EMERGENCY SEDATION AND PAIN MANAGEMENTProcedural sedation and analgesia represents one of the great advances in the maturationof emergency medicine as a discrete specialty within medicine. Once the exclusive domainof the anesthesiologist, sedation and pain management procedures are now a routine partof all emergency department practices. Emergency Sedation and Pain Management is a comprehensive medical textaddressing emergency sedation and analgesia with speciﬁc emphasis on treatment ofthe emergency department patient. The easily accessible, clinically oriented formatallows the reader fast and efﬁcient access to the key points in each chapter. The text presents a clinical approach to the treatment of pain in emergencypatients, including pediatric and adult populations. Analgesia, sedation, andanesthetic techniques are presented in an informative, authoritative, and conciseformat – written and edited by physicians with extensive research as well as clinicalemergency medicine expertise. The chapters are richly supplemented with tables,photographs, and step-by-step illustrations.john h. burton, md, has been the Residency Program Director in EmergencyMedicine and a Professor of Emergency Medicine at Albany Medical College inAlbany, NY, since 2006. From 1999 to 2003, Dr. Burton was the Medical Director forMaine Emergency Medical Services and, from 1995 to 2006, he worked in theDepartment of Emergency Medicine at the Maine Medical Center in Portland. Hewas the founding Research Director in the Department of Emergency Medicine atMaine Medical Center. Dr. Burton’s areas of research interest are procedural sedation and analgesia,emergency medical services, and management of cardiovascular emergencies. He haspublished extensively in the emergency medicine literature on these and relatedtopics. He has received awards and peer recognition throughout his academic careernoting a commitment to the specialty of emergency medicine. Dr. Burton completed medical school at the University of North Carolina at ChapelHill in 1992 and residency training at the University of Pittsburgh Afﬁliated Residencyin Emergency Medicine in 1995.james miner, md, facep, has been the Director of Performance Improvementand the Associate Research Director in the Department of Emergency Medicine atHennepin County Medical Center since 1999 and is an Associate Professor ofEmergency Medicine at the University of Minnesota Medical School. Dr. Miner has performed extensive research in the areas of pain management andprocedural sedation in the Emergency Department and has published numerousmanuscripts on these topics. He is an associate editor of Academic EmergencyMedicine. Dr. Miner completed medical school at Mayo Medical School in 1996 and residencytraining at the Hennepin County Medical Center in Emergency Medicine in 1999.
Emergency Sedationand Pain ManagementEdited byJOHN H. BURTONAlbany Medical CollegeJAMES MINERUniversity of Minnesota School of Medicine
ContentsAcknowledgments page ixList of Contributors xiSECTION ONE. OVERVIEW AND PRINCIPLES IN EMERGENCYANALGESIA AND PROCEDURAL SEDATION 1 1 Emergency Analgesia Principles James Miner and John H. Burton 1 2 Emergency Procedural Sedation Principles John H. Burton and James Miner 5 3 Analgesic and Procedural Sedation Principles Unique to the Pediatric Emergency Department Susan Fuchs 11 4 Pain and Analgesia in the Infant Michelle P. Tomassi 18 5 Provider Bias and Patient Selection for Emergency Department Procedural Sedation and Analgesia Knox H. Todd 25 6 Federal and Hospital Regulatory Oversight in Emergency Department Procedural Sedation and Analgesia Sharon Roy 30 7 Nursing Considerations in Emergency Department Procedural Sedation and Analgesia Tania D. Strout and Dawn B. Kendrick 38SECTION TWO. ANALGESIA FOR THE EMERGENCY PATIENT 43 8 Pharmacology of Commonly Utilized Analgesic Agents Eustacia Jo Su 43 9 Patient Assessment: Pain Scales and Observation in Clinical Practice Tania D. Strout and Dawn B. Kendrick 5510 Pathways and Protocols for the Triage Patient with Acute Pain Paula Tanabe 67 v
vi Contents 11 Patients with Acute Pain: Patient Expectations and Desired Outcomes David E. Fosnocht, Robert L. Stephen, and Eric R. Swanson 75 12 Analgesia for the Adult and Pediatric Multitrauma Patient Wayne Triner 79 13 Analgesia for the Emergency Department Isolated Orthopedic Extremity Trauma Patient Michael A. Turturro 87 14 Analgesia for Selected Emergency Eye and Ear Patients Matthew G. Dunn 91 15 Analgesia for the Emergency Headache Patient James Miner 96 16 Analgesia for the Emergency Chest Pain Patient Carl A. Germann and Andrew D. Perron 103 17 Analgesia for the Emergency Back Pain Patient Donald Jeanmonod 109 18 Analgesia for the Acute Abdomen Patient Martha L. Neighbor 120 19 Analgesia for the Renal Colic Patient Allan B. Wolfson and David H. Newman 127 20 Analgesia for the Biliary Colic Patient Allan B. Wolfson and David H. Newman 131 21 Analgesia for the Chronic Pain Patient James Miner 135 22 Outpatient Analgesia following Acute Musculoskeletal Injury John C. Southall 141 SECTION THREE. PROCEDURAL SEDATION FOR THE EMERGENCY PATIENT 147 23 Patient Assessment and Preprocedure Considerations Baruch Krauss and Steven M. Green 147 24 Monitoring for Procedural Sedation Baruch Krauss 152
Contents vii25 Pharmacology of Commonly Utilized Sedative Agents Eustacia Jo Su 15926 Procedural Sedation for Pediatric Laceration Repair Mark G. Roback 16827 Procedural Sedation for Pediatric Radiographic Imaging Studies Nathan Mick 17328 Procedural Sedation for Brief Pediatric Procedures: Foreign Body Removal, Lumbar Puncture, Bone Marrow Aspiration, Central Venous Catheter Placement Michael Ciccarelli and John H. Burton 17929 Procedural Sedation for Adult and Pediatric Orthopedic Fracture and Joint Reduction James Miner and John H. Burton 18530 Procedural Sedation for Electrical Cardioversion Christopher J. Freeman 19031 Procedural Sedation for Brief Surgical Procedures: Abscess Incision and Debridement, Tube Thoracostomy, Nasogastric Tube Placement Carl Chudnofsky 195SECTION FOUR. TOPICAL, LOCAL, AND REGIONAL ANESTHESIAAPPROACH TO THE EMERGENCY PATIENT 20532 Selected Topical, Local, and Regional Anesthesia Techniques Douglas C. Dillon and Michael Gibbs 20533 Topical Anesthesia Considerations for Pediatric Peripheral Intravenous Catheter Placement William T. Zempsky 22434 Regional Anesthesia for Adult and Pediatric Orthopedic Fracture and Joint Reduction Douglas C. Dillon and Michael Gibbs 23035 Regional Anesthesia for Dental Pain Kip Benko 23736 Local Anesthesia for Laceration Repair Joel M. Bartﬁeld 250
viii Contents SECTION FIVE. SPECIAL CONSIDERATIONS FOR EMERGENCY PROCEDURAL SEDATION AND ANALGESIA 255 37 Sedation and Analgesia for the Prehospital Emergency Medical Services Patient Michael Dailey and David French 255 38 Induction Agents for Rapid Sequence Intubation of the Emergency Department Patient Joseph Clinton and Arleigh Trainor 260 39 Sedation and Analgesia for the Critical Care Patient Richard Riker and Gilles L. Fraser 268 Index 277
AcknowledgmentsI am indebted to many professional and life mentors, including Darrell Sechrest; GerryUnks, PhD; Fred Hansen, MD; Abby Wolfson, MD; Don Yealy, MD; Herb Garrison, MD,MPH; Bud Higgins, MD; Mara McErlean, MD; and Vince Verdile, MD. I stand on theshoulders of mentors and friends (there have been many others). Thank you. This effort could not have transpired without the inspiration and constant support ofthe most important people of my life: Phyllis Burton-Sechrest, Allison Burton, CarolineBurton, and Tracy Burton. To you, I dedicate my efforts. John H. BurtonI am grateful for the guidance and support of the mentors who have shaped my career,especially Kenneth Watanabe, PHD, and Michelle Biros, MS, MD. I dedicate this work tomy loving family, Stephanie Miner, Isaac Miner, Natalie Miner, and Stella Miner, whosesupport made this possible. James MinerThe editors gratefully acknowledge the efforts of Tim Sweeney, MD, Maine MedicalCenter, Portland, for his contribution of a number of outstanding medical illustrationsfor this text. These illustrations are displayed as ﬁgures and color plates throughoutthe text. ix
ContributorsJoel M. Bartﬁeld Joseph ClintonOfﬁce of Graduate Medical Education Professor of Emergency MedicineAlbany Medical College Department of Emergency Medicine43 New Scotland Avenue, MC 50 University of Minnesota Medical SchoolAlbany, NY 12208-3479 Chief, Department of Emergency MedicineEmail: bartﬁj@mail.amc.edu Hennepin County Medical Center Minneapolis, MN 55415Kip Benko Email: email@example.comThe Mercy Hospital of Pittsburgh1400 Locust Street Michael DaileyPittsburgh, PA 15219 Department of Emergency MedicineEmail: Kippster1@aol.com Albany Medical College 43 New Scotland Avenue, MC 139John H. Burton Albany, NY 12208-3479Department of Emergency Medicine Email: firstname.lastname@example.orgAlbany Medical College Douglas C. Dillon43 New Scotland Avenue, MC 139 Department of Emergency MedicineAlbany, NY 12208-3479 Latter Day Saints (LDS) HospitalEmail: email@example.com Salt Lake City, UT 84132 Email: firstname.lastname@example.orgCarl ChudnofskyDepartment of Emergency Medicine Matthew G. DunnAlbert Einstein Medical Center Department of Emergency MedicineKorman B-6 Glens Falls Hospital5501 Old York Road Glens Falls, NY 12801Philadelphia, PA 19141 Email: email@example.comEmail: firstname.lastname@example.org David E. FosnochtMichael Ciccarelli Division of Emergency MedicineDepartment of Emergency Medicine University of UtahAlbany Medical College 30 North 1900 East Rm AC21843 New Scotland Avenue, MC 139 Salt Lake City, UT 84132Albany, NY 12208-3479 Email: email@example.com xi
xii List of ContributorsGilles L. Fraser Donald JeanmonodMaine Medical Center Department of Emergency MedicinePortland, ME 04102 Albany Medical CenterEmail: firstname.lastname@example.org 43 New Scotland Avenue Albany, NY 12208Christopher J. Freeman Email: email@example.comDepartment of Emergency Medicine Dawn B. KendrickAlbany Medical College Division of Emergency Medicine43 New Scotland Avenue, MC 139 Department of PediatricsAlbany, NY 12208-3479 University of Alabama at BirminghamEmail: firstname.lastname@example.org MTC 205 1600 7th Avenue SouthDavid French Birmingham, AL 35233-1711Department of Emergency Medicine Email: email@example.comAlbany Medical College43 New Scotland Avenue, MC 139 Baruch KraussAlbany, NY 12208-3479 Children’s Hospital BostonEmail: firstname.lastname@example.org Division of Emergency Medicine 300 Longwood AvenueSusan Fuchs Boston, MA 02115Professor of Pediatrics Email: email@example.comFeinberg School of MedicineNorthwestern University Nathan MickDivision of Pediatric Emergency Medicine Department of Emergency MedicineAssociate Director 47 Bramhall StreetChildren’s Memorial Hospital Maine Medical CenterChicago, IL 60614 Portland, ME 04102Email: firstname.lastname@example.org Email: email@example.com James MinerCarl A. Germann Department of Emergency MedicineMaine Medical Center Hennepin Medical CenterDepartment of Emergency Medicine 701 Park Avenue South22 Bramhall Street Minneapolis, MN 55415Portland, ME 04102-3175 Email: Miner015@umn.eduEmail: firstname.lastname@example.org Martha L. NeighborMichael Gibbs 1 Hawks Hill CourtDepartment of Emergency Medicine Lafayette, CA 94549-1900Maine Medical Center Email: email@example.comPortland, ME 04102 David H. NewmanEmail: firstname.lastname@example.org Director of Clinical ResearchSteven M. Green Assistant Professor of Clinical MedicineLoma Linda University Medical Center Department of Emergency MedicineDepartment of Emergency Medicine A-108 St Luke’s/Roosevelt Hospital Center11234 Anderson Street 1111 Amsterdam AvenueLoma Linda, CA 92354 New York, NY 10025Email: email@example.com Email: firstname.lastname@example.org
List of Contributors xiiiAndrew D. Perron Eustacia Jo SuDepartment of Emergency Medicine Chief, Pediatric Emergency Medicine SectionMaine Medical Center Associate Professor, Emergency MedicinePortland, ME 04102 and Pediatrics Oregon Health Sciences UniversityRichard Riker 3181 SW Sam Jackson Park RoadChest Medicine Associates CDW-EM335 Brighton Avenue, Suite 200 Portland, OR 97201Portland, ME 04102-2354 Email: email@example.comEmail: Rikerr@mmc.orgMark G. Roback Eric R. SwansonProfessor, Department of Pediatrics Division of Emergency MedicineUniversity of Minnesota Medical School University of UtahAssociate Director, Division of Pediatric 30 North 1900 East Rm AC218 Emergency Medicine Salt Lake City, UT 84132University of Minnesota Children’s Hospital/Fairview76 Variety Club Research Center Tim SweeneyMMC 814, 420 Delaware Street SE Department of Emergency MedicineMinneapolis, MN 55455 Maine Medical CenterEmail: firstname.lastname@example.org Portland, ME 04102Sharon Roy Email: email@example.comDepartment of Emergency MedicineHennepin County Medical Center Paula Tanabe701 Park Avenue South Department of Emergency Medicine and theMinneapolis, MN 55415 Institute for Healthcare StudiesEmail: firstname.lastname@example.org Northwestern University 259 E. Erie, Suite 100John C. Southall Chicago IL 60611Chief of Emergency Services Email: Ptanabe2@nmff.orgMercy Hospital144 State Street Knox H. ToddPortland, ME 04101 Professor of Emergency MedicineEmail: email@example.com Director, Pain and Emergency Medicine InstituteRobert L. Stephen Department of Emergency MedicineDivision of Emergency Medicine Beth Israel Medical CenterUniversity of Utah Albert Einstein College of Medicine30 North 1900 East Rm AC218 First Avenue at 16th StreetSalt Lake City, UT 84132 New York, NY 10003 Email: firstname.lastname@example.orgTania D. StroutMaine Medical Center Michelle P. TomassiDepartment of Emergency Medicine Department of Emergency MedicineResearch Nurse Albany Medical Center321 Brackett Street 43 New Scotland Avenue, A-139Portland, ME 04102 Albany, NY 12208-3478Email: email@example.com Email: firstname.lastname@example.org
xiv List of ContributorsArleigh Trainor The Mercy Hospital of PittsburghDepartment of Emergency Medicine 1400 Locust StreetHennepin County Medical Center Pittsburgh, PA 15219Minneapolis, MN 55415 Email: email@example.com Allan B. WolfsonWayne Triner Professor of Emergency MedicineDepartment of Emergency Medicine 230 McKee Place, Suite 500Albany Medical College Pittsburgh, PA 1521343 New Scotland Avenue, MC 139 Email: firstname.lastname@example.orgAlbany, NY 12208 William T. ZempskyMichael A. Turturro Associate Director, Pain Relief ProgramClinical Professor of Emergency Medicine Connecticut Children’s Medical CenterUniversity of Pittsburgh School of Medicine 282 Washington StreetVice Chair and Director of Academic Affairs Hartford, CT 06106Department of Emergency Medicine Email: email@example.com
SECTION ONE. OVERVIEW AND PRINCIPLES IN EMERGENCY ANALGESIA AND PROCEDURAL SEDATION1 Emergency Analgesia Principles James Miner and John H. Burton SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT SUMMARY BIBLIOGRAPHY suppression of the endorphin system with associatedSCOPE OF THE PROBLEM vegetative changes and physiologic dependence. It isPain is the presenting complaint for up to 70% of visits partially due to the early success of morphine that furtherto the emergency department (ED). There are a myriad advances in analgesic agents, aside from general anes-of strategies to treat and diagnose pain. The effective thesia, have been slow relative to other areas of medicine.strategies are those with adequate and timely pain relief There are a wide variety of approaches to the treatmentwithout adverse effects. of pain and very few single approaches that have clearly In 1992, the World Health Organization developed a been demonstrated as superior to others. Developingclinical guideline for the treatment of acute pain. This consistent and effective approaches to the management ofguideline includes basic instructions to select an a wide variety of painful conditions can optimize aappropriate pain medication for the patient’s pain physician’s ability to treat patients with pain. In addition,intensity, individualize the dose by titration of opioids, using effective analgesic strategies will allow one toand concomitantly provides adjuvant analgesic drugs as address the analgesic needs of patients while decreasingco-analgesics or to counteract side effects. the potential for side effects. It has been shown that patients frequently receiveinadequate analgesia in the ED. Oligoanalgesia, the in- CLINICAL ASSESSMENTadequate treatment of pain, frequently occurs in the ED,especially in those patients at the extremes of age and An accurate recognition and assessment of a patient’smembers of minority and ethnic groups. pain is the central aspect of effective pain management Treatment of pain is essentially a simple process, and a and is essential to any effective analgesic strategy. Thiswide variety of agents and techniques are available that process is subjective and complex with many of theare generally effective. Morphine has been recognized as a factors involved in an individual’s pain experience notbasic treatment for pain throughout the modern era of fully understood.allopathic medicine. It is effective, easy to obtain, and has Acute pain is deﬁned as an unpleasant sensory andnever been expensive. However, morphine has severe side emotional experience associated with actual or potentialeffects when overused, speciﬁcally in the acute setting tissue damage as well as activation of neurochemicalwith respiratory depression, hypotension, and a decreased receptor and mediator responses (Table 1-1).ability to report worsening symptoms. Issues with the Acute pain is primarily a subjective concept. Objectivechronic use of morphine, as with all opiates, include observations (grimacing, tachycardia) may be present, 1
