChief of Medical Staff, Emergency Medicine Consultant to Air Force SurgeonGeneralChapter13.Neonatal Emergencies; Pediatric AirwayManagement; Hirschsprungs

Disease or Congenital AganglionicMegacolon; Pyloric Stenosis; The AbusedChild;Tetralogy of Fallot; Pediatric Analgesia and Sedation

DEREKR.LINKLATER,MD,FACEP,FAAEMAssistant Program Director, Darnall Army Community Hospital EM ResidencyProgram, Assistant Clinical Professor of Emergency Medicine, Texas A&MSchool of Medicine, Assistant Clinical Professor of Military and EmergencyMedicine, USUHS School of MedicineChapter15.Pulmonary Embolism

REENIE LOPEZ,PA-CDepartment of Surgery, Division of Emergency Medicine, University of TexasHealth Science Center at San Antonio, San Antonio, TexasChapter13.Febrile Seizures

CLIFFORD C.LUTZ,MDMAJOR,MC,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapter 06.Hymenoptera Stings

JUSTINMADILL,DO CPT,MC,USADepartment of Emergency Medicine, Madigan Army Medical Center, Tacoma,WashingtonChapter 06. Submersion Incidents

ANANTHA K.MALLIA,DODepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapter17. AcetaminophenToxicity; Cyclic Antidepressant Toxicity; Digitalis Glycoside

Toxicity

MARGARET MANN-ZEBALLOS,MDDepartment of Surgery, Division of Emergency Medicine, University of TexasHealth Science Center at San Antonio, San Antonio, TexasChapter19.Prostatitis

DANIEL F.MCBRIDE,MDUnited States Army, Medical Corps

Chapter13.OtitisMedia

SAMUELTIMOTHYMCILRATH,MDMedical College of Georgia, Augusta, Georgia

Chapter13.Pediatric Bacteremia, Sepsis, andMeningitis; Pediatric Diarrhea

xiv CONTRIBUTORS

JOHNMCMANUS,MD,MCR,FACEP,LTC,MC,USAClinical Investigator at Army Institute of Surgical Research, Brooke ArmyMedical Center, San Antonio, Texas; Adjunct Assistant Professor EmergencyMedicine, Oregon Health and Science University, Portland, OregonChapters 06. Altitude-RelatedConditions; Frostbite; Hypothermia; 13.Cardiopulmon-

aryArrest in Children

CHRISTOPHERR.MCNEIL,MD,CPT,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapters 02. Automatic Implantable Cardioverter-Defibrillators; Cardiac Arrhythmias;

CardiacTamponade; Prosthetic Heart ValveDysfunction; Heart Transplant;08.Rhabdomyolysis; 13.Pediatric Cardiopulmonary Resuscitation; PediatricDiabetes andPediatric Diabetic Ketoacidosis

SUMERU GHANSHYAMMEHTA,MD,CAPT,MC,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapters 06.Heat Injuries; 10.OvarianTorsion; 19.Torsion of theTesticle

CARLMENCKHOFF,MD,FACEP,FAAEMAssociate Professor, Residency Director, Department of Emergency Medicine,Medical College of Georgia, Augusta, GeorgiaChapters 01.WoundManagement; 12. Injuries to the ForearmandWrist; Injuries to

the Lower Leg

KAZUOMIHATA,MDUnited States Air Force, Medical Corps

Chapter13.Neonatal Emergencies; HirschsprungsDisease or Congenital AganglionicMegacolon; Pyloric Stenosis; The AbusedChild; Tetralogy of Fallot

MICHAEL A.MILLER,MD,LTC,MC,USADepartment of Emergency Medicine, Darnall Army Community Hospital, FortHood, TexasChapter17. Amphetamines; Lithium; Organophosphorus andCarbamate Insecticides

Poisoning

JAMES ALANMORGAN,DO,COL,MC,USA (RET)Assistant Professor, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters 06.MarineFaunaEvenomations; 15. AcuteRespiratory Distress Syndrome;

Hemoptysis; 17.CarbonMonoxide

JULIE ANNMORGAN,MD,COL,MC,USA (RET)Brooke Army Medical Center, Fort Sam Houston, Texas

Chapters 06.Electrical Injuries; Marine Fauna Evenomations; 15. AcuteRespiratoryDistress Syndrome; Hemoptysis; 17.CarbonMonoxide

KARIMURPHEY, PA-CEmergency Medicine Physician Assistant, Medical College of Georgia, Augusta,GeorgiaChapter19.Renal Stones

Contributors xv

YOKONAKAMURA,MDVisiting Physician, Department of Emergency Medicine, Oregon Health andScience University, Portland, OregonChapter17.Clonidine; Phenytoin

ALICIA NASIR,RN,BSNAndrews Air Force Base, Maryland

Chapter 02.Mitral Valve Prolapse

JAVEDM.NASIRMedical Student, Uniformed Services University of the Health Sciences

Chapter13. AcuteRheumatic Fever

ROBERT NOLAN,DO,CPT,MC,USAChief Resident, Emergency Medicine, Madigan-University of Washington,Tacoma, WashingtonChapter15.Pneumothorax

BRENDAOSWALD,PA-C,MHEPhysician Assistant in Emergency Department at Medical College ofGeorgia, Assistant Emergency Medicine Physician Assistant ResidencyDirector, Clinical Faculty with Physician Assistant Department, Augusta,GeorgiaChapter12, Injuries to the ForearmandWrist; Injuries to the Lower Leg

STACEY BLACK PEARLMAN,PA-C,MPASSaint Vincent Hospital at Worcester Medical Center, Worcester, Massachusetts

Chapter15.TheBasics of VentilatorManagement in the Emergency Department;Ventilator Settings andOngoingMonitoring of Critical Patients in the EmergencyDepartment; Sedation and Analgesia in the IntubatedPatient

JAMES A.PFAFF,MD,COL,MC,USA (RET)Brooke Army Medical Center, Department of Emergency Medicine, Fort SamHouston, TexasChapter 05.Dental Emergencies; Maxillofacial Injuries; Ophthalmological

Emergencies; Otolaryngolical Emergencies; Pharyngitis; Sialolithiasis;Sinusitis; Dental Trauma

KRISTEN A.PLASTINO,MDAssistant Professor, Program Coordinator, Sex Education Program, AssociateResidency Program Director, Department of Obstetrics and Gynecology,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapter10.Placenta Previa

ERIC R.PRESSERTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20.Cardiac andLung Transplantation

xvi CONTRIBUTORS

LONRAMEY,PA-CFaculty Associate, Division of Neurosurgery, Department of Surgery, Universityof Texas Health Science Center at San Antonio, San Antonio, TexasChapter18. Spinal Cord Injuries

JAKE ROBERTS,DO,CPTDepartment of Emergency Medicine, Madigan Army Medical Center, Tacoma,WashingtonChapter13.UrinaryTract Infections in Children

DAWN F.RONDEAU,RN,MS, ACNP-CSAcute Care Nurse Practitioner, Washington State University, Pullman,WashingtonChapter13.Upper Respiratory Emergencies in Children

STEVENW.SALYER,PA-C,CPT,USA (RET)Emergency Medicine Physician Assistant, San Antonio, Texas

Chapters 09. Ataxia,Dizziness, and Vertigo; Headaches; 12.Basic Principles ofOrthopedic Injuries; AcuteBack Pain; 13.The Pediatric Patient: AnOverview;Seizures and Status Epilepticus; 15.Chronic Obstructive Pulmonary Disease;18.GenitourinaryTract Trauma; PediatricTrauma

KATHLEENM.SAMSEY,MD,CPT,MC,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapter12.HipTrauma

JOHNROBERT SCOTT,MDAssistant Professor, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters11.Blood Transfusions; 13.Reyes Syndrome

MICHAEL K. SHAFE, MD, FACEP, FAAEMAssistant Professor Department of Emergency, Medical College of Georgia,Augusta, GeorgiaChapters 08.Disseminated Intravascular Coagulation; 11. AcuteBleeding Diathesis;

Hemophilia; Sickle Cell Anemia

MARK S. SHORT,PA-C,CAPTU.S. Army

Chapter12.Hand Injuries

SEANMICHAEL SILER,DO,CAPT,MC,USADepartment of Emergency Medicine, Brooke Army Medical Center, Fort SamHouston, TexasChapter 06.Diving Injuries

JACQUELYN L. SIMONDS,PA-C,MPASDepartment of Emergency Medicine, Darnall Army Community Hospital, FortHood, TexasChapters10.Breast Abscesses andMastitis; 13.Kawasaki Disease

Contributors xvii

HOWELL J. SMITH III, PA-C,CPT,USA (RET)Orthopedic Physician Assistant, Veterans Administration, Tampa, Florida