2 Overview and Principles in Emergency Analgesia and Procedural Sedation Table 1-1. Opioid receptors, activities, and subsequent endorphin responses to acute pain Receptor Activity Endorphin Mu1 Euphoria, supraspinal analgesia Beta-endorphin Mu2 Respiratory depression, CV, and GI effects Beta-endorphin Delta Spinal analgesia Enkephalin Kappa Spinal analgesia, sedation, feedback inhibition Dynorphin Epsilon Hormone Beta-endorphin Gamma Psychomimetic effects, dysphioria Table 1-2. Pathway/barriers to effective pain assessment and treatment Phase Barrier Complaint/assessment Patient communication Physician bias Patient and physician concerns about the consequences of treatment Treatment Patient medical condition Physician knowledge of treatment modalities Adverse events Plan for ongoing Physician knowledge of treatment modalities treatment Patient compliance Adverse effects of medicationsbut these signs are often absent. As a consequence, of pain in the face of cultural differences is a difﬁcult, yetpatient pain assessment remains an indirect estimation important challenge to overcome in order to treat painby the treating physician. It is, therefore, important to adequately.use a consistent vocabulary in describing an assessment It should also be noted that many physicians haveof a patient’s pain. This process will allow patient encountered patients who have altered a prescription,ﬁndings to be communicated accurately and precisely have lost pain medications, seem to have pain out ofwhile a systematic treatment practice is implemented. proportion to their illness or injury, or who ignore follow- Because pain is assessed almost completely through up clinic appointments and return to the ED repeatedly.patient report, patients who have difﬁculty communi- These experiences can make it easy to view a patient’scating are at risk of oligoanalgesia due to under- report of pain with skepticism. Such observations andappreciation of their pain. Groups at risk include infants experiences, like the physician’s assessment of patientand children, patients whose cultural background differs pain, are signiﬁcantly dependent on verbal and nonverbalsigniﬁcantly from the treating physician’s, and patients subjective communication between the physician andwho are developmentally delayed, cognitively impaired, patient. This reality creates a substantial potential forunder severe emotional stress, or mentally ill. inaccurate interpretations of patient motives in clinical Unfamiliar or unrecognized attempts by the patient to conditions where the patient pain experience is largelyexpress pain may be misinterpreted by the physician, subjective (e.g., back pain) with minimal opportunityleading to a poor interaction and an unclear assessment for objective clinical assessment with modalities such asof the patient’s pain (Table 1-2). The accurate assessment radiographic imaging or laboratory testing.
Emergency Analgesia Principles 3 chronic pain states. Chronic pain is uncommonly associ-PAIN CONSIDERATIONS ated with signs of sympathetic nervous system activity.Acute pain follows injury and usually resolves as the The treatment of acute and chronic pain is different,injury heals. Acute pain may be, but is not always, asso- and confusion between the two leads to poor manage-ciated with objective physical signs of autonomic nervous ment of patients. Acute pain should be approached withsystem activity such as tachycardia, hypertension, dia- the intention of providing relief to a limited degree,phoresis, mydriasis, and pallor. When the cause of acute individualized to each patient, with a plan to taperpain is uncertain, establishing a diagnosis is the priority of medications as symptoms improve. Chronic painthe emergency physician. Symptomatic treatment of pain assumes a baseline level of pain that is best treated with ashould be initiated while the diagnostic evaluation is consistent approach to minimize baseline discomfortproceeding. In general, it is inappropriate to delay anal- and minimize the adverse effects of both pain and paingesic use until a diagnosis has been made. It is unlikely, treatment on the patient’s lifestyle.and unproven in medical literature, that treatment with ED personnel commonly identify patients who are0.1 mg/kg of morphine, or another analgesic equivalent, thought to seek pain medications, usually opioids, forwill mask signs or symptoms of progressive disease such illegitimate purposes. Drug addiction and prescriptionthat the effective treatment of pain will confound the abuse occur throughout medicine specialties, and thediagnostic approach. true prevalence of addiction and drug-seeking behaviors Chronic pain is pain that has persisted after the usual in the ED population is unknown.time of tissue healing has passed. This is clearly a vague When patients are undergoing treatment with opioiddeﬁnition with a great deal of ambiguity between acute and medications, the physician should be aware of the Intractable pain Brief procedural pain Sedation/anesthesia – Sedation/anesthesia – procedural sedation Oral/IM opioids Opioids IV opioids – nonsevere pain – titration required – titration unlikely – severe pain – quantity of pain – unknown quantity of pain medication required medications required established Peripheral nerve blocks as appropriate Nonselective NSAIDS, COX-2 inhibitors, tramadol Nonpharmacologic measures – assurance – stabilize situation Acetaminophen Pain assessment Figure 1-1. A generalized approach to the treatment of acute pain.
4 Overview and Principles in Emergency Analgesia and Procedural Sedationpotential for development of physical dependence and/ SUMMARYor tolerance. The clinician should be cautious, however,not to label the patient as an ‘‘addict’’ who is merely Pain is the most common complaint in the ED. Having aphysically dependent or tolerant of medications. Such consistent, integrated, and well-planned approach willscenarios have been characterized with the term iatro- optimize the experience for patients as well as medicalgenic pseudoaddiction. These patients have opioid doses providers.that are either too low or spaced too far apart to relievepain, and subsequently develop behavior resembling BIBLIOGRAPHYpsychological dependence. 1. Pain management in the emergency department. Ann Emerg Med 2004;44(2):198. 2. Rupp T, Delaney KA. Inadequate analgesia in emergencyPAIN MANAGEMENT medicine. Ann Emerg Med 2004;43(4):494–503. 3. Fosnocht DE, Swanson ER, Barton ED. Changing attitudesA generalized approach to the treatment of acute pain about pain and pain control in emergency medicine.should be consistently applied to patient encounters Emerg Med Clin North Am 2005;23(2):297–306.(Figure 1-1). Such an approach will optimize the 4. Jones JS, Johnson K, McNinch M. Age as a risk factor forpotential for effective analgesia across a broad range of inadequate emergency department analgesia. Am J Emerg Med 1996;14(2):157–160.painful conditions. 5. Friedland LR, Kulick RM. Emergency department analge- For injured patients whose pain progresses past the sic use in pediatric trauma victims with fractures. Anninitial acute phase and in patients with chronic pain, Emerg Med 1994;23(2):203–207. 6. Green CR, et al. The unequal burden of pain: Confrontingclose follow-up with a single practitioner can be an racial and ethnic disparities in pain. Pain Med 2003;4important aspect of their ongoing care. This practice (3):277–294.allows for the adoption of consistent approaches and the 7. Miner J, et al. Patient and physician perceptions as risksystematic trial of various strategies to determine a factors for oligoanalgesia: A prospective observational study of the relief of pain in the emergency department.strategy that best suits a given patient. Acad Emerg Med 2006;13(2):140–146. It is common for patients in the midst of ongoing 8. Bartﬁeld JM, et al. Physician and patient factors inﬂuencingprimary care to present with pain in the ED, or for the treatment of low back pain. Pain 1997;73(2):209–211.patients who have conditions warranting follow-up with 9. Cooper-Patrick L, et al. Race, gender, and partnership in the patient–physician relationship. JAMA 1999;282(6):583–589.a single practitioner to seek care from multiple sources 10. Merskey H. The taxonomy of pain. Med Clin North Amincluding the ED. If possible, these patients should be 2007;91(1):13–20.provided with a short course of medication and have 11. Thomas SH, et al. Effects of morphine analgesia on diagnostic accuracy in Emergency Department patientsclose follow-up arranged. In patients who are unwilling with abdominal pain: A prospective, randomized trial.or unable to obtain follow-up with a single physician, J Am Coll Surg 2003;196(1):18–31.the clinician should emphasize the development of a 12. Bijur PE, Kenny MK, Gallagher EJ. Intravenous morphine atconsistent patient analgesic strategy with clear expecta- 0.1 mg/kg is not effective for controlling severe acute pain in the majority of patients. Ann Emerg Med 2005;46(4):362–367.tions to minimize both undertreatment and the adverse 13. Weissman DE, Haddox JD. Opioid pseudoaddiction – aneffects of long-term opioid use. iatrogenic syndrome. Pain 1989;36(3):363–366
2 Emergency Procedural Sedation Principles John H. Burton and James Miner SCOPE OF THE PROBLEM PSA VS CONSCIOUS SEDATION Locations for PSA Practice The PSA Depth of Consciousness Spectrum CLINICAL ASSESSMENT PAIN/SEDATION CONSIDERATIONS PAIN/SEDATION MANAGEMENT Common ED PSA Agents FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY provision of a number of additional elements includingSCOPE OF THE PROBLEM relaxation of affected muscle groups and tissues adjacentProcedural sedation and analgesia (PSA) in the emer- to injured structures, reduction of patient anxiety, and asgency department (ED) is a common component of the a means to improve the broad experience of the proce-modern practice of emergency medicine. The concepts dure encounter not only for the patient but also forinherent to PSA, however, are not new to emergency patient family members and health-care providers alike.care for the sick and wounded. More recently, the understanding and practice of ED Medical accounts from authors as early as Hippo- PSA has beneﬁted from a great deal of interest fromcrates have included descriptions of painful procedures, researchers and clinicians. This interest has produced asuch as orthopedic dislocation and fracture reduction, in substantial amount of disseminated research, empirictheir accounts of the stabilization of patients with acute observations, and practical experience that havemedical and traumatic conditions. Along with these advanced the collective understanding of the roles anddescriptions, physicians have often described the use beneﬁts of procedural sedation.of certain techniques or adjuncts to assuage the pain Minimal, moderate, and deep sedation have all beenassociated with therapeutic procedures. described in the ED setting. Emergency patients fre- Historical depictions of procedure patients have fre- quently have conditions that require pain and complexquently included images of caregivers providing alcohol procedures. Unlike most patients who are undergoingor inhalational agents to alleviate procedure-related pain sedation in other settings, patients in the ED have un-and suffering. These concepts have become inherent to predictable NPO status, often have concurrent, severeour collective view of the role of medical caregivers as systemic disease, and usually are in severe pain beforeboth prescribing treatment as well as relief of pain and the procedure begins. In addition, concurrent eventssuffering throughout history. and time/bed constraints cannot be predicted in the ED. The rationale for administration of analgesic and/or As a consequence, ED PSA has evolved into a specializedsedative agents has generally relied upon the reduction of practice, responding to these many challenges, withpain and suffering. Modern medical practice recognizes unique approaches not common to other settings andthe importance of PSA as being equally important for the patients. 5
6 Overview and Principles in Emergency Analgesia and Procedural Sedation Table 2-1. PSA practice policy components Medical provider scope of practice and credentialing Patient PSA consent Standardized patient assessment, monitoring, and preparation practices for intended depth of consciousness Suggested PSA drug dosing strategies Patient history and physical examination documentation prior to procedure Documentation of medical procedure and patient monitoring data Discharge criteria following PSA Standards for routine reporting of adverse PSA-related eventsPSA VS CONSCIOUS SEDATION The PSA Depth of Consciousness Spectrum Many health-care locations will organize PSA clinicalThe term ‘‘procedural sedation and analgesia’’ has sup- practice guidelines based on categorical assessments ofplanted the often misused and misinterpreted historical expected sedation depth. PSA practitioners should rec-expression ‘‘conscious sedation.’’ In clinical practice, the ognize that a spectrum exists for the depth of patientconcepts implied with the use of PSA are less misleading sedation during any PSA encounter. This spectrum canto both the patient and the medical provider. In addition, be categorically characterized with levels that wouldthe use of the term PSA in clinical practice more accu- typically include minimal, moderate, and deep sedationrately captures the intent of this practice: sedation and/or (Figure 2-1). The distant end of the sedation depthanalgesia for an acute medical intervention with the depth spectrum would be occupied by a general anesthesiaof sedation and analgesia largely dependent on factors level of consciousness.dictated by the patient’s needs. Minimal sedation generally refers to a patient who retains a near-baseline level of alertness with the abilityLocations for PSA Practice to follow commands in an age-appropriate fashion.There are many locations within health-care facilities Minimal sedation is usually performed for procedureswhere PSA may take place. The areas with greatest that require compliance but are typically less painfulactivity are typically located within the hospital and with the use of local anesthesia. Typical light sedationwould include the ED, outpatient surgery units, radiol- procedures might include procedures such as lumbarogy, gastroenterology, and the intensive care unit (ICU). puncture, evidentiary exams, simple fracture reductions Each PSA site will have its unique patient population in combination with local anesthesia, and abscess inci-and procedures in addition to a unique set of caregivers sion and drainage. During minimal sedation, cardio-delivering care within this setting. The principles for vascular and ventilatory functions are usuallyPSA practice should not be ﬂuid across any collection of maintained, although patients should be monitored forhealth-care sites. Rather, procedural sedation practice inadvertent oversedation to deeper levels with oxygenshould be promulgated within a predetermined set of saturation monitors and close nursing supervision.clinical guidelines and requirements that emphasizes Agents typically utilized for minimal sedation includepatient PSA needs, patient safety, and provider training fentanyl, midazolam, and low-dose ketamine.speciﬁc to the intended level of consciousness depth as As one progresses along the sedation continuum to awell as the procedure (Table 2-1). PSA practice policies moderate sedation depth, levels of impaired conscious-should speciﬁcally address provider credentialing, doc- ness progress with the onset of eyelid ptosis, slurredumentation, patient consent, monitoring, and discharge speech, and delayed or altered responses to verbal sti-criteria for PSA patients in all areas. muli. Moderate sedation is performed on patients who
Emergency Procedural Sedation Principles 7 General Light Moderate Deep anesthesia Clinical signs Awake Responds to voice Responds to pain No response Relaxed Lid ptosis No gag reflex Slurred speech No speech Adverse event risk Pain Hypoventilation Apnea Aspiration Emesis Hypoxia Hypotension Airway obstruction Figure 2-1. The depth of consciousness spectrum for procedural sedation.would beneﬁt from either a deeper level of sedation to moderate sedation – the difference being the intendedaugment the procedure or would beneﬁt from amnesia level of sedation. Monitoring for deep sedation is theof the event. Patients usually have an intact airway and same as for moderate with oxygen saturation, cardiac,maintain ventilatory function without support. As with and blood pressure assessments augmented by directminimal sedation, inadvertent oversedation to deeper observation of the airway.levels can occur and appropriate monitoring including End tidal carbon dioxide (ETCO2) has also beenoxygen saturation, cardiac, and blood pressure assess- described in ED PSA, but its utility over direct ventila-ments should be done throughout the sedation with tion observation remains unclear. Deeply sedateddirect observation of the patient’s airway throughout the patients can develop respiratory depression but generallyprocedure. Agents used for moderate sedation in the ED maintain a patent airway and adequate ventilation.include propofol, etomidate, ketamine, and the combi- Patients sedated to this level can progress to a level ofnation of fentanyl and midazolam. sedation consistent with anesthesia and there is some As patient depth of consciousness progresses into a evidence that this may occur more frequently in patientsdeep sedation, the patient response to verbal commands intended to undergo deep sedation than in patients whois substantially impaired with preservation of response are going to undergo moderate sedation.to painful stimuli as well as preservation of airway A categorization of general anesthesia depicts aprotective reﬂexes. Deep sedation is performed on patient unresponsive to all stimuli as well as the absencepatients who would beneﬁt from a deeper level of of airway protective reﬂexes. Although it is acknowl-sedation in order to complete the procedure for which edged that deep sedation can inadvertently result in athey are receiving sedation. Amnesia of the procedure is level of sedation consistent with anesthesia, this is notsimilar between moderate and deep sedation, and it is typically the goal of ED PSA. Patients who progress to annot necessary to sedate patients to a deep level only to unintended level of sedation consistent with anesthesiaobtain amnesia of the procedure. Deep sedation gener- are unable to be aroused with verbal or painful stimuli.ally is achieved in the ED with the same agents as The ability to independently maintain ventilatory
8 Overview and Principles in Emergency Analgesia and Procedural Sedationfunction is usually impaired, and patients often require relief, anxiolysis, event amnesia, and sedation. The PSAassistance in maintaining a patent airway. Since patients intervention should be characterized as one with ancan quickly progress to this level using the agents typical emphasis on the balance between the intended beneﬁtsof moderate and deep sedation, physicians performing and the potential for PSA-related complications for anymoderate and deep sedation must be prepared to pro- given encounter allowing for the potential that manyvide ventilatory support until the patient has regained patients may experience discomfort despite the use of aconsciousness. PSA-augmented approach. Recent work with bispectral (BIS) monitoring has Patient monitoring should be a standardized processadded an objective assessment to the traditional un- for all PSA encounters. Moderate sedation and deepderstanding of the sedation depth spectrum during PSA sedation encounters should routinely include bloodand general anesthesia. Although much insight has been pressure, heart rate, hemoglobin-oxygen saturation, re-attained for the application of BIS ﬁndings to the general spiratory rate, and depth of sedation monitoring. Manyanesthesia patient, the implications and adaptability of practices have also begun routine ventilation monitoringthis work to the PSA patient are less clear. Precise levels with capnography. Capnography offers the beneﬁt ofof consciousness captured by the BIS monitor have more precise and sensitive monitoring of ventilationvarying degrees of correlation with clinically observed depth and rate through ETCO2 detection.moderate to deep levels of consciousness. As a conse- Depth of sedation is best monitored utilizing a stan-quence, the application of BIS monitoring technology to dardized sedation assessment scale (see Figure 2-1). ThePSA practice remains investigative. most common and clinically relevant complications during PSA encounters are adverse respiratory events such as apnea, hypoxemia, and airway obstruction.CLINICAL ASSESSMENT Therefore, the greatest emphasis for health-care providerPSA guidelines should include a history of present illness training and patient monitoring should be directedand physical examination for each patient. The pre- toward the prevention, detection, and treatment ofprocedure assessment should include consideration of adverse respiratory events.the patient age and any comorbidity that would impactthe selection of agents or dosing. PAIN/SEDATION CONSIDERATIONS The patient assessment should include considerationof the baseline airway status, including the American With the exception of ketamine, ED PSA sedativeSociety of Anesthesiologists’ (ASA) classiﬁcation of the medications have minimal to no inherent analgesicpatient as potentially uncomplicated or complicated properties. As the majority of sedation procedures will(Table 23-1). The ASA classiﬁcation and the patient’s involve a substantial amount of pain, most PSAage may prompt consideration for a more conservative encounters should offer a standardized analgesicagent selection and/or dosing strategy. The Mallampati approach to ensure proper attention to patient painscore is often employed as an assessment guide to assess prior to, during, and after any ED procedure.the potential for airway complications (discussed in The dosing of analgesic agents should be standardizedChapter 23). in a weight-based fashion. A typical approach should An informed consent document should be routinely include initial dosing of an analgesic agent based uponused for encounters where the expected depth of con- the patient’s preprocedural pain. Typical analgesicsciousness will exceed minimal sedation. As PSA consent agents will include morphine sulfate, hydromorphone,is obtained, the patient should be informed of any and fentanyl (Table 2-2). Selection of a speciﬁc analgesicpossible risks of the procedure, including potential should take into consideration the patient’s prioradverse complications and speciﬁc alternatives to the experience with similar analgesics as well as the desiredtreatment plan. The PSA consent should also assist the duration of clinical affects.patient in understanding that PSA for any given patient Patients who require longer periods of analgesia, suchmay or may not meet the patient’s expectations for pain as those with fractures, will beneﬁt from strategies
Emergency Procedural Sedation Principles 9 Table 2-2. Commonly utilized agents population. In the ED setting, the most common PSA for ED PSA procedures will be painful fracture and/or dislocation reduction maneuvers. These procedures typify encoun- Analgesia agents ters where optimum patient relaxation and analgesia are Fentanyl a beneﬁt to patients as well as providers. Morphine sulfate The selection of a proper PSA agent should rely upon Hydromorphone the consideration of a number of patient and procedure- related factors. The anticipated degree of muscle relax- Sedation agents ation and analgesia required for the procedure should be Midazolam contemplated. The expected duration of the procedure Propofol is of critical importance. Any anticipated positioning or Methohexital maneuvering of the patient may lend certain agent Etomidate selections more appropriate. Finally, the expectations of Ketamine the patient and medical consultants taking part in the procedure should be considered as well.emphasizing longer-acting agents, such as morphine or There remains a great deal of variance in ED PSA agenthydromorphone. These patients may also beneﬁt from selection and dosing strategies. Provider experience asintegration of patient-controlled elements such as well as institution or medical consultant preferences maypatient-controlled analgesia (PCA) pumps. Regardless of substantially inﬂuence individual approaches. An ‘‘evi-the analgesic agent selected, the analgesia approach dence-based’’ approach is now possible in clinical practiceshould be a continuous observational process with given the many reviews and investigations published intitration of additional medication in accordance with the medical literature.the ongoing patient needs. The ongoing titration of an analgesic agent during Common ED PSA Agentssedation procedures should be approached with caution. Agents commonly utilized for adult and pediatric EDIntravenous analgesics have inherent risks for ventilatory PSA include midazolam, etomidate, propofol, ketamine,depression as well as hemodynamic compromise. The and methohexital (Table 2-2).simultaneous titration of an analgesic and sedative agent Until recently, midazolam has been the PSA agentadds a compounded risk of these events during proce- that clinicians are most familiar with. Midazolam offersdural sedation as well as an element of confusion as to the beneﬁt of a rapid onset and low incidence of car-the agent or combination of agents responsible should diovascular complications in the ED PSA population.an adverse event occur. However, the utilization of shorter-acting sedative Selected procedures such as cardioversion or foreign agents has increased substantially, largely as a conse-body removal may be viewed as events in which the quence of physician familiarity with these medicationsaddition of an analgesic agent is of limited beneﬁt. In as induction agents in addition to many publishedsuch events, the PSA approach is simpliﬁed signiﬁcantly investigations in the medical literature.by the reduction of agents that place the patient at risk Short-acting sedative agents, speciﬁcally methohex-for adverse hemodynamic or respiratory events. ital, etomidate, and propofol, have consistently been demonstrated to confer similar or, in many cases, improved patient and provider experiences in the EDPAIN/SEDATION MANAGEMENT PSA setting. Adverse event rates associated with theseTypical PSA procedures in the adult and pediatric latter agents have not been characterized as substantiallypopulation might include incision and drainage of higher than the risk traditionally attributed to mid-abscess, fracture and/or dislocation reduction, laceration azolam. The current medical evidence has demonstratedrepair, and foreign body removal. Electrical cardiover- safety proﬁles associated with these agents comparablesion is a procedure commonly undertaken in the adult to midazolam.
10 Overview and Principles in Emergency Analgesia and Procedural Sedation An advantage of midazolam compared to short-acting may be deemed in the patient’s best interests. Generalsedative agents is the relatively light levels of sedation guidelines and participation in a planned approach toproduced with low-dose midazolam. In contrast, these patients is another beneﬁt of a multidisciplinedmethohexital, etomidate, and propofol will confer oversight process for ED PSA.moderate or deep sedation levels for nearly all encoun-ters. Since most ED-based PSA encounters require levels SUMMARYof sedation in the moderate to deep range, this argumentin favor of midazolam likely has little clinical application ED providers and patients beneﬁt from standardizedto the majority of ED patients. institutional and ED PSA practices. Concerns for patient Common arguments expressed in favor of shorter- safety should remain foremost in the provision of EDacting sedative agents promote the view that shorter PSA services. Medical providers responsible for PSAperiods of impaired levels of consciousness confer less practice encounters, particularly practices that routinelyrelative risk for adverse respiratory events, at the same confer levels of deep sedation, should be vigilant in theirtime offering the beneﬁt of substantially reduced moni- training and preparation for adverse hemodynamic andtoring times. The latter issue has gained a great deal of respiratory events.favor and pertinence with increasing ED patient volumesplacing great demands on ﬁxed ED personnel resources. BIBLIOGRAPHY 1. American Society of Anesthesiologists, Task Force onFOLLOW-UP/CONSULTATION Sedation and Analgesia by Non-Anesthesiologists. PracticeCONSIDERATIONS guidelines for sedation and analgesia by non-anesthesiologists. Anesthesiology 2002;96:1004–1017.A diverse medical provider group should be responsible 2. American Academy of Pediatrics. Committee on Drugs, Section of Anesthesiology. Guidelines for monitoring andfor development, maintenance, and ongoing review of management of pediatric patients during and after sedationED PSA practices for any given site. This approach is of for diagnostic and therapeutic procedures. PEDSparticular importance in locations where moderate and 1992;89:1110–1115.deep levels of patient sedation are frequently utilized. 3. Clinical policy for procedural sedation and analgesia in the emergency department. American college of emergencyConsultants routinely include providers with expertise physicians. Ann Emerg Med 1998; 663–677.in anesthesiology, pediatric, and radiology services. 4. Green SM, Krauss B. Procedural sedation terminology:Additional contributing services might include indivi- Moving beyond ‘‘conscious sedation.’’ Ann Emerg Medduals with orthopedics, plastics/reconstructive surgery, 2002;39(4):433–435. 5. Agrawal D, Manzi SF, Gupta R, Krauss B. Preproceduraland cardiology expertise. The goal of such a multi- fasting state and adverse events in children undergoingdisciplined group should be to enable a process of procedural sedation and analgesia in a pediatric emergencyensuring patient safety as well as ongoing performance department Ann Emerg Med 2003;42:636–646. 6. Joint Commission on Accreditation of Healthcare Organi-and evolution of PSA practices. zation. Standards for moderate and deep sedation and Selected patients may be deemed inappropriate for anesthesia hospital accreditation standards. Oakbrook Ter-ED PSA. These individuals may be considered to have an race, Illinois, 2002; Tx:2–Tx.2.4. 1, pp. 108–111.elevated risk for adverse events to such a degree that an 7. Miner JR, Biros MH, Seigel T, Ross K. The utility of bispectral index in procedural sedation with propofol inalternate approach of delaying or relocating the inter- the emergency department. Acad Emerg Med 2005;12:vention and sedation to an alternate time or location 190–196.