Chapter12. Acute Knee Pain

K.VINCENT SPEEG,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20. LiverTransplantation

RICHARD J. SPITZ,MDClinical Assistant Professor, Department of Surgery, Department of EmergencyMedicine, University of Texas Health Science Center at San Antonio, SanAntonio, TexasChapters 03.ErythemaMultiforme; 08. Alcoholic Ketoacidosis

LAURA ANN SPIVAK,MDMedical Toxicology, Oregon Health and Science University, Department ofEmergency Medicine, Oregon Poison Center, Portland, OregonChapter17. Arsenic; Beta-Blocker Overdose; Calcium-Channel Blockers; Caustic

Ingestions

MARK STEVENS,PA-C,CPT,USA (RET)Faculty Associate, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapter17. Salicylates

BENJAMINH.TAYLOR,PHD,PA-CMedical College of Georgia, Augusta, Georgia

Chapters 03.ExfoliativeDermatitis; 12. Infections of theBones and Joints

RALPH TERPOLILLI,MDAssociate Professor, Department of Surgery, University of Texas Health ScienceCenter at San Antonio, San Antonio, TexasChapter 09. Acute Stroke Syndromes

SHAWNM.VARNEY,MD,LTCOL,USAF,MCFlight Commander, 959 MSFS, Wilford Hall Medical Center, Lackland AirForce Base, TexasChapters 04.Diverticulosis andDiverticulitis; 08.Hypoglycemia

BROOKE ASHLEY VEALE,PA-CAssistant Professor, Department of Physician Assistant Studies, University ofTexas Southwestern Medical Center at Dallas, Dallas, TexasChapters 07.Malaria; 14.PanicDisorder; Generalized Anxiety Disorder; Conversion

Disorder; Personality Disorders; ParanoidPersonality Disorder; SchizoidPersonal-ity Disorder; Schizotypal Personality Disorder; Antisocial Personality Disorder; Bor-derline Personality Disorder; Histrionic Personality Disorder; Narcissitic PersonalityDisorder; Avoidant Personality Disorder; Dependent Personality Disorder; Obses-sive-Compulsive Personality Disorder; Suicide

xviii CONTRIBUTORS

SHAWNAWALL,MDDepartment of Obstetric and Gynecology, University of Texas Health ScienceCenter at San Antonio, San Antonio, TexasChapter10.Hyperemesis Gravidarum

KENNETHWASHBURN,MDTransplant Center, University of Texas Health Science Center at San Antonio,San Antonio, TexasChapter 20.LiverTransplantation

IANWEDMORE,MD,FACEP,LTC,MC,USAAssistant Chief, Department of Emergency Medicine, Madigan Army MedicalCenter, Tacoma, WashingtonChapter 06. Altitude-RelatedConditions; Hypothermia

RYANWELLS,MDWillford Hall Medical Center, Lackland Air Force Base, San Antonio, Texas

Chapters 01.Cholelithiasis and Cholecystitis; 15. Asthma

ALLENWHITFORD,DO,LTC,MC,USA (RET)Assistant Professor, Department of Emergency Medicine, University of TexasHealth Science Center at San Antonio, San Antonio, TexasChapter16. AirwayManagement; Shock

CLAUDIO F. ZEBALLOS,MDAssistant Professor, Department of Surgery, Division of Emergency Medicine,University of Texas Health Science Center at San Antonio, San Antonio,TexasChapters 04. Anorectal Disorders; 07.Rabies; 19.Epididymitis

DAVID ZINSMEISTER,PA-CAssistant Professor, Department of Orthopedics, University of Texas HealthScience Center at San Antonio, San Antonio, TexasChapter12. Acute Compartment Syndrome; OpenFractures

Preface

When I first walked into an Emergency Room in 1987, as a youngPA student, CTs were just coming into general use. MRIs were anexperimental radiological test, tPA and Streptolinase-plasminogen werestill voodoo medicine and cardiac catheterization labs were not yet ingeneral use. We had to practice medicine!

Back then we still examined patients. We had to! We did not have theradiological or laboratory tests we had today. We talked to patients andlistened to them. Patients told us what was wrong with them. You didn'thave to have three specialty consults before you could get someoneadmitted. No one got sued! Patients and insurance companies paid theirbills. Patient's respected doctors and PAs; we respected patients andtheir beliefs. We asked about their families. We were able to talk aboutfishing! Emergency Medicine wasn't yet a business.

With that said, things have gotten better. If you diagnosed someonewith HIV/AIDS in 1987, it was a death sentence. With the four drugtherapies of today, the life expectancy of someone with HIV is normal.Cardiac catheterization and stents save thousands of lives yearly. Wehave orthopedic replacement parts for just about every joint!

On the horizon, stem cell research will cure many diseases in ourlifetime. Gene splicing will prevent future human beings from everdeveloping the diseases that kill us today. We will develop a vaccinefor HIV.

Emergency Medicine will change and evolve just like all other medi-cal specialties. But we will always be the safety net of society. Emer-gency Medicine and the emergency room will always be the lastrefuge of the sick, injured, tired, and lonely. We will still see and treatall comers no matter what their insurance is or what side of town theylive on. They probably won't pay us. If they think we messed up, theywill find a lawyer on TV and sue us. We will still listen and console.We will be social worker, chaplain, big brother, and the giver of hopeat 3 AM. We will still see that one last patient 5 minutes before our shiftchange, and we will always leave late. This book is a continuum of theevolution of Emergency Medicine.

I spent 4 years in the 2nd Armored Calvary Regiment in Germany.I am a veteran of Desert Storm I. I have practiced a lot of emergencymedicine during my time in the Army in a tracked vehicle and a tent.Whether in a tent or a modern emergency center, the principles of emer-gency medicine are the same; care for the individuals body, save lives,and never forget to care about the person.

xix

xx PREFACE

The 2nd Calvary Regiment is the longest continuous active-duty unitin the U.S. Army (1832). During WWI in France, the regiment obtainedthe regimental motto of Toujours Pret (always ready). If EmergencyMedicine ever had a motto I believe it would also be Toujours Pret.

Steven W. Salyer, PA-C

Introduction

This is my second book on Emergency Medicine. I wrote the first bookin its entirety. This is not a second edition of the first book. I selectedthe best emergency medicine physician assistants and emergency medi-cine physicians in the country to contribute to this book. Many of thechapter's authors were or are faculty at Emergency Medicine residen-cies. These are the best emergency medicine minds I could find.

I also sought the best non-emergency medicine minds to write thecomplementary chapters to the book. There is no better an example ofthe quality of their writing than in the transplant chapters. I haveexpanded the transplant chapter to include topics on heart, lung, liverand kidney transplants. These topics are written by some of the besttransplant practitioners in the country.

This is a unique book in that the contributing chapter authors arePhysician Assistants, Nurse Practitioners and physicians. It is editedby a Physician Assistant. This collaboration of different practitionersis unique in the medical publishing community. The evolution of theteam process is evident in collaboration in the production of thisbook.

With the business concern over billing and reimbursement, we haveadded ICD codes to the beginning of each chapter. This addition willhelp with identification of the illness or disease and hopefully willincrease reimbursement.

We have also added Key Points and Emergency Actions at thebeginning of each topic. In a busy emergency department, the KeyPoints section will serve as a quick reference to give the practitionerthe key points of knowledge about the illness or condition. The Emer-gency Actions section of each topic will act as a quick reference for thepractitioner to refer to what emergency actions need to be takenimmediately.

This book is designed to be used, not to sit on a shelf. In a year'stime, its corners should be bent and its pages worn. Please enjoy anduse this book.

xxxv

Chapter 1

Acute Surgical Abdominal Emergencies

Abdominal Aortic Aneurysm (AAA)MARC L.DAYMUDE

ICD Code: 441.4

Key Points/Quick Reference

Abdominal aortic aneurysm (AAA) is diagnosed in most patients as anincidental finding on examination or radiologic procedure for anotherreason. Most patients who present with ruptured AAA, a life-threateningcondition, are unaware that they have an AAA. Ruptured AAA should besuspected in all patients at risk who report abdominal pain, back or flankpain, or symptoms of hypotension such as syncope, even if transient.

! Emergency Actions ! If an AAA is suspected, two large-bore intra-venous (IV) lines should be started, a cardiac monitor should be placed,emergent abdominal ultrasound and computed tomography (CT) scansshould be performed, and an emergent surgical consult should be obtained.