3 Analgesic and Procedural Sedation Principles Unique to the Pediatric Emergency Department Susan Fuchs SCOPE OF THE PROBLEM CLINICAL ASSESSMENT Presedation Assessment PAIN/SEDATION CONSIDERATIONS Pain Assessment in Pediatric Patients The Pediatric-Friendly ED as a Method of Distraction Personnel and Training Preprocedural Fasting Children with Special Health-Care Needs FOLLOW-UP/DISCHARGE CONSIDERATIONS SUMMARY BIBLIOGRAPHY allows for retention of protective airway reﬂexes andSCOPE OF THE PROBLEM spontaneous respirations.Analgesia and sedation of infants, children, and ado- There are numerous guidelines that exist for proce-lescents occur on a daily basis in pediatric emergency dural sedation and analgesia (PSA) in children, includ-departments (EDs) across the country. Some of the most ing those developed for sedation by nonanesthesiologistsimportant aspects of safely providing pain relief and/or by the American Society of Anesthesiologists and theanalgesia for painful procedures or sedation/anxiolysis American Academy of Pediatrics (AAP).for nonpainful procedures in children are The American College of Emergency Physicians has a an understanding of the deﬁnitions used for sedation clinical policy on procedural sedation and analgesia of children (PSA), as well as a policy on pharmacologic agents used proper presedation assessment in pediatric PSA. methods of pain assessment Since the Joint Commission on Accreditation of the presence of properly trained personnel and Healthcare Organization (JCAHO) developed standards monitoring devices for pain management and sedation, hospitals that are age-appropriate equipment certiﬁed by this organization must adhere to these guide- postprocedure assessment and discharge instructions. lines. The premise of these guidelines is to enhance pain assessment, patient safety, and to assure that PSA is being The terminology commonly used includes those performed consistently within the hospital, no matter thedeﬁned by the American Society of Anesthesiologists location: radiology, ED, patient ﬂoor, or procedure suite.(ASA) for minimal sedation or anxiolysis, moderatesedation, deep sedation, and general anesthesia. An CLINICAL ASSESSMENTappropriate addition to this structure for the pediatricpopulation is dissociative sedation, which is the trance- There are numerous pediatric patient scenarios that maylike state and analgesia induced by ketamine. This state require PSA in an ED. This includes simple analgesia for a 11
12 Overview and Principles in Emergency Analgesia and Procedural Sedationnondisplaced fracture, anxiolysis to decrease apprehension One concern with observational assessment is it is oftenof venipuncture, sedation for a painless procedure such difﬁcult to determine if the behavior is owing to pain oras a CT scan, and sedation for a painful procedure such as distress/agitation.a displaced fracture reduction. The appropriate selection Physiologic measurements of pain include tachycar-of agents is dependent upon the level of anxiolysis, dia, pupil dilatation, diaphoresis, and peripheral vaso-sedation, or pain relief required for the individual constriction. However, these can also occur because ofclinical encounter. fear, anxiety, or crying. Although a change of 10–20% in heart rate, respiratory rate, or blood pressure is associ-Presedation Assessment ated with pain, no pain assessment tool relies solely onA focused history and physical examination should these parameters. For children less than 3 years of age,include questions about past medical history, medica- the FLACC score is an observational pain assessmenttions, allergies, and prior sedation/analgesia or anes- tool that is commonly utilized (Figure 3-1).thesia experiences. The time of the last solid food intake, For children of age 3 and above, the ‘‘FACES’’ scalesoral intake, and clear liquids should be determined, and have been found to be an easy, well-accepted, reliable, anddecisions made about method and timing of sedation valid method of pain self-reporting. The Wong-Bakermay need to be adjusted. FACES Pain Rating Scale is often used for children between A thorough assessment of the airway for potential pro- the ages of 3 and 18, and consists of 6 faces ranging fromblems should be performed. This assessment should smiling to crying (Figure 3-2). This scale can be used withinclude evaluation for a small mandible, large tongue, brief age-appropriate verbal explanations and has beenshort neck, loose teeth, or limited neck mobility. A physical interpreted in several languages. The smiling face is scoredstatus classiﬁcation, such as that developed by the ASA, as zero, whereas the crying face is scored as 5.may serve to categorize the pediatric patient with regard to Another reliable and valid scale is the Bieri Scale, usedongoing illnesses and medical problems that would suggest for children 3–12 years of age. This scale consists ofa cautious approach toward PSA encounters. seven faces, showing a neutral expression (scored as 0) Consent for PSA should be obtained from the parent or to a face with a painful expression (scored as 6). Oneguardian. The method of drug administration, the actions concern with using a scale with a happy smiling face asof the drug(s), risks, as well as adverse events during and compared to one with a neutral face is that the painafter PSA should be routinely explained beforehand. score is higher with the former. No matter which scale is used, the key point is that the same scale should be used in the ED and throughout the hospital.PAIN/SEDATION CONSIDERATIONS For older children as well as adults, a visual analogPain Assessment in Pediatric Patients scale (VAS) is commonly used (Figure 3-3). The VASOne of the most important aspects of providing pain relief consists of a horizontal or vertical line with a descriptionto children is to understand how to assess the presence of pain at each end (usually no pain on one end with theand severity of pain and the relief of pain in infants and worst pain on the other). Marks are present on the scalechildren. Pain can be assessed in children using physio- at equal intervals, typically at 1 cm intervals, with eachlogic or behavioral observation as well as self-report. mark corresponding to a number along the scale. Since pain is a subjective experience, self-reporting is Studies have shown that when using a 10 cm VAS withfavored. Even children as young as 3 years old can use children, a change of 10 mm is interpreted by the patientself-reports by the use of pain-rating tools. Observa- as clinically signiﬁcant.tional pain assessment is used when the child cannotself-report, or it can be used to supplement physiologic The Pediatric-Friendly ED as a Method ofmeasures and self-reporting. Distraction It should be noted that health-care professionals Because anxiety and fear may play a large role in anyconsistently underestimate a child’s pain, as do parents, child’s ED experience, simple methods of distractionyet the parents are closer to the child’s own pain rating. can be built into the ED or made readily available
Sedation in the Pediatric Department 13 Categories Scoring 0 1 2 Faces No particular Occasional Frequent to expression or grimace or constant smile frown, quivering chin, withdrawn, clenched jaw disinterested Legs Normal position Uneasy, restless, Kicking, or legs or relaxed tense drawn up Activity Lying quietly, Squirming, Arched, rigid or normal position, shifting back jerking moves easily and forth, tense Cry No crys (awake Moans or Crying steadily, or asleep) whimpers; screams or sobs, occasional frequent complaint complaints Consolability Content, relaxed Reassured by Difficult to occasional console or touching, comfort hugging or being talked to, distractable Note: Each of the five categories is scored from 0–2, with a total score between zero and ten. Figure 3-1. FLACC Scale. 0 1 2 3 4 5 NO HURT HURTS HURTS HURTS HURTS HURTS LITTLE BIT LITTLE MORE EVEN MORE WHOLE LOT WORST Alternate coding 0 2 4 6 8 10Figure 3-2. Wong-Baker FACES Scale. (From Hockenberry MJ. Wong’s essentials of pediatric nursing, 7th edn. St. Louis, MO: Mosby,2005, p. 1301. Copyrighted by Mosby, Inc. Reprinted by permission.)
14 Overview and Principles in Emergency Analgesia and Procedural Sedation No pain Worst pain 1. Skilled medical personnel to administer the medication. 2. An individual skilled in airway management and 0 1 2 3 4 5 6 7 8 9 10 cardiopulmonary resuscitation. 3. An individual speciﬁcally assigned to watch the patient during and after the procedure. ThisFigure 3-3. Visual Analog Scale (VAS) for the assessment of pain. includes monitoring and documenting the cardio- respiratory status, watching for chest rise, head(a ‘‘distraction box’’). Distraction involves focusing a position, and following pulse oximetry. Thechild’s attention away from the procedure. This can be as person monitoring the patient must be able tosimple as having child-friendly wallpaper or objects on assist in any supportive or resuscitative measuresthe ceiling, such as mobiles or kites, that a child can focus (providing basic pediatric life support).on (Figure 3-4). A television, with appropriate movies or 4. All settings must have age- and size-appropriateprogramming popular with children, is a great distraction equipment available including oxygen, suctiontool. Depending on the procedure, having a child or apparatus and catheters, bag-mask ventilationparent blow bubbles, blow a pinwheel, or look into a device, airway adjuncts, intubation equipment,kaleidoscope may provide a helpful distraction (Figure 3- reversal medications, IV equipment (if not already5). Older children and adolescents may prefer to listen to in place), IV ﬂuids, and resuscitation medications.music or play a hand-held video game.Personnel and Training Preprocedural FastingAccording to the AAP Committee on Drug Guidelines Preprocedural fasting remains an area of controversy forfor Monitoring, the management of patients during and pediatric patient sedation and analgesia in the ED.after sedation for diagnostic and therapeutic procedures Guidelines have been developed for elective proceduresshould routinely include the following: by the ASA and AAP to reduce the risk of pulmonaryFigure 3-4. Child-friendly wallpaper can serve as a distraction for children in the ED. (For color reproduction, see Color Plate 3.4.)
Sedation in the Pediatric Department 15 Figure 3-5. Toys can serve as visual distracters to allow for a less-threatening examination for children in the ED. (For color reproduction, see Color Plate 3.5.)aspiration of gastric contents. The AAP and ASA agree between a preprocedural fasting state and adverse eventsthat there should be no oral intake of clear liquids for in the ED setting.2 hr prior to the procedure for any age infant or child. Ultimately, the routine preprocedural assessmentThese ASA guidelines assert that the length of NPO should include a query regarding time of last food andstatus should be 6 hr after infant formula or a light meal, liquid intake. The implications of this history should beand 4 hr after breast milk, whereas the AAP guidelines evaluated against the risks and beneﬁts of the plannedadvise that infants 5 months and under should have no depth of sedation and the urgency of the situation.milk or solids for 4 hr, infants 6–36 months no milk orsolids for 6 hr preprocedure, and those older than 36 Children with Special Health-Care Needsmonths should NPO for 8 hr. Of note, the Canadian Children with special health-care needs represent aAnesthesiologists’ Society has indicated that an NPO growing number of patients seen in the ED, especially inrule of no ﬂuid intake for periods beyond 3 hr prior to tertiary care institutions. Although the initial assessmentsurgery is unnecessary. of these children is no different when compared to the The extrapolation of elective procedure practices to the nonspecial needs population, some of these children willemergency setting and population remains a point of have comorbidities and illnesses suggesting signiﬁcantcontention. The primary issue in the ED is that one is risk for analgesic and sedation practices.often faced with an emergency procedure, such as a Information regarding the patients’ current medica-fracture reduction, yet the child does not meet the fasting tion is important to predict any adverse drug interac-guidelines owing to the nature of the unplanned event. tions. Asking the parents about prior experiences with There have been several recent studies considering sedation can be beneﬁcial, as these may provide infor-preprocedural fasting and adverse events in pediatric PSA. mation revealing agents that have previously been usedThree studies, from 3 different institutions with 3,420 for success or complications.patients of ages ranging from 5 days to 32 years, have The pain assessment of the special health-caredemonstrated that there appears to be no association needs child should be adjusted for a developmental
16 Overview and Principles in Emergency Analgesia and Procedural Sedationage-appropriate level. If the patient is nonverbal, use of age-speciﬁc equipment, and discharge criteria should bean infant score, such as the FLACC Scale, may be routine in all pediatric patient analgesia and sedationnecessary. In addition, the parents may be able to assist encounters.in describing some of the child’s pain behaviors orfacial expressions. BIBLIOGRAPHY Monitoring requirements for these children may 1. Krauss B, Green SM. Procedural sedation and analgesia inrequire the addition of cardiac rhythm assessment for children. Lancet 2006;367 (9512):766–780.children with cardiovascular problems. After the pro- 2. Doyle L, Colletti JE. Pediatric procedural sedation. Pediatrcedure, these children may require monitoring for a Clin North Am 2006;53:279–292.longer period than typically utilized to guard against an 3. Green SM, Krauss B. Clinical practice guideline for emergency department ketamine dissociative sedation inenhanced risk for respiratory depression. Discharge children. Ann Emerg Med 2004;44(5):460–471.criteria should still be met, although reaching some of 4. American Society of Anesthesiologists, Task Force on Sedationthe child’s baseline behaviors may depend on the par- and Analgesia by Non-Anesthesiologists. Practice guidelines for sedation and analgesia by non-anesthesiologists. Anesthesi-ents’ assessment. ology 2002;96(4):1004–1017. 5. American Academy of Pediatrics, Committee on Drugs. Guidelines for monitoring and management of pediatricFOLLOW-UP/DISCHARGE CONSIDERATIONS patients during and after sedation for diagnostic and therapeutic procedures: Addendum. Pediatrics 2002;110Speciﬁc discharge criteria for children following seda- (4):836–838.tion events should include the following: 6. EMSC Grant Panel on Pharmacologic Agents Used in Pediatric Sedation and Analgesia in the Emergency 1. Cardiovascular function and airway patency are Department. Clinical policy: Evidence-based approach to satisfactory and at baseline. pharmacologic agents used in pediatric sedation and 2. The patient is easily arousable and protective analgesia in the emergency department. Ann Emerg Med 2004;44:342–377. reﬂexes are intact. 7. American College of Emergency Physicians, Clinical 3. The patient can talk (if age appropriate). Policies Subcommittee on Procedural Sedation and 4. The patient can sit up unaided (if age appropriate). Analgesia. Clinical policy: Procedural sedation and 5. The patient has returned to the presedation level analgesia in the emergency department. Ann Emerg Med 2005;45:177–196. of responsiveness. 8. American Academy of Pediatrics, Committee on Psycho- 6. The child’s hydration status is adequate. social Aspects of Child and Family Health, and American Pain Society, Task Force on Pain in Infants, Children, and A reliable adult should be given discharge instructions Adolescents. The assessment and management of acutefor the pediatric patient at the time of discharge from pain in infants, children, and adolescents. Pediatricsthe ED. These should note that the child may be drowsy 2001;108:793–797. 9. Askin DF, Wilson D. Health problems of newborns. Infor a few hours, the adult should not leave the child Wong’s essentials of pediatric nursing, 7th edn, ed. MJunattended in a car seat, and the child should be pro- Hockenbery. St Louis, MO: Elsevier Mosby, 2005, pp. 244–hibited from unattended swimming or bathing for 8 hr. 247.Postdischarge feeding should include precautions con- 10. Merkel SI, Shayevitz JR, Voepel-Lewis T, Malviya S. The FLACC: A behavioral scale for scoring postoperative paincerning the avoidance of a heavy meal for a few hours, as in young children. Pediatr Nurs 1997;23:293–297.some children will have mild nausea after PSA. 11. Wong DL, Baker CM. Pain in children: Comparison of assessment scales. Pediatr Nurs 1988:14:9–17. 12. Powell CV, Kelley A-M, Williams A. Determining theSUMMARY minimum clinically signiﬁcant difference n visual analog pain score for children. Ann Emerg Med 2001;37:28–31.Over the years, emergency physicians are increasingly 13. Soud TE Rogers JS. Nonpharmacologic intervention forasked to provide sedation and analgesia to pediatric pain relief. In Manual of pediatric nursing, ed. TE Soud, JS Rogers. St Louis, MO: Mosby, 1998.patients for numerous diagnostic and therapeutic pro- 14. Rusy LM, Weisman SJ. Complementary therapies for acutecedures. Adherence to existing guidelines for patient pediatric pain management. Pediatr Clin North Amassessment, medical personnel, patient monitoring, 2000;47(3):589–599.
Sedation in the Pediatric Department 1715. Roback MG, Bajaj L, Wahen JE, Bothner J. Preprocedural 17. Hoffman GM, Nowakowski R, Troshynski TJ, Berens RJ, fasting and adverse events in procedural sedation and Wesiman SJ. Risk reduction in pediatric procedural analgesia in a pediatric emergency department: Are they sedation by application of an American Academy of related? Ann Emerg Med 2004;44:454–459. Pediatrics/American Society of Anesthesiologists process16. Agrawal D, Manzi SF, Gupta R, Krauss B. Preprocedural model. Pediatrics 2002;109:236–243. fasting state and adverse events in children undergoing 18. Sacchetti A, Turco T, Carraccio C, Hasher W, Cho D, procedural sedation and analgesia in a pediatric emergency Gerardi M. Procedural sedation for children with special department. Ann Emerg Med 2003;42:636–646. health are needs. Pediatr Emerg Care 2003;19:231–239.
4 Pain and Analgesia in the Infant Michelle P. Tomassi SCOPE OF THE PROBLEM CLINICAL ASSESSMENT Deﬁnition of Pain in Infants Development of Nociception PAIN CONSIDERATIONS Pain and Memory Pain Assessment in the Infant Pain Scales for Infants PAIN MANAGEMENT Nonpharmacologic Interventions Pharmacologic Interventions Topical and Injected Local Anesthetics FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY This inability to verbalize pain contributes to the failureSCOPE OF THE PROBLEM of health-care professionals to recognize and treat painPain in infants poses a major challenge for health pro- aggressively in infants.fessionals. Although infants are uniquely vulnerable to It has also been hypothesized that pain perceptionpain and its consequences, pain is less adequately con- occurs in a less-organized fashion in the infant than thetrolled in this patient population than in any other. child or adult. Pain is a combination of sensory (dis-Many reasons account for the undertreatment of pain in criminative) and emotional (affective) components. Theinfants with the most common problem being a paucity sensory component of pain is deﬁned as nociception.of knowledge regarding pain and analgesia for the infant Nociception incorporates the physiologic and behavioralpopulation. responses of infants to a painful stimulus but not the cognitive responses that are part of pain perception. Consequently, health-care professionals are required toCLINICAL ASSESSMENT rely on physiologic and behavioral responses whenDeﬁnition of Pain in Infants assessing pain in an infant. Finally, the IASP deﬁnitionThe International Association for the Study of Pain indicates that pain is an association based on previous(IASP) has deﬁned pain as ‘‘an unpleasant sensory and actual or potential tissue damage. In most neonates andemotional experience associated with actual or potential infants, no opportunity has existed for gaining previoustissue damage or described in terms of such damage’’ experience with pain recognition.(from reference 3). It has been suggested that this deﬁ-nition is inappropriate for infants. Development of Nociception The interpretation of pain is subjective and infants Health-care professionals have historically believed thatlack the ability of self-report in the traditional sense. infants are unable to feel pain because of inadequately18
Pain and Analgesia in the Infant 19developed central and peripheral nervous systems. It has A repeated painful experience may cause the newbornbeen hypothesized that immature myelinated nerves to eventually recognize the activities of the event andwould not allow for transmission of noxious stimuli demonstrate altered conduct. Barba et al. (see reference 7)from the site of the injury to the central nervous system. have analyzed the behavioral and physiologic responsesAn abundance of evidence refutes these beliefs and of newborns to repeated heel lancing. In their ﬁndings,demonstrates that the fetus has the anatomic, neu- infants exhibit responses indicating awareness of arophysiologic, hormonal, and functional requirements forthcoming painful event after experiencing repeatedfor processing pain by mid- to late gestation. painful stimuli with similar procedures. By 20 weeks gestational age, the fetal cerebral cortexhas a full complement of neurons and sensory receptors Pain Assessment in the Infantspread to all cutaneous and mucosal surfaces. At birth, The misconception that infants are incapable ofthe density of nociceptive nerve endings in the new- expressing pain has been pervasive. Although infants areborn’s skin is sometimes greater than in adults. Lack of unable to verbalize their pain, the combination ofmyelination does not support the argument that infants physiologic indicators and behavioral cues are consid-are incapable of perceiving pain given that adults may ered by many to be a valid and reliable means ofhave as many as 80% of unmyelinated ﬁbers that are assessing pain in this patient population.responsible for transmitting pain information. It should Physiologic indicators of pain in the infant includebe noted that incomplete myelination does affecttransmission by slowing the conduction speed of pain increases in heart rate, respiratory rate, bloodimpulses. However, this decrease in conduction speed is pressure, mean airway pressure, muscle tone, andbelieved to be offset by the shorter distance traveled for intracranial pressureimpulses to the central nervous system. decreases in vagal tone, oxygen saturation, and peripheral blood ﬂow autonomic changes (mydriasis, diaphoresis, ﬂushing,PAIN CONSIDERATIONS pallor, and palmar hydrosis).Pain and Memory Acute behavioral cues of pain in the infant includeThe issue of whether infants remember pain has been atopic of signiﬁcant debate. Memory and learning depend crying (robust, intense, extended, high-pitched cries)on cerebral malleability, which is particularly evident facial expression (Figure 4-1)during the late prenatal and neonatal periods. Although body posturing (ﬁnger clenching, limb thrashing,the structural and functional capacity for memory is writhing, backarching, tremulousness).thought to be present in neonates, there is no evidenceto support that an infant has the ability to remember Pain Scales for Infantspain. Nevertheless, a growing number of research studies Several composite measures for assessing pain in infantssuggest that early exposure to unrelieved pain and the have been developed. The two neonatal scales that arestress related to an event may exaggerate affective and most comprehensive and have been tested more thor-behavioral responses during subsequent painful events. oughly for reliability are the Taddio et al. have explored the effect of neonatal Neonatal Infant Pain Scale (NIPS)circumcision on pain response during subsequent rou- CRIES Neonatal Postoperative Pain Measurementtine vaccination at 4 and 6 months of age. Their ﬁndings Score.reveal that circumcised infants demonstrate a strongerpain response to subsequent routine vaccination than The NIPS is composed of six indicators of pain: ﬁveuncircumcised infants. Among circumcised infants, an behavioral and one physiologic. This scale evaluates painattenuated pain response to vaccination has been for an average gestational age of 33.5 weeks. A score ofobserved with preoperative eutectic mixture of local zero represents no pain whereas a score of seven suggestsanesthetics (EMLAÔ) treatment. severe pain (Table 4-1).
20 Overview and Principles in Emergency Analgesia and Procedural Sedation Grimacing, furrowed brow bulging Eye squeezing Nasal flaring, deepened nasolabial folds Tongue curving, chin quivering Figure 4-1. Facial expression of infant pain (photo courtesy of Jennifer Grove). Table 4-1. Neonatal Infant Pain Scale (NIPS) NIPS 0 1 2 Facial expression Relaxed muscles Grimace Restful neutral expression Tight facial muscles Furrowed brow, chin, jaw Negative facial expression Cry No cry Whimper Vigorous cry Quiet Mild intermittent moaning Loud scream (rising, shrill, continuous) Silent cry Breathing patterns Relaxed Change in breathing Usual pattern for infant Irregular and faster chest indrawing Gagging Breath holding Arms Relaxed Tense, straight arms No muscular rigidity Rapid extension and ﬂexion Occasional random arm movement Legs Relaxed Tense, straight legs No muscular rigidity Rapid extension and ﬂexion Occasional random leg movement State of arousal Quiet, peaceful sleeping Awake, Fussy alert, and settled Awake, alert, and restless Thrashing The CRIES Scale was developed for the assessment of It is important to note that the CRIES Scale becomesneonate postoperative pain. The acronym CRIES an eight-point scale when used in healthy neonates whorepresents ﬁve physiologic and behavioral indicators of do not require supplemental oxygen administration.pain. Responses to each indicator can total a maximum Although the implementation of the CRIES observationsof two points with a maximum scale score of 10 is facility dependent, most centers provide analgesia when(Table 4-2). pain ratings are greater than three on the CRIES Scale.
Pain and Analgesia in the Infant 21 Table 4-2. CRIES Neonatal Postoperative Pain Measurement Scale 0 1 2 Crying No High pitched High pitched Consolable Inconsolable Requires oxygen (goal O2 sat 95%) No 30% O2 required 30% O2 required Increased vital signs HR and BP HR, BP 20% HR, BP 20% Normal Preop value Preop value Expression No grimace Grimace Grimace/grunt Sleeplessness No Frequent awakening Continuously awake Note: O2, oxygen; HR, heart rate; BP, blood pressure characterized as a potent intervention against the painPAIN MANAGEMENT experienced during heel stick stimuli in newborns.The management of infant pain relies primarily on Oral sucrose solutions, with nonnutritive sucking, brieﬂy produce analgesia in neonates. Sucrose con- awareness of an infant’s capacity to perceive pain centrations between 24% and 50% are most often sensitivity toward clinical situations where pain may recommended as several studies have shown lower be encountered concentrations to be less effective for analgesia. The appropriate steps to prevent and treat pain. initial dose should be given within 3 min of the painfulThere is a wide variation in strategies for pain man- procedure and repeated as needed throughout theagement in the infant population. Like other popula- duration of the procedure. Oral sucrose is most appro-tions, the general consensus among health-care priately used for brief painful events, not exceedingproviders is that pain management is likely most effec- 2–3 min duration, such as heel stick or venipuncture.tive when a combination of both nonpharmacologic and For treatment of moderate to severe pain with longerpharmacologic interventions is employed. duration, oral sucrose may be used in conjunction with other analgesics techniques.Nonpharmacologic InterventionsNonpharmacologic interventions have the allure of Pharmacologic Interventionsbeing easy to administer and requiring no intensive For moderate to severe pain, pharmacologic interven-monitoring. These techniques are believed to enhance tions should be added to the pain management regimen.activity in descending neuronal inhibitory pathways Although all medications used most commonly forwith a corresponding decrease in pain experience. infant analgesia and sedation are potentially dangerous,Attenuation of spinal cord impulse transmission can be they can be administered safely when carefully titratedachieved by stimulation of large sensory nerve ﬁbers (Figure 4-3).mediating tactile and temperature sensations. Some The most commonly used analgesic for mild infantrecommended nonpharmacologic infant analgesic pain remains acetaminophen, as it is considered safe andinterventions are listed in Figure 4-2. effective in all age groups, including newborns. Proper Kangaroo care or skin-to-skin contact between initial dosing of rectal acetaminophen is 25–40 mg/kg,mother and child was developed as a low-cost method of followed by 20 mg/kg q6 hr for subsequent dosing.assisting low birth weight infants with thermoregulation. Codeine is not typically used in neonates, but is utilized inPatterned after marsupial caregiver behaviors, kangaroo older infants, often in combination with acetaminophen.care consists of placing the naked infant against the Nonsteroidal anti-inﬂammatory drugs (NSAIDs),mother’s bare chest, between her breasts, in an upright such as ibuprofen and ketorolac, can be used as anposition for several hours a day. This technique has been alternative to acetaminophen in children over 6 months
Pain and Analgesia in the Infant 23of age. NSAID agents should not be used in children Benzodiazepines are often used as sedative andallergic to aspirin due the cross-sensitivity of aspirin and amnesiacs during painful procedures in infants. Mid-NSAIDs. Ketorolac is a potent analgesic agent with a azolam has been approved for use in neonates. If mid-more attractive side effect proﬁle (less gastrointestinal azolam is used, a continuous infusion (0.02 mg/kg/hr,irritation) when compared to other NSAID agents. The no loading required in neonates) or administration ofduration of ketorolac therapy should not exceed 5 days individual doses (0.5–0.75 mg/kg PO, 0.3–1 mg/kg IM,in infants. Additionally, limited clinical data exists for 0.05–0.1 mg/kg IV) over at least 10 min is recommendedthe use of ketorolac in patients less than 16 years of age. to reduce the risk of adverse effects.The efﬁcacy and safety of cyclooxygenase-2 inhibitors, Although excellent as a sedative analgesic for proce-such as celecoxib, have not been evaluated in patients dural sedation in children, ketamine is contraindicatedyounger than the age of 18. in those less than 3 months of age. Opiates are the most ﬂexible and widely used narcoticanalgesics, with morphine and fentanyl being the most Topical and Injected Local Anestheticsappropriately used for pain due to invasive procedures. A eutectic mixture of 2.5% lidocaine and 2.5% prilo-Morphine and fentanyl should be administered as fre- caine, designated EMLA, may provide excellent topicquent small aliquots or as a continuous infusion. For anesthesia. This combination is a mixture of the twoprolonged use, continuous infusion is preferred to avoid drugs in a 1:1 weight ratio, whereby the two crystallinelarge variations in plasma concentration. Whenever powders melt at a lower temperature than they domedications in this category are administered, there separately. This amalgamation increases the concentra-must be accompanying vigilance for potential adverse tion of the local anesthetics in the emulsion droplets,effects on the respiratory and cardiovascular systems. making them more synergistically effective. Intravenous boluses of the synthetic opiates, such as EMLA cream should be applied in a thick layer andfentanyl (80–100 more potent than morphine), may be left undisturbed, ideally for 60–90 min prior to theassociated with glottic and chest wall rigidity. The risk of intended procedure. EMLA penetrates skin surfaces to aadverse effects is a result of immature hepatic and renal depth of 5–10 mm, providing anesthesia for 1–2 hr. Thefunction in the infant and is, therefore, directly related depth of EMLA penetration can be increased by apply-to rate of drug administration, total dose, and combi- ing occlusive dressings over the unguent-covered area.nation with other medications capable of central ner- The major concern for EMLA use is the risk of met-vous system depression. The propensity for adverse hemoglobinemia. This side effect is typically noteffects, such as marked ﬂuctuations in intracranial encountered without repeated applications. Despite nopressure and subsequent brain damage, is reduced by data demonstrating additive risk, caution should beavoiding rapid bolus injection. taken when other agents capable of causing methemo- Naloxone should be readily available when opiates are globinemia, such as acetaminophen, are coadministered.being utilized in infants. Naloxone can be administered In addition, EMLA must not be used on abraded skinin incremental doses of 0.01–0.1 mg/kg, to a maximum surfaces; a cotton ball soaked with lidocaine-epinephrine-dose of 2 mg (Table 4-3). tetracaine (LET) solution should be used instead. Table 4-3. Morphine and fentanyl infusion rates for neonates and infants Patient population Morphine Fentanyl Neonate (4 weeks old) 0.1 mg/kg (loading) 1 mcg/kg (loading) 0.01–0.15 mg/kg/hr (infusion) 1 mcg/kg/hr (infusion) Infant (4 weeks old) 0.1 mg/kg (loading) 1–2 mcg/kg (loading) 0.02–0.04 mg/kg/hr (infusion) 1–2 mcg/kg/hr (infusion)
24 Overview and Principles in Emergency Analgesia and Procedural Sedation Table 4-4. Doses of injectable local anesthetics without epinephrine (doses increase slightly with epinephrine) Drug Concentration (%) Standard dose (mg/kg) Toxic dose (mg/kg) Bupivacaine 0.25 1.5–2 2.5 Lidocaine 1 3.5–4 4.5 Cardiac arrhythmias and seizures, although rare, are BIBLIOGRAPHYcomplications of local anesthetic injection, particularly 1. Alanis MC, Lucidi RS. Neonatal circumcision: A review ofwhen administered with improper dosing. It is prudent the world’s oldest and most controversial operation.to initially use the smallest possible dose for adequate Obstet Gynecol Surv 2004;59(5):379–395.anesthesia and later titrate to effect (Table 4-4). 2. American Academy of Pediatrics, Committee on Psycho- social Aspects of Child and Family Health, Task Force on Pain in Infants, Children, and Adolescents. The assessmentFOLLOW-UP/CONSULTATION and management of acute pain in infants, children, andCONSIDERATIONS adolescents. Pediatrics 2001;108(3):793–797. 3. Anonymous. Prevention and management of pain andAs in older patient populations, the goal of pain manage- stress in the neonate. American Academy of Pediatrics.ment is to keep the infant within a therapeutic window by Committee on Fetus and Newborn. Committee on Drugs. Section on Anesthesiology. Section on Surgery. Canadianproviding enough medication to reduce pain without Paediatric Society. Fetus and Newborn Committee.causing unwanted deleterious effects. Although the poten- Pediatrics 2000;105(2):454–461.tial for adverse side effects such as respiratory depression 4. Aucott S, Donohue PK, Atkins E, Allen MC. Neurodeve-and hypotension exist, especially in premature or neuro- lopmental care in the NICU. Ment Retard Dev Disabil Res Rev 2002;8(4):298–308.logically impaired infants, knowledge of the pharmacoki- 5. Birenbaum D, Mattison DR. Analgesics for the treat-netics and proper dosing will reduce this risk substantially. ment of pain in children. N Engl J Med 2003;348(10): The practice of treating infant pain with analgesic 959–960. 6. Gray L, Watt L, Blass EM. Skin-to-skin contact is analgesicagents requires close monitoring by professionals expe- in healthy newborns. Pediatrics 2000;105(1):e14.rienced in infant pain management. Infants should be 7. McCaffery M, Pasero C. Pain: Clinical manual, 2nd edn.monitored regularly for common complications such as St. Louis, MO: Mosby, 1999, pp. 626–696.constipation, as well as those less common such as 8. Peters JW, Koot HM, De Boer JB, et al. Major surgery within the ﬁrst 3 months of life and subsequentallergic reactions or central nervous system depression. biobehavioral pain responses to immunization at later age. Pediatrics 2003;111(1):129–135.SUMMARY 9. Taddio A, Shah V, Gilbert-MacLeod C, Katz J. Condition- ing and hyperalgesia in newborns exposed to repeated heelThe assessment and treatment of pain in infants are lances. JAMA 2002;288(7):857–861. 10. Walco GA, Cassidy RC, Schecter NL. Pain, hurt, andimportant components of medical care for the sick and harm: The ethics of pain control in infants and children. Ninjured infant. Many pain assessment processes exist for Engl J Med 1994;331(8):541–544.pain evaluation in the infant. These practices should be 11. White-Traut R. Providing a nurturing environment forcombined with a meaningful analgesic approach with infants in adverse situations: Multisensory strategies for newborn care. J Midwifery Women’s Health 2004;pharmacologic and nonpharmacologic agents selected 49(4 Suppl 1):36–41.according to infant pain severity, clinical scenario, and 12. Wood M. The case for pediatric drug development inprovider experience. clinical pain research. Anesthesiology 2004;100(1):2–4.