DEFINITION

An aneurysm is a permanent, focal dilation of an artery to greater than1.5 times its expected diameter, involving all layers of the arterial wall(i.e., intima, media, and adventitia). Although any artery can develop ananeurysm, it is most commonly found in the infrarenal aorta. An infrarenalaortic diameter of 3 cm or greater is defining. This is a different entity fromdissection, in which blood flows through a tear in the intima, resulting in afalse lumen and dilation of the artery. Pseudoaneurysms are localizedarterial wall ruptures that are contained by the adventitia and fibrousreaction and result in focal arterial wall expansion. They commonly resultfrom trauma, infection, or previous surgical intervention of the arterialwall.

EPIDEMIOLOGY

AAA is a disease primarily of the elderly. Risk factors include atheroscle-rotic disease, age older than 50 years, and hypertension. Smoking is themost important risk factor. Men are affected twice as often as women.AAA in first-degree relatives represents an 11.6-fold increased risk.Patients with connective tissue disorders such as Ehlers-Danlos or

1

2 ESSENTIAL EMERGENCY MEDICINE FOR THE HEALTHCARE PRACTITIONER

Marfan syndromes may develop AAA at an earlier age. Incidence in theUnited States is estimated at 2%4% in patients older than 50 years andincreases to 5%10% in men over the age of 65 years. The majority ofAAAs occur distal to the renal arteries. Two percent extend proximallyto include the renals and thoracic portion of the aorta. Forty percent extenddistally to involve the iliac arteries. The natural progression of AAA is togradually expand, then rupture, resulting in fatal hemorrhage. The aver-age rate of enlargement is 0.4 cm/yr. The risk of rupture increases withdiameter. AAAs less than 4 cm in diameter have very low risk of rupture,whereas the risk for 4- to 5-cm AAAs is 1%3%/yr, for those 57 cm is6%11%/yr, and for those greater than 7 cm is 20%/yr. The mortality ratefor ruptured AAA is 78%94%, with only half of patients surviving thejourney to the hospital. The operative mortality rate for ruptured AAAis approximately 50%. Ruptured AAA accounts for an estimated 15,000deaths per year in the United States and is the tenth leading cause of death.Seventy-five percent of patients presenting to the hospital with a rupturedAAA are unaware that they have an AAA. AAA management is aimed atprevention of rupture and usually involves elective surgical repair. Electivesurgical mortality is less than 5%. Patients who survive repair have anexcellent prognosis, with life expectancy similar to nonaffected cohorts.The cause of death in these patients is usually from cardiac causes.

CLINICAL PRESENTATION

Most patients are diagnosed with AAA as an incidental finding duringphysical examination or radiographic procedure performed for anotherreason; most patients are asymptomatic at the time of presentation. Thetriad of abdominal pain, palpable pulsatile abdominal mass, and hypoten-sion is present in only 30%50% of patients with ruptured AAA. Patientsoften present with atypical complaints. The majority of ruptures are leftretroperitoneal and may result in left lower quadrant pain and tenderness.Flank pain mimicking renal colic is common, and ureterolithiasis ismisdiagnosed in 10% of patients with AAA. Expansion of a retroperito-neal hematoma may result in compression of nerve roots, most commonlyfemoral and obturator. Five percent of patients report neurologic prob-lems, including anterior thigh pain and numbness with hip flexorweakness. Syncope, diaphoresis, nausea, and vomiting may be the onlysymptoms related to transient hypotension. Twelve percent of AAAs areinitially diagnosed as diverticulitis. Five percent present with peripheralmicroemboli resulting in blue toe syndrome. Hypotension and shockmay dominate the presentation. Retroperitoneal ruptures may tamponadeand have delayed presentations of days to weeks. Free intraperitoneal rup-tures that occur in 10%30% result in rapid exsanguination, and thesepatients rarely survive long enough to make it to the hospital. The

Abdominal Aortic Aneurysm (AAA) 3

expanding mass of the AAAmay erode into adjacent structures. Aortoen-teric fistula results from erosion into the duodenum (most common)and can present as massive upper gastrointestinal tract bleeding. Erosioninto the inferior vena cava results in aortocaval shunting and high-outputheart failure manifested as dyspnea, jugular venous distention, venousdistention, and pulmonary edema.

EXAMINATION

Physical examination is not a reliable method to exclude AAA in thepatients at risk. A pulsatile abdominal massespecially if it extends tothe right of midlineis suggestive. However, only 30% of AAAs 34cm in diameter, 50% of AAAs 45 cm, and 75% of AAAs greater than5 cm are palpable. Abdominal bruits are present in only 5%10% andmay indicate atherosclerotic occlusive disease of other vessels. Femoralpulses usually are normal.

LABORATORY FINDINGS

Laboratory findings are not helpful in establishing the diagnosis ofAAA and may be misleading. Hematuria may result from compressionof the ureters and is common in aortocaval fistula due to increased renalvein pressure. This, in the face of reports of flank pain, may suggestureterolithiasis.

DIAGNOSIS

Ruptured AAA should be in the differential diagnosis of any patient overthe age of 50 years who presents with flank or abdominal pain, hypoten-sion, or syncope. In a patient whose condition is unstable, a palpable, pul-satile abdominal mass is all that is needed to obtain emergent surgicalconsultation for immediate surgery. In other patients, ultrasound or CTscans may be necessary to establish the diagnosis.

RADIOGRAPHS

Plain radiography of the abdomen may reveal the eggshell appearanceof a calcified AAA, but it is not helpful in excluding AAA from the differ-ential diagnosis in patients who are at risk. Multiple studies have demon-strated that ultrasound is 100% sensitive in the detection of AAA and thatthis can be done at the bedside in the emergency department (ED) byemergency physicians using portable ultrasound devices with the sameaccuracy. ED bedside ultrasound for AAA has been demonstrated to sig-nificantly decrease time to diagnosis and disposition. Obesity and bowel


gasmay limit visualization of the aorta in some patients, making diagnosisdifficult. All patients who are at risk for AAA should have bedside ultra-sound scanning performed in the ED. Stable patients can undergo a formalultrasound or CT scan. The advantages of CT over ultrasound are that CTcan better define the extent of disease, identify retroperitoneal hemor-rhage or rupture, or identify alternative diagnoses in the setting of a nor-mal aorta. The major disadvantage is that the patient must leave the EDto go to receive the CT scan, and resuscitation is often difficult in thatsetting. Aortography is helpful for preoperative planning in electiverepairs but is not indicated for diagnosis in the ED.

TREATMENT AND OUTCOME

For patients whose AAA is found incidentally and is truly asymptomatic,outpatient referral to surgery for elective repair is appropriate. These patientsshould be cautioned to return for any symptoms potentially referable toAAA. Patients who have suspected rupture of AAA require access via twolarge-bore IV lines. Blood samples should be drawn for baseline completeblood count (CBC), blood urea nitrogen (BUN)/creatinine and electrolytemeasurements, coagulation studies, and type and cross-match for 10 unitsof blood. Definitive treatment requires operative repair. An emergencysurgical consultation should be made as soon as the diagnosis of rupturedAAA is suspected. Preoperative hypotension is themost important prognos-ticator of mortality. Patients whose conditions are unstable require aggres-sive fluid/blood product resuscitation to maintain a systolic blood pressureof 90100 mmHg or adequate cerebral (i.e., normal mental status) andcardiac (no ischemic chest pain/electrocardiographic changes) perfusion.

Bibliography

Barkin AZ, Rosen CL: Ultrasound detection of abdominal aortic aneurysm, Emerg MedClin North Am 2004;22(3):675682.

Bessen HA: Abdominal aortic aneurysm. In Marx J (ed): Rosens Emergency Medicine:Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 11761186.

Lin PH, Bush RL, McCoy SA, et al: A prospective study of a hand-held ultrasound devicein abdominal aortic aneurysm evaluation, Am J Surg 2003;186(5):455459.

Rogers RL,McCormack R:Aortic disasters,EmergMedClin North Am 2004; 22(4):887908.Salen P, Mclanson S, Buro D: ED screening to identify abdominal aortic aneurysm in

asymptomatic geriatric patients, Am J Emerg Med 2003;21(2):133135.Zarins CK, Heikkinen MA, Hill BB: Aneurysmal vascular disease. In Townsend CM (ed):

Sabiston Textbook of Surgery, ed 17. Elsevier: St Louis, 2004, pp 19691981.

AppendicitisMARC L.DAYMUDE

Appendicitis 5

ICD Code: 541


Classically acute appendicitis develops as diffuse, periumbilical painfollowed by nausea, vomiting, low-grade fever, and anorexia. Over thecourse of 12^18 hours, the pain localizes to the right lower quadrantwith evidence of local peritoneal irritation on examination. The CBC anddifferential that usually show an elevated white blood cell count (WBC)with a left shift andnormal urinalysis results are themost relevant labora-tory findings. Diagnosis may be made purely on the basis of history andphysical examination in classic cases, or it may require an ultrasound orCT scan in conjunction with surgical consultation. Treatment is primarilysurgical.