5 Provider Bias and Patient Selection for Emergency Department Procedural Sedation and Analgesia Knox H. Todd SCOPE OF THE PROBLEM PATIENT ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT CONCLUSION BIBLIOGRAPHY Emergency medicine, by virtue of its mission toSCOPE OF THE PROBLEM provide universal and timely access to health care,In 1999, the U.S. Congress requested that the Institute of affords a unique perspective on the problems of healthMedicine (IOM) investigate and report on disparities in disparities. The emergency department (ED) clinicalhealth-care delivery among racial and ethnic minorities. interaction is characterized by lack of patient-physicianIn its landmark report, Unequal treatment: Confronting continuity, diagnostic uncertainty, and signiﬁcantracial and ethnic disparities in health care, the IOM demands on time. Given this environment, perhaps it isdocumented widespread disparities throughout the not surprising that ethnic disparities in analgesic ad-health-care delivery system and recommended a number ministration were ﬁrst documented in an ED setting.of countermeasures to address these inequities. Theseﬁndings are summarized in Table 5-1. Speciﬁcally, the PATIENT ASSESSMENTIOM reported that racial and ethnic disparities wer-econsistent across a broad range of clinical conditions, In a 1993 retrospective cohort study, investigators reportedmedical specialties, and treatment settings and that that Hispanics with isolated humerus, radius, ulna, fem-health disparities persisted after controlling for multiple oral shaft, tibia, and ﬁbula fractures were twice as likely aspotential confounders, including socioeconomic status non-Hispanic whites to receive no pain medication duringand access to care. With regard to clinician-level factors, their ED stay. Although only 26% of non-Hispanic whitesphysician bias, stereotyping, and clinical uncertainty received no analgesics in the ED, 55% of Hispanics wentwere felt to contribute to the observed disparities. without pain medication. These results were not explained Given the subjective nature of pain experience and by differences in patient characteristics (e.g., gender, pri-assessment, particularly in clinical conditions where mary language, and insurance status), injury severity, orovert tissue damage is not involved (e.g., migraine, low the likelihood of associated alcohol or drug intoxication.back pain), it is not surprising that disparities in pain The observed effect of ethnicity even persisted after con-management are prominent in the emerging health trolling for primary language use, suggesting that differ-disparities literature. Although ﬁndings are not uniform, ential analgesic administration was not based purely on thea number of reports from a variety of settings indicate patient’s degree of U.S. acculturation or on his or herthat African Americans and Hispanics are more likely to ability to communicate directly with ED staff.be undertreated for pain than similarly presenting white Though this study had several methodologicalpatients. limitations, the results suggested that ethnicity might 25
26 Overview and Principles in Emergency Analgesia and Procedural Sedation Table 5-1. Summary of ﬁndings of the IOM Unequal treatment report Finding 1-1: Racial and ethnic disparities in health care exist, and because they are associated with worse outcomes in many cases, these are unacceptable Finding 2-1: Racial and ethnic disparities in health care occur in the context of broader historic and contemporary social and economic inequality, and there is evidence of persistent racial and ethnic discrimination in many sectors of American life Finding 3-1: Many sources – including health systems, health-care providers, patients, and utilization managers – may contribute to racial and ethnic disparities in health care Finding 4-1: Bias, stereotyping, prejudice, and clinical uncertainty on the part of health-care providers may contribute to racial and ethnic disparities in health care. Although indirect evidence from several lines of research supports this statement, a greater understanding of the prevalence and inﬂuence of these processes is needed and should be sought through research Finding 4-2: A small number of studies suggests that racial and ethnic minority patients are more likely than white patients to refuse treatment. These studies ﬁnd that differences in refusal rates are generally small and that minority patient refusal does not fully explain health-care disparities Finding 5-1: As a result of the increasing linguistic diversity in the United States, professional interpretation services are increasingly needed to assist in low-English proﬁcient racial and ethnic minority patients in health-care settings Finding 5-2: Community health workers offer promise as a community-based resource to increase racial and ethnic minorities’ access to health care and to serve as a liaison between health-care providers and the communities they serve Finding 5-3: Culturally appropriate patient education programs offer promise as an effective means of improving patient participation in clinical decision-making and care-seeking skills, knowledge and self-advocacy Finding 6-1: Sociocultural differences between patient and provider inﬂuence communication and decision making. Evidence suggests that provider-patient communications are directly linked to patient satisfaction, adherence, and health outcomes. Finding 6-2: A signiﬁcant body of literature deﬁnes and supports the importance of cross-cultural education in the training of health professionals Finding 6-3: Cross-cultural education offers promise as a tool to improve health-care professionals’ ability to provide quality care to diverse patient populations thereby reducing health-care disparities Source: IOM of the National Academies. Unequal treatment: Confronting racial and ethnic disparities in health care. Washington, DC: National Academies Press, 2003.differentially inﬂuence ED pain management patterns in was no difference in physicians’ estimates of painfour ways: (a) differences in patient pain perceptions; between the two groups. The report suggested that(b) ethnic differences in communications regarding the previous observations of differential analgesic adminis-presence of pain to the physician (by the patient, patient tration could not be attributed to differences in physi-advocate, or a member of the ED team); (c) differential cians’ abilities to accurately assess pain in the two ethnicassessments of pain intensity by the health-care pro- groups. When these studies were conducted, guidelinesvider; and (d) actual differences in action by the emer- to promote routine pain assessment within health-caregency physician and ED staff to order and administer systems were only beginning to have an impact onanalgesics unrelated to the patient’s pain experience. Of practice. The authors suggested that the routine incor-the proposed mechanisms, logic suggested that pain poration of standardized assessments into patient careassessment was the most likely mediator of differences in might prove an effective intervention to minimize thethe medical decision-making process. presence of ethnic disparities in treatment. Following up on this issue, the investigators con- The third in this series of studies raised doubts aboutducted a second study at the same institution to deter- the effectiveness of standardizing physician pain assess-mine the inﬂuence of patient ethnicity on emergency ment alone as a method to decrease racial and ethnicphysicians’ ability to assess acute pain. For 138 non- disparities in analgesic administration. In this retrospec-Hispanic whites and 69 Hispanic ED patients with tive cohort study of patients with acute, isolated long-isolated extremity trauma no differences in patient self- bone fractures at a single ED in Atlanta, Georgia, 127assessed pain intensity were found. Although physicians’ African American and 90 non-Hispanic whites receivedestimates of pain were lower than patients’ reports, there analgesics in 57% and 74% of cases, respectively. This
Provider Bias and Patient Selection 27corresponded to an estimated 1.66 relative risk of A later study, from the University of California at Sanreceiving no analgesics for African Americans when Francisco, used a retrospective cohort design to reexam-compared with non-Hispanic white patients. ine racial and ethnic disparities in analgesic administra- As in prior studies, this disparity persisted after con- tion. In that study, long-bone fractures were identiﬁed introlling for multiple potential confounders. Importantly, 323 ED patients, including 181 non-Hispanic whites, 58the medical records in these cases now contained explicit African Americans, 46 Hispanics, and 38 Asian Americans.notations regarding pain in nearly identical proportions Overall, 80% of the patients received analgesics, and therefor African American and non-Hispanic white patients. were no observed differences in analgesic administrationThese ﬁndings suggest that reducing racial and ethnic related to patient ethnicity.disparities in analgesic practice is unlikely to occur by The high rate of analgesic administration observed ininitiatives solely designed to standardize pain assess- this study could indicate that, as analgesic practicement, and that improved pain management practice improves for all groups, interethnic racial and ethnicmight depend upon interventions that target analgesic disparities might tend to decrease. However, the last twoadministration itself. reports also raise the question of publication bias as an Other investigators have examined the role of patient explanation for the preponderance of published studiesexpectations as an explanatory factor for observed dis- reporting differences in analgesic administration betweenparities in analgesic practice. In a survey of 58 Hispanic ethnic groups.and 408 non-Hispanic white patients presenting to a To date, there are no multicenter studies of this issueuniversity ED, expectations for pain relief and estimates with broad geographic representation in a variety of EDof reasonable waiting times for analgesics were com- settings, and most of our inferences regarding broad-pared. The two ethnic groups had similar chief com- based analgesic practices derive from publicly availableplaints and presenting pain-intensity levels. national databases, speciﬁcally the NHAMCS and the When asked to indicate the amount of pain relief they ED component. The most recent available informationexpected from the ED, Hispanics and non-Hispanic from this database (years 2003–2004) suggests thatwhites indicated similar expected levels of relief. In ethnic disparities in analgesic use persist. In Health,addition, the groups’ expectations for waiting times United States, 2006, the Department of Health andprior to receiving analgesics were almost identical. These Human Services’ overview of national trends in healthﬁndings argued against disparate patient expectations as statistics, it is reported that among ED patients report-an explanation for differential analgesic practice. ing severe pain, only 40% of African Americans received A subsequent report, using national databases, docu- opioid analgesics vs 53% of whites.mented racial and ethnic differences in ED parenteralanalgesic and sedative use. These researchers examined PAIN CONSIDERATIONSthe National Hospital Ambulatory Medical Care Survey(NHAMCS) from 1992 to 1997, focusing on patients Beyond the ED, systemic barriers to adequate painreceiving a variety of parenteral analgesics or sedative treatment are common and are inﬂuenced by socio-agents. For patients with fractures, African American economic status and geography, in addition to minoritychildren covered by Medicaid insurance were the group ethnicity. With regard to ﬁnancial status, research sug-least likely to receive parenteral analgesics or sedatives. gests that pain specialists give preferential treatment to Not all researchers have found racial and ethnic dis- more proﬁtable patients. Low socioeconomic statusparities in ED analgesic administration. In a prospective is associated with impaired heath-care access, fewerstudy of 91 patients with low back pain, investigators community health-care resources, and higher overallexamined the inﬂuence of physician pain assessment, as morbidity and mortality rates.well as patient gender, age, and insurance status on the Health insurance allows improved access; however,decision to administer analgesics. Only physician pain 15% of U.S. non-Hispanic whites are uninsured com-assessment was predictive of analgesic administration in pared with 18% of Asians and Paciﬁc Islanders, 20% ofa multiple logistic regression model. African Americans, and 32% of Hispanics. Minority
28 Overview and Principles in Emergency Analgesia and Procedural Sedationmembers without insurance are half as likely to have a providers may be an effective intervention. At theregular physician when compared with insured African regional and national levels, health plans should incor-Americans, thus limiting their access to specialty-level porate ethnic identiﬁers to determine whether evidencepain medicine care. of ethnic disparities in pain management exist. Place of residence is also predictive of access to heath Deﬁnitions of quality ED care should include thecare. Minority neighborhoods tend to lack access to absence of such disparities, and when unmet, largespecialty-level pain medicine. Given the high prevalence providers should receive notice from third-party pur-of chronic pain, there is a relative dearth of pain spe- chasers of our services. Finally, health services researchcialists nationally, and primary care physicians may should be conducted to identify the most promisingprovide care for patients with complex pain manage- interventions to improve the quality of pain manage-ment needs, particularly in rural settings. Many of these ment for all of our patients, speciﬁcally for racial andpatients will seek care in the ED during ﬂares of chronic ethnic minorities.pain syndromes. Of particular concern are recent reports of small area CONCLUSIONgeographic variations in availability of prescriptionopioids. Pharmacies in minority and low-income neigh- Emergency medicine is an inherently egalitarian spe-borhoods appear less likely to carry opioid analgesics than cialty, and its practitioners should be guided by princi-those in nonminority neighborhoods. This variation in ples of distributive justice. One of our specialty’s mostthe availability of analgesics varies geographically, even important roles within the U.S. health-care system is towithin metropolitan areas (New York City) and across a promote fairness and equal access to quality medicalstate (Michigan). The inability to obtain prescribed care. The provision of superior ED analgesia and pro-analgesics may again increase the number of ED visits for cedural sedation, as well as the elimination of analgesia-pain that has spiraled out of control. related health disparities in our departments, should be a fundamental goal of emergency medicine practice.PAIN MANAGEMENT BIBLIOGRAPHYAmong the recommendations in the IOM Unequaltreatment report were calls to increase the proportion of 1. Institute of Medicine of the National Academies. Unequal treatment: Confronting racial and ethnic disparities in healthminorities in the health professions, promote consis- care. Washington, DC: National Academies Press, 2003.tency through evidence-based guidelines, and include 2. Johnson S. Introduction: Legal and regulatory issues inmeasures of disparities in performance measurement. pain management. J Law Med Ethics 1998;26:265–266.Although most would agree that the health professions 3. Bonham VL. Race, ethnicity, and pain treatment: Striving to understand the causes and solutions to the disparities inshould better reﬂect the ethnic makeup of our popula- pain treatment. J Law Med Ethics 2001;29:52–68.tion, it is unlikely that such efforts will yield rapid 4. Lasch KE. Culture, pain, and culturally sensitive pain care.results. Pain Manag Nurs 2000; 1(Suppl 1):16–22. In the short term, the last two recommendations – 5. Todd KH, Samaroo N, Hoffman JR. Ethnicity as a risk factor for inadequate emergency department analgesia.evidence-based guidelines and performance measure- JAMA 1993;269:1537–1539.ment – hold more immediate promise and should be 6. Kirkman-Liff B, Mondragon D. Language of interview:pursued within all treatment settings. Evidence-based Relevance for research of southwest Hispanics. Am J Public Health 1991;81:1399–1404.guidelines will promote consistent treatments for all 7. Todd KH, Lee T, Hoffman JR. The effect of ethnicity ongroups if used; however, there are many barriers to their physician estimates of pain severity in patients withroutine use. isolated extremity trauma. JAMA 1994;271:925–928. Quality assurance and improvement activities con- 8. Todd KH, Deaton C, D’Adamo AP, Goe L., Ethnicity and analgesic practice. Ann Emerg Med 2000;35:11–16.ducted at the institutional level should use ethnic 9. Lee WW, Burelbach AE, Fosnocht D. Hispanic and non-identiﬁers in order to identify ethnic disparities should Hispanic white patient pain management expectations.they exist. Simply supplying feedback to health-care Am J Emerg Med 2001;19:549–550.
Provider Bias and Patient Selection 2910. Hostetler MA, Auinger P, Szilagyi PG. Parenteral analgesic 17. Stewart AL, Napoles-Springer AM. Advancing health and sedative use among ED patients in the United States: disparities research: Can we afford to ignore measurement Combined results from the National Hospital Ambulatory issues? Med Care 2003;41(11):1209. Medical Care Survey (NHAMCS) 1992–1997. Am J Emerg 18. Kaiser Commission on Medicaid and the Uninsured. The Med 2002;20:139–143. uninsured and their access to health care. Washington, DC:11. Bartﬁeld JM, Salluzzo RF, Raccio-Robak N, Funk DL, Henry J. Kaiser Family Foundation, 2003. Verdile VP. Physician and patient factors inﬂuencing the 19. Collins KS, Hughes DL, Doty MM, et al. Diverse treatment of low back pain. Pain 1997;73:209–211. communities, common concerns: Assessing health care12. Fuentes EF, Kohn MA, Neighbor ML. Lack of association quality for minority Americans. New York: Commonwealth between patient ethnicity or race and fracture analgesia. Fund, 2002. Acad Emerg Med 2002;9:910–915. 20. Baicker K, Chandra A, Skinner JS. Geographic variation in13. National Center for Health Statistics. Health, United health care and the problem of measuring racial States, 2006, with Chartbook on Trends in the Health of disparities. Perspect Biol Med 2005;48(Suppl 1): S42–S53. Americans, Hyattsville, MD, 2006. 21. Green CR, Ndao-Brumblay SK, West B, Washington T.14. Lebovits A. The ethical implications of racial disparities in Differences in prescription opioid analgesic availability: pain: Are some of us more equal? Pain Med 2005;6:3–4. Comparing minority white pharmacies across Michigan.15. Cohen DA, Farley TA, Mason K. Why is poverty J Pain 2005;6:689–699. unhealthy? Society and physical mediators. Soc Sci Med 22. Morrison RS, Wallenstein S, Natale DK, Senzel RS, Huang 2003;57(9):1631–1641. LL. ‘‘We don’t carry that’’ – Failure of pharmacies in16. Lillie-Blanton M, Rushing O, Ruiz S., Key facts: Race, predominantly nonwhite neighborhoods to stock opioid ethnicity, and medical care. Washington, DC: Henry J. analgesics. N Engl J Med 2000;342:1023–1026. Kaiser Family Foundation, 2003.