! Emergency Actions ! Patients who present having experienced1218 hours of abdominal pain and the above symptoms should have theirfluids replenished; should be treated for their pain, nausea, and vomiting;and should undergo an emergent abdominal CTscan. If an acute appendicitisis present, an emergent surgical consult should be obtained.

DEFINITION

The appendix is an appendage off the base of the cecum of uncertain func-tion. It contains lymphoid and mucus-producing tissues. In an adult, itslength averages 9 cm but may range from 2 to 22 cm. The location ofthe tip varies from retrocecal, intraperitoneal in 65% to pelvic in 30%and retroperitoneal in 2%. Acute appendicitis is an inflammatory processof the appendix, usually precipitated by luminal obstruction caused bylymphoid hyperplasia, appendicolith, fecal material, or other foreign bodyresulting in bacterial overgrowth.

EPIDEMIOLOGY

Normal appendiceal lymphoid tissue gradually increases through adoles-cence then slowly decreases after the third decade, corresponding to peakincidence of appendicitis in the late teens to 20s. The lifetime risk ofacute appendicitis is 8.6% in men and 6.7% in women, with a general


population perforation rate of 17%20% and a mortality rate of 0.25%.Although appendicitis is less common in young children and elderly per-sons, perforation rates are as high as 30%65% in children and 70% inpatients older than 60 years. Children also have a higher rate of generalperitonitis. The mortality rate in elderly persons is 4%8%, and the riskof complications and mortality increase with perforation. Annually,250,000 appendectomies are performed in the United States. Historically,attempts were made to balance the risk of perforation with its higher inci-dence of complications and mortality in patients with unrecognizedappendicitis with the removal of normal appendices. Negative appendec-tomy rates were accepted at 15%20% to decrease the chances of missinga case of appendicitis that would go on to perforate.


The typical history of appendicitis is of generalized abdominal pain fol-lowed by nausea and anorexia. Pain is initially most prominent in the epi-gastrium, then migrating to the periumbilical region, and over a period ofhours localizing in the right lower quadrant. Pain typically precedes theonset of nausea and vomiting. As the pain becomes localized, patientsmay report that activities that jar the abdomen such as jumping, bumpsin the road while driving, or coughing exacerbate the pain. Diarrhea isuncommon except in children. Low-grade fever may be present. Becauseof the varied location of the tip of the appendix, atypical presentations arenot uncommon and occur in 20%33% of affected patients. Atypicalpresentations are more likely in elderly persons and in young children.The location of the appendix is also affected by pregnancy, with its positionbecoming more cephalad and lateral as the gravid uterus displaces abdomi-nal contents with the progression of pregnancy; this alters the site of pain, aswell. Eighty-three percent of patients present in the first 48 hours of theinflammatory process. Patients who present beyond that time are morelikely to have a perforated appendix, fever, and evidence of peritonitis.

EXAMINATION

Examination of the abdomen may reveal diminished bowel sounds andlocalized tenderness in the right lower quadrant. With the progression ofinflammation, abdominal muscle spasm may progress from voluntary inresponse to pain to involuntary guarding. Rebound tenderness may alsodevelop. Signs of peritoneal irritation are often present but are not specificfor appendicitis. Psoas sign is elicited by having the patient lie on his orher left side while the right thigh is flexed backward. Pain may indicatean inflamed appendix overlying the psoas muscle. Rovsing sign is pain

Appendicitis 7

referred to the right lower quadrant when the left lower quadrant is pal-pated. A positive obturator sign is pain that is elicited in a supine patientby internally and externally rotating the flexed right hip. Rectal examina-tion may reveal right rectal tenderness or an inflammatory mass. Womenrequire pelvic examination to identify possible gynecologic sources oftheir pain. With perforation, abdominal pain, tenderness, and guardingmay be more pronounced and diffuse.

LABORATORY FINDINGS

The total leukocyte count is elevated over 10,000 in 88% of patients withappendicitis. An elevation of the percentage of neutrophils (left shift) isimportant even in the setting of a normal totalWBC. A completely normalWBC and differential is uncommon. The C-reactive protein level may beelevated but is not specific. Urinalysis may reveal pyuria due to the prox-imity of the ureter to the appendix. Other laboratory tests are neither spe-cific nor helpful in establishing the diagnosis, except to exclude otherpossible diagnoses. A pregnancy test should be performed on all womenof childbearing age.

DIAGNOSIS

The diagnosis of appendicitis is made primarily based on history and theresults of a physical examination. Corroborative evidence includes eleva-tion of theWBC or left shift. In patients who do not have a typical presen-tation or physical findings or in whom alternative diagnoses cannot beexcluded, radiologic studies can help establish the diagnosis.

RADIOGRAPHY

Plain radiographs may reveal an appendicolith but are generally not useful.Ultrasound scanning using graded compression has been shown inmultiplestudies to have greater than 85% sensitivity and 90% specificity. Sono-graphic criteria for the diagnosis of acute appendicitis are noncompressibleappendix greater than 7 mm in diameter, the presence of an appendicolith,submucosal incontinuity, or periappendiceal fluid or mass. It is less sensi-tive for perforated appendicitis. Sonography is operator dependent, andpatient body habitus can affect performance. CT has essentially supplantedultrasound scanning, except in specific patient populations such as pregnantwomen or persons with contrast allergy. The sensitivity and specificity ofCT for appendicitis are both around 90%, depending on the clinical studyand the use of oral, IV, and rectal contrast. CTcriteria for diagnosing appen-dicitis are an appendix greater than 57 mm in diameter, a target sign of


circumferential thickening, and periappendiceal inflammation. CT in con-junction with serial examinations and clinical observation in patients whohave atypical presentations or equivocal findings or who are at high riskhave lowered the negative appendectomy rate to 2% in some studieswithout increasing the rate of perforation.


When the diagnosis of appendicitis is suspected, urgent surgical consulta-tion is required. Vomiting and anorexia can result in dehydration. Patientsshould receive replenishing fluids and not receive anything by mouthbefore possible surgery. Narcotic pain medications have been shown notto significantly change physical examination findings. The patients painshould be addressed. If perforation is suspected, treatment with broad-spectrum antibiotics that cover coliform and anaerobic bacteria shouldbe initiated. Definitive treatment requires surgical removal of the inflamedappendix, either laparoscopically or by open technique, as determined bythe consultant.

Bibliography

Cydulka RK: Meta-analysis of the clinical and laboratory diagnosis of appendicitis[abstract], Ann Emerg Med 2005;45(1):105.

Jones K, Pena AA, Dunn EL, et al: Are negative appendectomies still acceptable? AmJ Surg 2004;188(6):748754.

Lally KP, Cox CS, Andrassy RJ: Appendix, In Townsend CM (ed): Sabiston Textbook ofSurgery, ed 17. Elsevier: St Louis, 2004.

Lin CJ, Chen JD, Tiu CM, et al: Can ruptured appendicitis be detected preoperatively inthe ED? Am J Emerg Med 2005;23(1):6066.

McCollough M, Sharieff GQ: Abdominal surgical emergencies in infants and young chil-dren, Emerg Med Clin North Am 2003;21:909935.

Morris KT, Kavanagh M, Hansen P, et al: The rational use of computed tomography scansin the diagnosis of appendicitis, Am J Surg 2002;183(5):547550.

Storm-Dickerson TL, Horattas MC: What have we learned over the past 20 years aboutappendicitis in the elderly? Am J Surg 2003;185(3):198201.

Wolfe JM, Smithline HA, Phipen S, et al: Does morphine change the physical examinationin patients with acute appendicitis? Am J Emerg Med 2004;22(4):280285.

Cholelithiasis and CholecystitisRYANWELLS

Cholelithiasis and Cholecystitis 9

ICD Codes: Calculus of gallbladder with acute cholecystitis574.0, Calculus of gallbladder with othercholecystitis 574.1, Acute cholecystitis 575.0,Other cholecystitis (without mention ofcalculus) 575.1

Key Points

Cholelithiasis (gallstones) is a very common presenting feature in obese,fertile female patients. Cholecystitis causes prolonged pain in the upperabdomen.The diagnosis of cholelithiasis should be entertained in any dia-betic patient with right upper quadrant pain, fever,nausea, and vomiting.

! Emergency Actions ! Any patient who presents with fever, sepsis,and cholelithiasis should be administered IV fluids and antibiotics, and animmediate right upper quadrant ultrasound scan should be performed. Animmediate surgical consultation should be sought.