6 Federal and Hospital Regulatory Oversight in Emergency Department Procedural Sedation and Analgesia Sharon Roy SCOPE OF THE PROBLEM Regulatory Assessment Deﬁnitions Sedation Regulatory Considerations SEDATION MANAGEMENT FOLLOW-UP CONSIDERATIONS SUMMARY BIBLIOGRAPHY Sedation in the ED is a specialized practice utilizingSCOPE OF THE PROBLEM treatment approaches that are not common to otherRegulatory oversight of procedural sedation and anal- settings where procedural sedation is administered.gesia (PSA) in the emergency department (ED) is mul- The Joint Commission on Accreditation of Healthcaretifaceted involving federal, state, institutional, and Organizations (JCAHO) has recently focused a greatprofessional mandates (Figure 6-1). The stated goals of deal of attention on procedural sedation. Unfortunately,these regulatory bodies are patient safety, standardiza- much of this attention had led to advisory materials thattion of care, and clinical guidance. are not evidence based. Developing protocols can be challenging for organi- The Clinical Policies Committee of the Americanzations and practitioners when ﬁltering recommenda- College of Emergency Physician (ACEP), in 2005, issuedtions from multiple regulatory agencies and practice an update to their original clinical policy that makesdisciplines. The reality for the ED practitioner is often an recommendations for procedural sedation that are evi-increased frustration owing to regulations that are often, dence based. Though these recommendations are rele-simultaneously, restrictive yet general and broad. The ED vant to the practice of emergency medicine and usefulis a unique setting that necessitates practice guidelines for the development of local sedation guidelines, it wasand procedures that are clear, yet ﬂexible enough to meet carefully noted that individual institutions will still bethe broad spectrum of situations encountered. accredited on the basis of the criteria of the respective Although the need for consistency across organiza- accrediting organization, such as JCAHO. Evidencedtions, practice disciplines, and departments may maxi- based or not, the criteria of accrediting organizationsmize patient safety, the square-peg-into-a-round-hole must be addressed.method of standardization will not work in the imple-mentation of guidelines for sedation in emergency med- Regulatory Assessmenticine. ED patients present with complex sedation needs, JCAHO now implements the Tracer Methodology of siteoften complicated by concurrent diseases, hemodynamic survey for accreditation. This process is a real-timeinstability, unpredictable NPO status, and untreated pain. assessment of a facilities’ compliance with regulations and30
Federal and Hospital Regulatory Oversight 31 Level of oversight Agency Federal JCAHO: Enforcement of federal standards that meet the federal “Conditions of Participation” Accreditation is voluntary. To participate in Medicare or Medicaid programs, organizations must meet eligibility requirements. State State Department of Health State Medical Licensing Board State Surveyors: Accreditation on behalf of Centers for Medicare and Medicaid Services Professional Specialty Board Certification American College of Emergency Physicians Emergency Nurses Association Institutional Organizational Policies Multidisciplinary PSA Guidelines ED Standards of Care Figure 6-1. Levels of oversight and responsible agencies.level of care delivery. A retrospective review will no longer and accurate assessment of existing procedural sedationsatisfy the requirements for renewal of accreditation. clinical practices and procedures.Health-care organizations and practitioners need to be in The JCAHO has refreshed the Comprehensive accred-a continual state of readiness for regulatory review. itation manual for hospitals: The ofﬁcial handbook Paramount to the development and review of proce- (CAMH). Recommendations and regulation standardsdural sedation policies and procedures is maintaining a regarding PSA can be found in ‘‘Provisions of care,patient-centered focus. If a sedation policy addresses the treatment and services’’ section of the handbook titledneeds of the patient (Figure 6-2), it will likely adhere to the Standards for additional special procedures. Each facilityregulatory threshold for safe, acceptable delivery of care. is charged with the responsibility to develop speciﬁc and The JCAHO states that sedation standards and anes- appropriate protocols for moderate and deep sedation.thesia care apply in any setting, for any purpose, and by The guidelines set forth the minimal professionalany route for standards that must be addressed but are generally not prohibitive in the establishment of hospital and/or general, spinal, or other major regional anesthesia departmental sedation protocols (Figure 6-3). moderate or deep sedation (with or without analgesia), which in the manner used may result in Deﬁnitions the loss of protective reﬂexes. Sedation is a continuum and the patient response is not Reviews of compliance with sedation protocols should always predictive or static. Levels of sedation are deﬁnedbe performed continually, and a risk management pro- as minimal, moderate, deep, or anesthesia (Figure 6-4).cess must be in place for corrective actions when deﬁ- ED PSA policies and procedures must address the ﬂu-ciencies are found. An understanding of the regulatory idity of the sedation continuum, especially given thedeﬁnitions and requirements is central to a thorough unpredictable presentations of ED patients. Sedation is
32 Overview and Principles in Emergency Analgesia and Procedural Sedation Health-care Professional’s responses to the question: “ . . . What would you expect of the people who were responsible for that anesthesia or sedation?” • Pick the safest, most effective anesthetics or sedatives • Know how to administer them properly • Know the contraindications and side effects with those medications • Learn something about my past experiences with anesthesia or sedation ahead of time • Tell me what to expect • Allow me ample opportunity to ask questions • Answer my questions with honesty and authority • Know how I’m doing at all times during the procedure • Check to make sure that the equipment you are using is functioning properly • Have a back up plan in place in case I get into trouble • Know when I’m in too deep and you need to call for help • Don’t rush off to the next patient and procedure before making sure the practitioners and nurses monitoring my recovery have the information they need to do a good job Figure 6-2. Expectations for sedation management.deﬁned by the level of sedation achieved rather than the be presented. There is no supportive literature indicatingagents used to achieve it. that informed consent separate from the general consent Qualiﬁed individuals performing and/or monitoring obtained at registration in the ED has an effect on clinicalthe patient during PSA must have competency-based outcomes. Implied consent may be appropriate in situa-education, training, and experience. Health-care orga- tions that impair the patient’s ability to comprehendnizations meet this regulatory oversight criterion by the issues presented in the consent process.processes of Credentialing and Privileging. A facility must The JCAHO does make a distinction in the consentestablish medical bylaws by which an applicant is process between moderate and deep sedation proceduresaccepted by meeting requirements of licensure, relevant and other procedures, in that operative procedures maytraining, and current competence to perform moderate occur without procedural sedation and sedation may beand deep procedural sedation. The requirements are not administered for noninvasive procedures.speciﬁc except that they must be uniform throughout all Regulations on documentation of care are not speciﬁc inspecialties and practice environments in the hospital. form. Patient education and comprehension is reﬂected in Signed consent is acknowledgment of the preprocedural the informed consent. Monitoring equipment, personneldiscussion with the patient. Intervention and medication present, and interventions must be reﬂected in some formrisks and beneﬁts should be discussed. Possible side of documentation. The documentation guidelines (Figureeffects and alternatives to the planned procedure should 6-5) must reﬂect preprocedural baseline, patient status
Federal and Hospital Regulatory Oversight 33 Standard # Standard Statement Standard Elements PC.13.20 Operative or other • Sufficient numbers of qualified staff are present procedures and/or the administration of moderate • Individuals administering moderate or deep sedation and or deep sedation or anesthesia are qualified and credentialed anesthesia are planned • An RN supervises perioperative nursing care • Appropriate equipment to monitor the patient’s physiologic status is available • Appropriate equipment to administer IV fluids and drugs, including blood products, is available as needed • Resuscitation capabilities are available • Anticipated needs of the patient are assessed to plan for the appropriate level of post procedure care • Preprocedural education, treatments, and services are provided according to the plan for care, treatment, and services • Conduct a “time out” immediately before starting the procedure • A presedation or preanesthesia assessment is conducted • Before sedating or anesthetizing a patient, a licensed independent practitioner with appropriate clinical privileges plans or concurs with the planned anesthesia • The patient is reevaluated immediately before moderate or deep sedation and before anesthesia induction PC.13.30 Patients are monitored • Appropriate methods are used to continuously monitor during the procedure and/or oxygenation, ventilation, and circulation during procedures administration of moderate that may affect the patient’s physiological status or deep sedation or anesthesia • The procedure and /or the administration of moderate or deep sedation or anesthesia for each patient is documented in the medical record PC.13.40 Patients are monitored • The patient’s status is assessed immediately after the immediately after the procedure and/or administration of moderate deep sedation or procedure and/or anesthesia administration of moderate or deep sedation or • Each patient’s physiological status, mental status, and pain anesthesia level are monitored • Monitoring is at a level consistent with the potential effect of the procedure and/or sedation or anesthesia • Patients who have received sedation or anesthesia in the outpatient setting are discharged in the company of a responsible, designated adult Figure 6-3. Standards for sedation oversight.during the procedure, and postprocedural recovery to modalities utilized, intervention effectiveness, unpre-baseline. A standardized scale that is universally under- dicted sedation levels, and patient experiences.stood and accepted facility-wide should be utilized. Focusing on the purpose of regulations, to ensure the Monitoring of outcomes is essential data that must be delivery of safe patient care, can assist in the developmentcollected. ED PSA audits should include the treatment of policies and protocols that expedite care, ensure
34 Overview and Principles in Emergency Analgesia and Procedural Sedation Level of Sedation Definition Minimal A drug-induced state during which patients respond normally to verbal commands. Although cognitive function and coordination may be impaired, ventilatory and cardiovascular functions are unaffected. Moderate A drug-induced depression of consciousness during which patients respond purposefully to verbal commands-either alone or accompanied by light tactile stimulation. No interventions are required to maintain a patent airway, and spontaneous ventilation is adequate. Cardiovascular function is usually maintained. Deep A drug-induced depression of consciousness during which patients cannot be easily aroused but respond purposefully after repeated or painful stimulation. The ability to independently maintain ventilatory function may be impaired. Patients may require assistance in maintaining a patent airway and spontaneous ventilation may be inadequate. Cardiovascular function is usually maintained. Anesthesia Consists of general anesthesia and spinal or major regional anesthesia. It does not include local anesthesia. General anesthesia is a drug-induced loss of consciousness during which patients are not arousable, even by painful stimulation. The ability to independently maintain ventilatory function is often impaired. Patients often require assistance in maintaining a patent airway, and positive pressure ventilation may be required because of depressed spontaneous ventilation or drug-induced depression of neuromuscular function. Cardiovascular function may be impaired. Figure 6-4. Levels of sedation.patient safety, and increase patient satisfaction. Regula- of an emergency physician given compliance with regu-tory oversight is not meant to be punitive. It should be latory, legislative, institutional, and professional standardsviewed as a blueprint to guide facilities and practitioners. of care.Sedation Regulatory Considerations SEDATION MANAGEMENTResearch and practical experience have advanced thepractice of procedural sedation in the ED, to the point ED procedural sedation is not without risk. Standards ofwhere previous policies and standards were outdistanced procedural sedation care that adhere to regulatoryand required revision. The resultant examination of oversight contribute to the minimization of those risks.procedural sedation in the ED initiated discussion The basic management principles are very clear withamong many disciplines and has led to new practice regard to regulatory oversight:guidelines, standards of care, and the advancement of 1. Sufﬁcient qualiﬁed individuals are present duringprocedural sedation usage in other treatment areas. In- the procedure and recovery (Figure 6-6).stitutional policy development should be a collaborative 2. Appropriate equipment for care and resuscitationprocess. A multidisciplinary approach should be utilized are available and in working order.to establish criteria to guide departments in developing 3. Monitoring of vital signs at regular intervals:functional, realistic practice standards. The ACEP believes that emergency physicians and nur- a. Heart rateses under their supervision are qualiﬁed to provide pro- b. Oxygenationcedural sedation in the ED. ACEP is typically recognized as c. Adequacy of pulmonary functionthe authoritative body for the establishment of guidelines d. Blood pressurefor procedural sedation by emergency physicians. e. Cardiac monitoring when indicated by the The Emergency Nurses Association (ENA) recognizes patient’s condition.this position and has stated that it is within the scope ofpractice for credentialed registered nurses in the ED to 4. Documentation of care.manage procedural sedation under the direct supervision 5. Monitoring of outcomes.
Federal and Hospital Regulatory Oversight 35 1. Complete a history and physical prior to the procedure. 2. Complete a presedation assessment a. History of sedation/anesthesia complications b. Physical exam of airway, heart and lungs, level of consciousness c. Clinical impression or diagnosis d. Anticipated procedure e. Pertinent lab or test results f. Current medications g. Sedation risk assessment (e.g. ASA score) 3. Complete a plan for sedation 4. Obtain and document appropriate informed consent process 5. Assess pre procedure data a. Vital signs b. Oxygen saturation c. Pain level d. Level of consciousness e. Baseline phase 1 recover score (assessment tool to score recovery from sedation) 6. Immediate reassessment just prior to sedation administration 7. Vital signs minimally every 5 minutes 8. Sedation Score (e.g. Ramsey Sedation Scale) every 15 minutes 9. Monitor vital signs every 5–15 minutes until sedation recovery score returns to baseline 10. Vital signs every 30 minutes until patient returns to pre procedure baseline 11. Assess pain level 12. Provide discharge instructions to patient and/or caregiver. Note: Data collection on all moderate and deep sedation patients should be collected for performance improvement planning to monitor sedation practices and patient outcomes. Figure 6-5. PSA documentation standards guideline. ED practitioners who are responsible for the direct but not limited to, an emergency physician, an EDcare of the ED patient should develop speciﬁc ED nursing manager, and both a physician and a nursingpractice standards and are responsible for overseeing educator.compliance with the standards. Practitioners incor- A member of this group should also be a liaisonporated in this process should be comprised of, involved with an organizational sedation group for
36 Overview and Principles in Emergency Analgesia and Procedural Sedation Practitioner Qualifications ED Physician • Board certified or board-eligible in Emergency Medicine • Competency Based Education/Experience in patient assessment and ED Procedural Sedation ED Registered Nurse • Licensed Registered Nurse • Basic Life Support • Advanced Cardiac Life Support • Advanced Pediatric Life Support • Trauma Nurse Core Course • Competency Based ED specific education in patient assessment and ED PSA Figure 6-6. Examples of criteria for qualiﬁcation to perform moderate or deep procedural sedation. before, during, and after the administration of ED PSA Patient (Figure 6-7). SUMMARY ED physician ED registered nurse Health-care organizations are required by the JCAHO to develop a policy for moderate and deep procedural sedation that is uniform throughout the organization Multidisciplinary consultation After care provider education and to oversee compliance with this policy. The required Figure 6-7. Communication pathways during ED procedural criteria in these policies are deﬁned by the level of sedation. sedation achieved, not the agents used or the treatment area in which the procedure is performed. The devel-multidisciplinary consultation and assurance of consis- opment of this policy can provide an institution thetent practice throughout the health-care facility. opportunity to develop standards that are safe and uniform throughout the practice environment.FOLLOW-UP CONSIDERATIONSPlanning for after care of the patient who has received BIBLIOGRAPHYED PSA should begin during the initial assessmentphase. Standards for postprocedure care need to be 1. Godwin SA, et al. Clinical policy: Procedural sedation and analgesia in the emergency department. Ann Emerg Medincluded in any ED PSA policy. Once the patient’s 2005;45:177–196.condition has returned to a preprocedural baseline, 2. Malviya S, Naughton NN, Tremper KK. Sedation anddisposition needs to be arranged. Postsedation educa- analgesia for diagnostic and therapeutic procedures. St. Louis,tion should emphasize patient safety factors. MO: Humana Press, 2003. 3. Lin DM, Wightman MA. Sedation, anesthesia and the Communication is the most effective tool a health- JCAHO, 3rd edn, chapter 2. Marblehead, MA: HCPro, 2005,care provider can use to deliver safe patient care p. 4.when meeting regulatory requirements. Patients, ED 4. Comprehensive accreditation manual for hospitals: The ofﬁcial handbook. Standards for additional special procedures.personnel, consulting disciplines, and after-care providers 5. The Joint Commission on Accreditation of Health Careshould communicate clearly and reafﬁrm comprehension Organizations, Joint Commission Resources, 2007.