DEFINITION

Gallstones are crystalline structures formed from both normal and abnor-mal bile components. Bile is a pigmented, isotonic fluid that is composedof primarily water and bile acids. Bile is formed in the hepatocytes and isrequired for the breakdown and absorption of fats in the intestines. Thebiliary tract consists of the gallbladder, the hepatic bile canaliculi, theintrahepatic bile ducts, the extrahepatic bile ducts, the cystic duct, andthe common bile duct. Bile is manufactured in and secreted from hepato-cytes before being transported via portions of the biliary tract to the gall-bladder for storage. While in the gallbladder, stored bile is concentratedand acidified. Cholelithiasis is the formation of gallstones in any part ofthe biliary tract. Seventy percent of gallstones are cholesterol stones,and the remainders are pigment stones. The principal cause of biliary tractdisorders is related to the formation of gallstones. Gallstones can beasymptomatic, or they can lead to obstruction of the gallbladder and bileducts, resulting in symptomatic cholelithiasis, cholecystitis, pancreatitis,or cholangitis. Cholecystitis is an acute inflammation of the gallbladdertypically caused by gallstone obstruction of the neck of the gallbladder


or at the cystic duct. However, between 5% and 10% of cholecystitis isacalculous (without gallstones).

EPIDEMIOLOGY

An estimated 10%20%ofAmericans have gallstones, and asmany as onethird will develop cholecystitis. Risk factors for the development of chole-lithiasis and subsequent cholecystitis include increasing age, obesity,female sex, rapid weight loss, pregnancy, oral contraceptives, medications,chronic intravascular hemolysis, andmultiparity. There is also an increasedfamilial tendency for the formation of gallstones. There is an increasedincidence in Pima Indians and persons of Scandinavian heritage. Choleli-thiasis is less common in children, yet the condition does occur in thisage group. Diseases involving hemolytic anemia (e.g., spherocytosis andsickle cell anemia) increase the likelihood of developing gallstones.

It is important to note that even patients without classic risk factorsdevelop gallstones and cholecystitis. Therefore, a high index of suspicionshould be maintained for anyone presenting with symptoms consistentwith gallbladder disease.

PATHOPHYSIOLOGY

Bile is formed in the hepatocytes and is transported via the biliary tree tothe gallbladder. The gallbladder stores approximately 50 ml of bile at anyone time. When the stomach receives food (especially fatty food), bothvagal responses and secretion of cholecystokinin cause the gall bladderto contract. Bile is released into the duodenum for digestion of a meal.

The purpose of the gallbladder is to concentrate and acidify the bile.When this process is increased or rapidly reproduced andwhen rising cho-lesterol levels are present, lecithin and bile acids act to solubilize choles-terol. While cholesterol levels rise and lecithin and bile acids decline,cholesterol comes out of solution and forms crystals or stones.

Gallstones can consist of three types: cholesterol, pigmented, andmixed. Between 70% and 80% of gallstones are cholesterol stones. Pig-mented gallstones come in two types: brown and black. Black gallstonesoccur in the gallbladder and contain high concentrations of calcium bilir-ubinate. Black gallstones are found more often in elderly persons and inthose with sickle cell disease and hereditary spherocytosis. Brown gall-stones are found in the gallbladder, intrahepatic duct, and extrahepaticduct. Brown gallstones are more often associated with infection.

Gallstones may migrate into either the cystic or common bile duct andbecome lodged, leading to symptomatic cholelithiasis. The consequentobstruction leads to increased intraluminal pressure and distention of thegallbladder, causing pain in the right upper quadrant or epigastric regionof the abdomen, nausea, and vomiting.


If the obstruction persists, acute cholecystitis may develop. This oftenoccurs when a gallstone is lodged in either the cystic duct or the infun-dibulum of the gallbladder. Gallstones are found in 95% of the patientswith cholecystitis. Duct obstruction can also occur from external causessuch as tumor, parasites, fibrosis, or kinking of the duct. The inflamma-tory response may be complicated by infection and bacterial organismscan be isolated in 50%75% of patients with a diagnosis of cholecysti-tis. The infection is often polymicrobial, but the most common individ-ual pathogens include Escherichia coli and Klebsiella species. Althoughbacteria are often isolated from inflamed gallbladders, it is unclear whatrole infection plays in cholecystitis.

The small amount of cholecystitis not associated with gallstonesis called acalculous cholecystitis. Acalculous cholecystitis makes upapproximately 5%10% of cases of cholecystitis. Conditions associatedwith acalculous cholecystitis include major surgery, severe trauma,debilitation, sepsis, long-term total parenteral nutrition, prolonged fast-ing, sickle cell disease, Salmonella infections, cardiac events, and othermicrobial infections in patients with acquired immunodeficiencysyndrome.

Avery small percentage of patients will develop serious complicationsassociated with cholecystitis, including gallbladder empyema and emphy-sematous (i.e., gangrenous) cholecystitis. These patients are often elderlyand diabetic. The patient typically presents in extremis with fever, septicshock, and right upper quadrant pain.


Gallbladder disease can produce a wide range of symptoms. Patients mayhave asymptomatic cholelithiasis or they may experience biliary colic(i.e., symptomatic cholelithiasis) or acute cholecystitis. Biliary colic isthe right upper quadrant or epigastric abdominal pain associated with gall-stones. The classic presentation for symptomatic cholelithiasis or chole-cystitis is biliary colic associated with nausea and vomiting. This oftenfollows ingestion of foods (typically fatty foods) by about 3060minutes.However, it is important to note that gallstone pain is not related to mealsin at least one third of patients. This pain is typically present in the rightupper quadrant and may initially be colicky but often becomes constant.The pain may radiate to the right shoulder or scapula. The patient maybe in severe discomfort and diaphoretic. Patients with cholecystitis mayalso have fever. If the patient has known gallstones or a history of similarepisodes, this will aid in diagnosis.

Differentiating the clinical presentation of symptomatic cholelithiasisfrom cholecystitis may be difficult, especially early in the presentation.Cholecystitis is more likely if the symptoms persist longer than 46 hoursor if fever is present.


EXAMINATION

Patients with biliary colic may be in severe discomfort. On examination,they may be tachycardic and diaphoretic. Abdominal examinationreveals tenderness in the right upper quadrant or epigastric region. Ifthe patient has cholecystitis, he or she may have fever and a Murphyssign. Murphys sign is the inspiratory arrest that occurs upon palpationof the right upper quadrant during a deep breath. Fever makes thediagnosis of acute cholecystitis much more likely than simple biliarycolic. However, in a retrospective chart review by Gruber et al, 71%of patients with pathologically diagnosed cases of acute nongangrenouscholecystitis were afebrile. Physicians should be cautious in consi-dering lack of fever a comforting finding in a patient with possiblecholecystitis.

LABORATORY FINDINGS

Unfortunately, no single laboratory test or combination of tests will catchall cases of acute cholecystitis. Laboratory test values are expected to benormal with cholelithiasis and are often normal in cholecystitis. None-theless, a multitude of laboratory tests are often ordered for these patients.A CBC, urinalysis, urine pregnancy test, and measurements of electrolytes,aspartate aminotransferase (AST), alanine aminotransferase (ALT), biliru-bin, international normalized ratio, alkaline phosphatase, and lipase maybe ordered. The most important lab testsclinically and diagnosticallyare the urine pregnancy test and the lipase analysis. With cholecystitis,one may find an elevated CBC, AST, ALT, and alkaline phosphatasedepending on the location of the gallstone in the biliary tract and thedisease progression. If the lipase is elevated, the patient likely has pancrea-titis. Of note, however, no lab test will make or break the diagnosis ofcholecystitis.

DIAGNOSIS

A diagnosis is made using a history, physical examination, and imagingstudy. Ultrasound, CT, and hepatobiliary scintigraphy (hepatobiliary imi-nodiacetic acid [HIDA] scans) are imaging options. Symptomatic choleli-thiasis is differentiated from cholecystitis by complete resolution ofsymptoms and an ultrasound scan that reveals no evidence of cholecystitis.

The differential diagnosis of gallbladder pain includes pancreatitis,cholangitis, gastritis, peptic ulcer disease, hepatitis, hepatic abscess,pyelonephritis, renal colic, right lower lobe pneumonia, pleural effusion,appendicitis, atypical myocardial infarction, pelvic inflammatory disease,and ectopic pregnancy.


RADIOGRAPHS

Plain radiographs can be useful if one is looking for another cause ofthe pain. In general, plain radiographic films will not help one to diag-nose gallbladder problems.

Ultrasound has become the imaging modality of choice in the ED.Ultrasound provides greater than 95% sensitivity and specificity forthe diagnosis of gallstones more than 2 mm in diameter. Ultrasound isalso 90%95% sensitive for cholecystitis. Ultrasound findings consis-tent with acute cholecystitis include gallstones, sonographic Murphyssign, thickened gallbladder wall, and pericholecystic fluid.

HIDA has been found to have a sensitivity approaching 100% anda specificity of 90% for diagnosing acute cholecystitis. Many believethat the HIDA scan is the gold standard imaging study. However, it isa difficult study to attain from most EDs.

CT and magnetic resonance imaging (MRI) have recently been advo-cated for diagnosing gallbladder pathology. There are reports of signifi-cantly improving capabilities in diagnosing gallbladder disease in newer-generation CT scanners. CT is preferred over MRI in the ED because it ismuch quicker and more accessible than MRI. CT has an advantage overultrasound in that it can make other diagnoses if the gallbladder is not thecause of the symptoms.

TREATMENTS AND OUTCOMES

Some patients may be quite ill, especially elderly persons. The ABCs oflife support (i.e., airway, breathing, and circulation) must be evaluatedand treated. Oxygen administration and cardiac monitoring should beused at least until a cardiac cause is ruled out.

The treatment of biliary colic consists of the administration ofIV fluids, analgesics, and antiemetics and, rarely, nasogastric suctioningfor intractable vomiting. Analgesia can be accomplished with ketorolacor ibuprofen (if tolerating oral) and narcotics. Some practitioners prefermeperidine over morphine because it is thought to cause less spasm tothe sphincter of Oddi. However, many authorities feel this is not clini-cally relevant. Antiemetics include promethazine (Phenergan), prochlor-perazine (Compazine), metoclopramide (Reglan), or ondansetron(Zofran). Treatment and time will cause symptoms of symptomatic cho-lelithiasis/biliary colic to resolve, usually within 46 hours. If symp-toms are initially thought to be due to symptomatic cholelithiasis butthey do not resolve, early acute cholecystitis should be considered.

Treatment of acute cholecystitis consists of all of the above plus antibi-otic coverage and immediate surgical evaluation. Ampicillin/sulbactam,ticarcillin/clavulanic acid, or piperacillin/tazobactam is a good option.One may also use clindamycin with gentamicin in a penicillin-allergic


patient. If intra-abdominal sepsis is a concern, a regimen of ampicillin,gentamycin, and metronidazole can be used.

All patients with cholecystitis should be admitted to the hospital. Theirdefinitive care will require surgery and a cholecystectomy. The timing ofsurgery is not universally accepted, however. Some surgeons perform thecholecystectomy on the same day, whereas others wait 2472 hours forthe gallbladder to cool off.

Patients with acalculous cholecystitis tend to have a more aggressivecourse with a mortality rate as high as 41%. Emphysematous cholecys-titis is a rare form of cholecystitis. Gas-producing organisms likelyinvade the mucosa, and gas will be found in the gallbladder wall. Treat-ment in the ED is the same, but surgery is performed emergently.

DISPOSITION

Patients with symptomatic cholelithiasis who have complete resolution ofsymptoms can be discharged home. They should have close follow-up witha surgeon because definitive care for gallstone-related pain is surgery. Otherless common options include medical dissolution therapy and gallstonelithotripsy. Patients may be discharged with a prescription for ibuprofenand oral narcotics to treat further episodes of biliary colic. The patientshould be instructed to return to the ED immediately if fever or worseningor persistent pain (greater than 23 hours) occurs, if the patient is unable totolerate food or liquids, or if a change in his or her symptoms occurs.

If a patient with gallstones has persisting symptoms, he or she shouldnot be discharged without a surgical evaluation. This is true even if thelaboratory test results are all normal and possibly even if an ultrasoundscan has shown gallstones, as long as no evidence of acute cholecystitisexists. Remember that none of our diagnostic studies are 100% sensitive.

All patients with acute cholecystitis should be admitted to the hospital.

Bibliography

Aufderheide TP, Brady WJ, Tintinalli JE: Cholecystitis and biliary colic, In Tintinalli JE(ed): Emergency Medicine: A Comprehensive Study Guide, ed 5. McGraw-Hill: NewYork, 2000, pp 576580.

Gladden D, Clinton B, Wolf J, et al: Cholecystitis Emedicine online journal. August 2004.Available at www.emedicine.com.

Gruber PJ, Silverman RA, Gottesfeld S, Flaster E: Presence of fever and leukocytosis inacute cholecystitis, Ann Emerg Med 1996;28(3):273277.

Guss DA: Cholelithiasis and cholecystitis, In Marx J (ed): Rosens Emergency Medicine:Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 12651272.

Riviello RJ, Brady WJ: Presentation and management of acute biliary tract disorders in theemergency department: Optimizing assessment and treatment of cholelithiasis and cho-lecystitis, Emergency Medicine Reports 2002 Aug 12:23(17).

Rosen P, Barkin RM, Braen GR, et al: Cholelithiasis and cholecystitis, In SchaiderJ, Hayden SR,Wolfe R, et al (eds): The 5 Minute EmergencyMedicine Consult. Lippincott,Williams & Wilkins: Philadelphia, 1999, pp 226229.
http://www.emedicine.com

Hernias 15

Shea JA, Berlin JA, Escarce JJ, et al: Revised estimates of diagnostic test sensitivity andspecificity in suspected biliary tract disease, Arch Intern Med 1994;154(22):25732581.

Singer AJ, McCracken G, Henry MC, et al: Correlation among clinical, laboratory, andhepatobiliary scanning findings in patients with suspected acute cholecystitis, AnnEmerg Med 1996;28(3):267272.

HerniasMARC L.DAYMUDE

ICD Codes: Femoral 553, Inguinal 550.9, Umbilical 553.1,Incisional 553.21


A hernia represents an abnormal protrusion of an organ or tissue througha defect in its surrounding wall. A hernia that cannot be reduced, an incar-cerated hernia, is a surgical urgency because of its contents risk loss ofblood flow,which is known as a strangulated hernia.

! Emergency Actions ! Any hernia that is suspected to be incarcer-ated or strangulated and cannot be reduced should be considered a medi-cal emergency. Two large-gauge IV lines should be placed, the patientsfluids should be replenished, an emergent CT scan should be obtained,and an emergent surgical consult should be sought.

DEFINITION

The most common hernias involve the abdominal wall and are inguinal,femoral, umbilical, and incisional. Inguinal hernias occur in the groinsuperior to the inguinal ligament through a defect in processus vaginalis.A direct inguinal hernia protrudes through the muscle and fascia of theabdominal wall, whereas an indirect inguinal hernia protrudes throughthe internal inguinal ring into the inguinal canal. Femoral herniasprotrude inferior to the inguinal ligament through a defect in the transver-salis fascia into the femoral canal. Umbilical hernias pass through thefibromuscular ring of the umbilicus and can be present at birth or acquiredin adulthood due to increased abdominal pressure from obesity, ascites, or


pregnancy. Incisional hernias protrude through areas of postincisionalweakness after abdominal surgery. A hernia is considered reducible if,when the abdominal muscles are relaxed and the patient is supine, the her-nia contents either spontaneously or under gentle pressure return to anintra-abdominal position. An incarcerated hernia does not reduce withthe above measures. A strangulated hernia is an incarcerated hernia inwhich the blood supply to the hernia contents is compromised by the nar-row hernia defect and/or swelling. This can lead to ischemia, bowelobstruction, or perforation.

EPIDEMIOLOGY

The lifetime risk of developing a hernia is 5% for males and 2% forfemales. Approximately 75% of all hernias are inguinal, and two thirdsof these are indirect. Incisional hernias account for 15%20% of hernias.Ten percent are ventral or umbilical, and 5% are femoral. Men are 25 timesmore likely to have an inguinal hernia, though this is still the most commonhernia in women.Women are 10 times more likely to have a femoral herniaand twice as likely to have an incisional hernia. Femoral hernias have thehighest rate of strangulation at 15%20%. Strangulation is more commonat either extreme of age.


Asymptomatic hernias present as a painless lump or bulge at the site. Lesscommonly, painmay be part of the reported symptoms caused by the com-pression of local nerves or the hernia defect by the contents as it slides inand out. Incarcerated hernias present with progressive pain and swelling,often at the site of a known hernia. A strangulated hernia may involve fea-tures suggestive of bowel obstruction with pain, swelling, nausea, vomit-ing, and obstipation. The strangulated hernia may become blue or purpleand have significant tenderness. There may also be clinical evidence ofperforation with fever, shock, and peritoneal tenderness.

EXAMINATION

A complete examination must include examination of the suspected her-nia in positions that place it both dependent and not dependent to the pullof gravity. For most abdominal hernias, this could be the standing positionin which gravity would pull hernia contents through the defect and thesupine position, which would allow gravity to pull the hernia contentsback into the intraperitoneal cavity. These can be augmented by havingthe patient perform a Valsalva maneuver to increase intra-abdominal pres-sure and thereby demonstrate the hernia. Direct palpation over the areas of

Hernias 17

concern during position changes and resultant changes in the herniamass help to differentiate hernias from other causes of a lump andmay demonstrate the actual abdominal wall defect.

LABORATORY FINDINGS

In hernias found to be uncomplicated by examination, laboratory testingis not necessary. In patients with suspected incarcerated or strangulatedhernias, CBC, electrolyte measurements, and renal function tests mayreveal an elevated WBC with left shift and evidence of volume depletion.In patients in whom the diagnosis is not clearly hernia, laboratory valuesmay help differentiate other causes of a lump, especially in the inguinalregion where adenopathy or genital pathology may mimic a hernia.

DIAGNOSIS

The diagnosis of hernias is primarily clinical, with the demonstration onexamination of a mass that protrudes when under increased pressure,such as with gravity or a Valsalva maneuver, and recedes when the pres-sure is decreased or with gentle palpation. Incarcerated or strangulatedhernias or bulges that are not clearly hernias may require radiologicevaluation.

RADIOGRAPHS

Plain supine and upright films of the abdomen may demonstrate free airfrom perforation or evidence of bowel obstruction in cases of suspectedincarceration or strangulation, but these are generally not useful in theevaluation of hernias. Ultrasound is highly sensitive and specific in thediagnosis of inguinal and femoral hernias. CT may be useful in detectingless common hernias and in identifying ischemic hernia contents.


Patients with hernias that are easily reduced in the ED may be dischargedhome with outpatient surgical consultation and precautions to return ifthey experience increased pain, fever, nausea and vomiting, or irreducibil-ity of the hernia mass. Reduction of hernias may require adequate painmanagement to relax the abdominal wall and putting the patient intoTrendelenburgs position and applying gentle pressure. Hernias shouldnot be forced back in because of the risk of reducing necrotic bowelinto the peritoneal cavity and inducing diffuse peritonitis. Patients with


suspected incarcerated or strangulated hernias require urgent surgicalevaluation in the ED. If there is evidence of strangulation and bowelobstruction or perforation, fluid resuscitation and treatment with broad-spectrum antibiotics should be initiated while surgical consultation isawaited.

Bibliography

Blaivas M: Ultrasound-guided reduction of a Spigelian hernia in a difficult case: An unusualuse of bedside emergency ultrasonography, Am J Emerg Med 2002;20(1):5961.

Fitzgibbons RJ, Jonasson O, Gibbs J: The development of a clinical trial to determine ifwatchful waiting is an acceptable alternative to routine herniorrhaphy for patients withminimal or no hernia symptoms, J Am Coll Surg 2003;196(5):737742.

Frager D: Intestinal obstruction: Role of CT, Gastroenterol Clin 2002;31(3):777799.Malangoni MA, Gagliardi RJ, Hernias. In Townsend CM: Sabiston Textbook of Surgery,

ed 17. Elsevier: St Louis, 2004, pp 11991217.Manthey DE: Abdominal hernia reduction. In Roberts JR, Hedges JR: Clinical Procedures

in Emergency Medicine, ed 4. Elsevier: St Louis, 2004, pp 860866.Perrott CA: Inguinal hernias: Room for a better understanding, Am J Emerg Med 2004;22

(1):850.

Intestinal ObstructionMARC L.DAYMUDE

ICD Code: 560.9


In adults themost common cause of small bowel obstruction (60%^75%)are adhesions fromprevious abdominal surgery.Malignancy, fromprimaryor secondary metastatic lesions, is the second most common cause ofobstructions in adults. In infants aged 2^3 weeks, pyloric stenosis is themost likely cause of obstruction. In children aged 3 months to 6 years,intussusception is themost likely cause of bowel obstruction.

! Emergency Actions ! Any patient who is suspected to have anintestinal bowel obstruction should have two large-gauge IV lines placed,and aggressive fluid resuscitation should be started. Upright and flat plainradiographs should be obtained. If an intestinal bowel obstruction is sus-pected, an abdominal CT scan and an emergent surgical consult should beobtained.

Intestinal Obstruction 19

DEFINITION

Bowel obstruction represents a mechanical interruption in the flow ofintraluminal intestinal contents. The etiology and treatment of the obstruc-tion vary widely depending on whether the interruption occurs in thesmall or large bowel. The terms pseudo-obstruction, ileus, or Ogilvie'ssyndrome represent a functional decrease in bowel motility and progres-sive dilation that is thought to result from autonomic imbalance frommultiple causes.

EPIDEMIOLOGY

In adults, the most common cause of small bowel obstruction (60%75%)is adhesion after abdominal surgery, especially lower abdominal and pel-vic surgeries such as appendectomy, hysterectomy, and colectomy.Malig-nancy, primarily metastatic with peritoneal implants, account forapproximately 20%. The third most common cause of small bowelobstruction in adults, representing 10%, is incarcerated hernia, most com-monly inguinal or ventral. Crohns disease accounts for 5% either by acuteinflammation or chronic scarring and strictures. The remaining 2%3%are from intraluminal obstruction from intussusception, gallstones thatpass through a cholecystoduodenal fistula, enteroliths, foreign bodies,and bezoars. Rarely, intra-abdominal inflammatory masses such as fromdiverticulitis can cause small bowel obstruction.

Large bowel obstruction in adults is predominantly caused by primarymalignancy, representing 60% of obstructions. Volvulus (sigmoid 60%and cecal 40%) make up 10%13% of large bowel obstruction. Sigmoidvolvulus usually occurs in an elderly patient with debilitating diseasesor in patients with severe psychiatric or neurologic diseases. A commonhistory is of long-standing constipation. Diverticular disease with inflam-matory masses or chronic scarring accounts for almost all other cases oflarge bowel obstruction in the United States.

In children, the most common causes of bowel obstruction are agedependent. In the first 23 weeks of life, pyloric stenosis causes gastricoutlet obstruction in 1 in 150 males and 1 in 750 females. From 3 monthsto about 6 years, the most common cause of small bowel obstruction isintussusception. The second most frequent cause is incarcerated hernias,especially in the younger age group. Less common causes are postsurgicaladhesions, sigmoid volvulus, and Meckels diverticula.

Pseudo-obstruction or ileus has multiple etiologies to include commonmedications, intra-abdominal processes, or severe stresses to the body.Common precipitants include narcotic medications, medications withanticholinergic effects, withdrawal of laxative abuse, intra-abdominal sur-geries, sepsis, severe burns, pelvic or lumbar trauma or surgeries, spinalcord injuries, and retroperitoneal hematomas.



The classic symptoms of bowel obstruction are progressive abdominaldistention, colicky abdominal pain, nausea and vomiting, and obstipationor inability to pass flatus or stool. Vomiting is a more prominent symptomthe more proximal the obstruction. The crampy abdominal pain tends tooccur in paroxysms 45 minutes apart as the bowel peristalses againstthe obstruction. Obstipation is a late finding. The early course may actu-ally be marked by diarrhea due to the increased peristaltic activity bothproximal and distal to the obstruction. Later in the course of obstruction,the vomitus may become feculent due to bacterial overgrowth of pooledintestinal contents proximal to the obstruction. Bowel obstruction causesthe loss of absorptive properties of the bowel, leading to accumulationof fluids in the lumen, bowel wall edema with third-space fluid losses,and marked intravascular depletion. This can progress to hypotensionand shock.

EXAMINATION

The patients vital signs may reflect the severity of volume depletionwith tachycardia and hypotension. Tachypnea may reveal an attempt tocompensate a metabolic acidosis. Fever may suggest bowel strangulationand perforation. The abdominal examination typically reveals diffuse dis-tention, tenderness, and tympany to percussion. Early in the course ofobstruction, bowel sounds are high pitched and hyperactive with rushesand tinkles. As the obstruction progresses and the bowel becomes moredistended, the abdomen may become quiet. A complete physical examina-tion is essential to identify possible causes of the obstruction. In adults, theabdomen likely will reveal surgical scars from previous surgeries. Incarcer-ated hernias should be sought, especially inguinal, femoral, or incisional.A rectal examination may reveal an obstructing mass of colon cancer.Similarly, a bimanual pelvic examination may identify ovarian masses.Infants may have an epigastric olive of pyloric stenosis or the sausagemass of intussusception. Current jelly stools of intussusception are alate finding indicative of bowel mucosal sloughing. Focal tenderness orperitoneal signs suggest bowel strangulation, necrosis, or perforation.

LABORATORY FINDINGS

Laboratory findings in bowel obstruction are nonspecific and not helpfulwith the diagnosis. There often will be an elevated WBC with left shift.Elevation of BUN and creatinine levels give evidence of volume deple-tion. Electrolyte level abnormalitiesespecially hypokalemia, hypo-chloremia, and metabolic alkalosis from vomitingare not uncommon.Lactic acidosis may be present.

Intestinal Obstruction 21

DIAGNOSIS

Diagnosis is made primarily based on history and physical examinationwith the support of plain upright and supine abdominal radiographs.The diagnostic accuracy of plain radiographs for small bowel obstructionis 60%. Characteristic findings include dilated loops of small bowel with-out colonic gas. Upright radiographs reveal multiple layers of air-fluidlevels that resemble stacked coins. Cecal volvulus may have a dilatedkidney-beanshaped dilated loop of colon in the left upper quadrant.Radiographs in sigmoid volvulus reveal dilated sigmoid colon with atapered end pointing to right upper quadrant resembling a bent inner tube.On equivocal cases, CT is 90% sensitive and specific in the diagnosis ofsmall bowel obstruction and helpful in identifying extrinsic causes ofobstruction such as internal hernias, tumors, or inflammatorymasses. Bar-ium enema may be both diagnostic and therapeutic for intussusceptionand sigmoid volvulus. Enteroclysis, in which contrast is instilled directlyinto the small bowel by a nasogastric tube then followed fluoroscopicallythrough the bowel, may be necessary to diagnose partial or intermittentobstruction.

RADIOGRAPHS

Formost cases of bowel obstruction, supine and upright radiographs are theonly radiographs needed to establish the diagnosis. These may also revealsome causes of obstruction such as foreign bodies or gallstones. CT, bariumenema, and enteroclysis increase the diagnostic accuracy in less certaincases or in cases of partial or intermittent obstruction.


Emergency management hinges on establishment of the diagnosis, vol-ume resuscitation, and prevention of further distention of the bowel.In the case of small bowel obstruction more so than large bowel obstruc-tion, third-space fluid losses can be substantial and patients will requireisotonic crystalloid fluid boluses to restore intravascular volume. Correc-tion of electrolyte abnormalities should be initiated. A urinary cathetermay aid in managing fluid resuscitation. All patients should have a naso-gastric tube placed at low, intermittent suction to decompress the boweland prevent further accumulation of fluids and swallowed air. Antibioticsare indicated for patients who have evidence of bowel strangulation,necrosis, or perforation. All patients will require surgical consultationand admission. Many patients with ileus or partial obstruction may bemanaged conservatively with fluid resuscitation, bowel decompression,and rest. Patients with complete obstruction or evidence of strangulation,necrosis, or perforation will require operative management.


Bibliography

Bitterman R, Peterson M: Large intestine, In Marx J (ed): Rosens Emergency Medicine:Concepts and Clinical Practice, ed 5. Mosby: St Louis, 2002, pp 13271342.

Evers BM: Small intestine. In Townsend CM (ed): Sabiston Textbook of Surgery, ed 17.Elsevier: St Louis, 2004, pp 13231375.

Frager D: Intestinal obstruction: Role of CT, Gastroenterol Clin North Am 2002;31(3):777799.

Garcia EA: Intestinal obstruction in infants and children, Center Pediatr Emerg Med2002;3(1):1421.

Kahi CJ, Rex DK: Bowel obstruction and pseudo-obstruction, Gastroenterol Clin NorthAm 2003;32(4):12291247.

Nagle A, Ujiki M, Denham W, et al: Laparoscopic adhesiolysis for small bowel obstruc-tion, Am J Surg 2004;187(4):464470.

Thoracic Aortic DissectionMARC L.DAYMUDE

ICD Code: 441.01 (thoracic)


Aortic dissection represents a splitting between the three layers of theaortic arterial wall: the intima, media, and adventitia. This separation ofthemedia allows blood to flow througha false lumenand can result in rup-ture of the weakenedarterial wall.Themost common symptom is sudden,sharp chest pain that radiates to the back.Dissection, a potentially lethalcondition, should be on the differential diagnosis of any patient with chestor upper back pain.

! Emergency Actions ! Any patient suspected of having an aortic dis-section should immediately have two large-gauge IV lines placed, shouldbe placed on the cardiac monitor, and should have an immediate CTangiogram and blood pressure control. If an aortic dissection is present,immediate surgical consult should be obtained.

DEFINITION

Aortic dissection is a separation between the layers of the aorta caused bythe shear forces of blood flow. This results from a weakening or

Thoracic Aortic Dissection 23

degeneration of the middle layer of the aorta (i.e., the media). A tear in thearterial lining (i.e., the intima) allows blood to flow between the layers ofthe wall of the aorta, creating a false lumen. The weakened aortic wall candilate and rupture. The dissection may involve arterial branches off theaorta, resulting in decreased blood flow distal to the involved area andcausing additional symptoms due to ischemia. The dissection may propa-gate both distally and proximally from the intimal tear. Dissection istermed acute if it is diagnosed within 14 days of symptom onset andchronic if diagnosed after 14 days. Aortic dissection is distinctly differentin pathogenesis, prognosis, and management from aortic aneurism, whichrepresents a diffuse expansion of all three layers of the aortic wall to 50%or more than the normal diameter. There are two major classification sys-tems based on the site of dissection that correlate with prognosis and guidetreatment decisions: Stanford and DeBakey.

Stanford A: Involves the ascending aorta Stanford B: Does not involve the ascending aorta DeBakey I: Involves the ascending and descending thoracic aorta DeBakey II: Involves only the ascending aorta DeBakey IIIA: Does not involve the ascending aorta and is proximalto the diaphragm

DeBakey IIIB: Does not involve the ascending aorta and extendsdistal to the diaphragm

EPIDEMIOLOGY

Acute aortic dissection is the most common aortic disaster. It occurs morecommonly in men and the incidence increases with age, rarely occurringbefore the age of 40 years. Mortality rates from dissection are 1 to5/100,000 per year. Seventy-five percent of untreated patients with dissec-tion die within 2 weeks of symptom onset. The most common risk factoris hypertension. Atherosclerosis is not a contributing factor in most cases.Connective tissue disorders and congenital heart syndromes such asMarfan syndrome, Ehlers-Danlos syndrome, Turners syndrome, giant-cell arteritis, polycystic kidney disease, bicuspid aortic valve, and coarcta-tion of the aorta contribute to increased risk of dissection at an earlier age.Pathophysiology is theorized to be due to degeneration of the media aspart of the aging process that is exacerbated by hypertension. Accumu-lated stresses from the shear forces of blood flow and flexion of the aortawith every contraction of the heart induce a tear in the intima that allowsblood to flow into the medial layer. The depth and distance of dissection isrelated to the degree of medial degeneration and magnitude of shear forcescaused by hypertension. Dissections involving the ascending aorta aremore lethal and are more often associated with complications of the aorticbranch arteries than those confined to the descending aorta.



Pain is the most common symptom named at presentation and is present in90% of patients with dissection. It is typically described as sharp and ofsudden onset, with maximal pain from the start. The pain is sometimesdescribed as tearing or ripping. It may involve the anterior chest with orwithout radiation to the neck and jaw, the interscapular region of the back,or the lumbar and abdominal areas; alternatively, it may migrate throughthose regions with progression of the dissection from the ascending to des-cending aorta. Vagal symptoms of nausea and vomiting, diaphoresis, light-headedness, and anxiety are commonly associated. Syncope, representingacute hemorrhage and hypotension, rupture into the pericardium and tam-ponade or involvement of the carotid arteries interrupting cerebral bloodflow occurs in 9%. Involvement of the carotid arteries may also resultin stroke-like neurologic symptoms in 6%. The coronary arteries, mostcommonly the right coronary artery, may be occluded by the dissectionand result in acute myocardial infarction, most commonly an inferopos-terior myocardial infarction, when the right coronary artery is involved.

EXAMINATION

Most patients will appear apprehensive, pale, and diaphoretic. Patientsmay be hypertensive from acute catecholamine release or hypotensivedue to rupture, tamponade, or impaired blood flow through the subclavianarteries (pseudohypotension). With ascending dissections, involvementof the subclavian arteries may result in pulse deficits and blood pressurediscrepancies between the upper extremities. This is evident in 24% ofpatients with ascending dissection. Involvement of the carotid arteriescan result in cerebral ischemia and stroke-like findings of hemiparesisand altered mental status. Ascending dissections can propagate proxi-mally, resulting in aortic valve regurgitation or rupture into the pericar-dium. Aortic regurgitation (occurs in 18%50%) is evidenced by a loudpansystolic murmur and can resul

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Essential Emergency Medicine For the Healthcare Practitioner