Federal and Hospital Regulatory Oversight 376. Emergency Nurses Association Position Statement 2006 7. Practice guidelines for sedation and analgesia by nonanesthe- Procedural Sedation and Analgesia in the Emergency siologists. An updated report by the American Society of Department, at www.ena.org, last accessed on January Anesthesiologists Task Force on Sedation and Analgesia by 2007. Nonanesthesiologists. Anesthesiology 2002;96:1004–1017.
7 Nursing Considerations in Emergency Department Procedural Sedation and Analgesia Tania D. Strout and Dawn B. Kendrick SCOPE OF THE PROBLEM CLINICAL ASSESSMENT Preprocedure Phase Nursing Considerations for ED PSA Intraprocedure Phase Nursing Considerations for ED PSA Postprocedure Phase Nursing Considerations for ED PSA SUMMARY BIBLIOGRAPHY education, stafﬁng adequate to ensure that nurses caringSCOPE OF THE PROBLEM for PSA patients have no other responsibilities thatProcedural sedation and analgesia (PSA) is a standard might interfere with the care of the PSA patient, andcomponent of emergency medicine practice. Emergency guidelines and protocols for aspects of PSA, includingnurses are frequently called upon to assist in the drug administration, monitoring, discharge criteria, andassessment of and provision of care to this patient complication management.population. Although the administration of PSA medi- Recognizing that the emergency nurse’s role in seda-cations by the registered nurse is regulated by institu- tion encounters varies, based upon institutional policytional policy and state law, compliance with regulatory and nurse practice acts within each state, nursing con-requirements and professional practice standards is also siderations for ED PSA can be discussed within a pre-essential to ensure patient safety and quality care. procedure, intraprocedure, and postprocedure phase Both the Emergency Nurses Association (ENA) and framework.the American College of Emergency Physicians (ACEP)support the delivery of medications used for PSA by CLINICAL ASSESSMENTcredentialed emergency nurses who are working underthe direct supervision of an emergency physician. These Preprocedure Phase Nursing Considerationsprofessional organizations state that PSA agents poten- for ED PSAtially administered by the emergency nurse include, but During the preprocedure phase of emergency sedationare not limited to, etomidate, propofol, ketamine, fen- and analgesia, the nursing assessment should be com-tanyl, and midazolam. pleted and documented according to institutional stan- In addition to ENA and ACEP, several other profes- dards. Monitoring equipment necessary for continuoussional organizations have developed clinical policies and patient assessment should be applied and baseline phys-guidelines surrounding emergency department (ED) iologic parameter measurements should be recorded.PSA. Important aspects of these guidelines recommend These should include heart rate and rhythm, bloodformal institutional-based programs of education and pressure, respiratory rate, and oxygen saturation, andcredentialing for nurses who administer PSA, programs others including BIS and ETCO2 as appropriate byto evaluate and document competency, continuing institutional policy.38
Nursing Considerations 39 Medication, allergy, past medical and surgical histo- this phase sets the stage for an efﬁcient, successful, andries must be evaluated and recorded for each patient. safe PSA experience.The patient’s prior sedation and anesthesia experiencesshould be assessed. Pain state and level of consciousness Intraprocedure Phase Nursing Considerationsshould be evaluated using a standardized measurement for ED PSAtools that will continue to be used throughout the PSA During the intraprocedure phase of ED sedation, theexperience. Patient weight and the time of their last solid emergency nurse may administer PSA medicationsand liquid oral intake are important elements of the under the direct supervision of the emergency physicianpreprocedure assessment, as are the date of the last according to institutional and state regulations. Accuratenormal menstrual period and pregnancy status in female documentation of medications administered, doses,patients. routes, administration times, and patient responses Imperative to a safe and successful sedation procedure should occur.is an evaluation for the existence of barriers to effective Ongoing monitoring and documentation of physio-communication with the patient. The emergency nurse logic parameters, level of consciousness, pain, inter-should ensure that adjuncts supporting clear commu- ventions, and occurrence of events, such as vomiting,nication, such as hearing aids or medical interpreters, takes place during the intraprocedure phase. Emergencyare in place prior to beginning PSA interventions. nurses caring for PSA patients should have a thorough Nursing interventions that must take place in the knowledge of sedation and analgesia medications andpreprocedure PSA phase include the veriﬁcation and their expected and potential effects. They should bepreparation of sedation and analgesic medications, the prepared to anticipate patient needs, intervene asestablishment of patent intravenous access, and the ex- required, and assist in resuscitative efforts. Table 7-2planation of anticipated procedures and medication displays nursing interventions essential to successfuleffects to patients and their families. When circum- navigation of the intraprocedural phase of ED sedation.stances permit, the emergency nurse should review theanticipated discharge plan and instructions with the Postprocedure Phase Nursing Considerationspatient and family in order to alleviate anxiety and allow for ED PSAthe patient time to ask questions prior to the adminis- Upon completion of the intraprocedural PSA phase, thetration of PSA agents. emergency nurse should continue monitoring the Emergency nurses caring for sedation patients should patient’s physiologic parameters, level of consciousness,ensure the availability of operational resuscitation and pain state. Criteria to discontinue this monitoringequipment, airway adjuncts, medications, suction, and are set by individual institutions, but typically includereversal agents. Table 7-1 lists essential nursing activities the patient returning to baseline vital signs and level ofduring the preprocedure phase of ED PSA. consciousness, having intact protective reﬂexes, and As part of the preprocedure phase of the PSA inter- having the ability to respond verbally when questioned.vention, the clinical team should clearly deﬁne the indi- The emergency nurse should monitor PSA patients forvidual roles of the team members, for example, sedation adverse events or complications. These should bephysician, procedure physician, and monitoring nurse. documented and any resulting intervention and theThe group should discuss the planned depth of sedation patient’s response to the intervention should be noted.required for procedure completion, the activities around When PSA patients meet all discharge criteria, thethe actual procedure (e.g., laceration repair, shoulder patient should be provided with a written set of dis-reduction), who is preparing and administering the charge instructions, including medication instructions,medications, and any untoward events that may be postprocedure instructions, activity restrictionsanticipated. (including alcohol consumption, motor vehicle/dan- Family presence during the procedure should be gerous equipment operation, and important decisionaddressed with the team during this phase as well. making), a plan for follow-up care, and instructions forEffective communication and role clariﬁcation during any potential complications.
40 Overview and Principles in Emergency Analgesia and Procedural Sedation Table 7-1. Essential nursing interventions in preprocedural PSA phase Assess and document Existence of barriers to communication Height and weight Age Last normal menstrual period and pregnancy status, if applicable Allergies Medications Medical and surgical history Historical anesthesia experiences Alcohol, tobacco, illicit substances usage history Airway patency Last solid food and drink Level of consciousness using standard scale Level of pain or discomfort using standard scale Physiologic parameters: heart rate and rhythm, blood pressure, respiratory rate, oxygen saturation, others (BIS, ETCO2) by institutional policy Temperature, color, moisture of skin Nursing actions Verify signed, informed consent Verify presence of a responsible adult to accompany and/or transport patient upon discharge Establish intravenous access Explain procedure, medications, and expected effects to patient and family Review anticipated discharge plan prior to PSA with patient and family Ensure availability of airway adjuncts and resuscitation equipment/medications Ensure functional suction equipment and medical gases Verify and prepare ordered medications Ensure availability of appropriate reversal agents Table 7-2. Essential nursing interventions in intraprocedural PSA phase Assess and document Level of consciousness using standard scale Level of pain or discomfort using standard scale Physiologic parameters: heart rate and rhythm, blood pressure, respiratory rate, oxygen saturation, others (BIS, ETCO2) by institutional policy Temperature, color, moisture of skin Patient’s ability to tolerate procedure Presence of nausea/vomiting Medication dosages, routes, times administered Patient response to medications administered Nursing actions Administer sedation and analgesic medications as ordered Provide verbal reassurance to patient and family Administer supportive interventions as required (e.g., airway adjuncts) Participate in resuscitation efforts as required
Nursing Considerations 41 Table 7-3. Essential nursing interventions in postprocedural PSA phase Assess and document Level of consciousness using standard scale Level of pain or discomfort using standard scale Physiologic parameters: heart rate and rhythm, blood pressure, respiratory rate, oxygen saturation, others (BIS, ETCO2) by institutional policy Temperature, color, moisture of skin Occurrence of adverse events Medication dosages, routes, times administered Patient response to medications administered Nursing actions Administer medications as ordered Ensure patient meets institutional discharge criteria Provide written discharge instructions to patient and family or responsible adult Ensure presence of a reliable mode of transportation Discharge instructions should be provided to both the BIBLIOGRAPHYpatient and another responsible adult, owing to the 1. American College of Emergency Physicians (ACEP). Clinicalamnestic effects of various PSA agents. Conﬁrmation policy: Procedural sedation and analgesia in the emergencythat the PSA patient has reliable transportation and is department. Ann Emerg Med 2005;45:177–196.not driving should be made prior to discharge from the 2. American College of Emergency Physicians (ACEP). PolicyED. Table 7-3 lists nursing actions during the post- statement: Delivery of agents for procedural sedation and analgesia by emergency nurses. Ann Emerg Medprocedure phase of the PSA intervention. 2005;46:368. 3. Emergency Nurses Association (ENA). Emergency Nurses Association position statement: Procedural sedation andSUMMARY analgesia in the emergency department. Retrieved from http://www.ena.org/about/position/PDFs/DF08CCBA0E4The emergency nurse is an essential member of the 6430288A9EB30B835E350.pdf, last accessed on August 22,sedation and analgesia team, typically responsible for 2006.patient assessment and monitoring during all phases of 4. EMSC Grant Panel (Writing Committee) on Pharmacologicthe sedation intervention. Qualiﬁed registered nurses Agents Used in Pediatric Sedation and Analgesia in the Emergency Department. Clinical policy: Evidence-basedmay administer sedation and analgesia medications approach to pharmacologic agents used in pediatric sedationunder the direct supervision of a physician, where and analgesia in the emergency department. J Emerg Nursallowed by institutional and state regulations. 2004;30:447–461. 5. American Society of Anesthesiologists. Practice guidelines Nurses involved with the care of the sedation patient for sedation and analgesia by non–anesthesiologists.population should be familiar with the speciﬁc regula- Anesthesiology 1996;84:459–471.tions affecting their participation during sedation 6. Society of Gastroenterology Nurses and Associates, Inc.encounters. Nurses should also have an in-depth (SGNA) Practice Committee. SGNA guidelines for nursing care of the patient receiving sedation and analgesia in theknowledge of PSA medications and their effects and gastrointestinal endoscopy setting. Gastroenterol Nursshould be prepared to participate in resuscitative efforts 2000;23:125–129.as needed. Adequate and clear communication between 7. O’Donnell JM, Bragg K, Sell S. Procedural sedation: Safelyall sedation team members, throughout all phases of navigating the twilight zone. Nursing 2003;33:36–44. 8. Brown TB, Lovato LM, Parker D. Procedural sedationpatient sedation and analgesia, is imperative to ensure in the acute care setting. Am Fam Physician 2005;71:patient safety, satisfaction, and procedural success. 85–90.
SECTION TWO. ANALGESIA FOR THE EMERGENCY PATIENT8 Pharmacology of Commonly Utilized Analgesic Agents Eustacia Jo Su SCOPE OF THE PROBLEM CLINICAL ASSESSMENT Approach to the Patient/Situation PAIN CONSIDERATIONS PAIN MANAGEMENT Nonopioid Agents Acetaminophen (paracetamol) Pharmacology Dosing Contraindications Precautions Adverse effects Important drug interactions Comments and controversies Nonsteroidal anti-inflammatory agents Nonselective COX inhibitors Contraindications Adverse effects Drug interactions Comments and controversies Ketorolac tromethamine (toradol) COX-2 inhibitors Description Pharmacology Efficacy Drug interactions Safety and adverse effects Specific agents Comments and controversies Opioids Pharmacology Speciﬁc Agents Morphine Meperidine Hydromorphone Fentanyl Oxycodone Hydrocodone Codeine Tramadol FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY 43
44 Analgesia for the Emergency Patient produce greater overall relief of pain and distress thanSCOPE OF THE PROBLEM can be accomplished by drugs alone.Emergency physicians must recognize and treat pain from Using nonopioid drugs, such as acetaminophen, non-many causes, from shingles to severe trauma, myocardial steroidal anti-inﬂammatory drugs (NSAIDs), tricyclicinfarction to ureterolithiasis. Pain management is an antidepressants, and sedating drugs can provide syner-important skill in emergency medicine, requiring recog- gistic relief with lower doses of opiates. Knowing how tonition and acknowledgment of the patient’s pain, combine different drugs and modalities of delivery inadequate treatment, and prompt reevaluation. order to harness the synergy of their mechanisms of Analgesia is the ‘‘loss of sensitivity to pain,’’ or the action can greatly enhance the emergency physician’sreduction of pain through therapy. The therapy is not ability to relieve a patient’s pain.solely pharmacologic in nature: psychological and social Combinations of drugs in ﬁxed doses, such assupport as well as physical positioning for maximum oxycodone and acetaminophen, are convenient but maycomfort, all help to reduce a patient’s perceived pain. predispose to acetaminophen toxicity if the patient hasSimply reassuring the patient that the provider is aware already taken a full dose of acetaminophen prior toof the patient’s pain and is actively working to relieve presenting at the ED. Clinicians should consider thethe pain can be as important as any medications used. patient’s speciﬁc situation and prescribe the best com- bination therapy according to the patient’s physiologic and psychologic needs.CLINICAL ASSESSMENTApproach to the Patient/SituationIt is imperative for physicians to detect and measure PAIN MANAGEMENTpain rapidly so that they can begin treatment promptly Pharmacologic therapy can be either curative or pallia-and assess its effect. To the physician, the patient may tive. Relief of cardiac chest pain by the vasodilatorynot appear to be in pain, but he or she may actually effect of nitroglycerin is an example of curative therapy.be in severe pain. Careful listening, observation, and This chapter will deal with palliative therapy; once therepeated solicitation may be necessary to fully elicit an diagnosis is established, if curative therapy is available,admission of pain. Assessment must be both qualitative it is obviously preferable to palliation alone.(is pain present?) and quantitative (how much does ithurt? Has it improved with treatment?). Early reassess- Nonopioid Agentsment must follow any treatments to ensure that it was Acetaminophen (paracetamol)adequate and without adverse effects, and that repeated Acetaminophen is a synthetic, nonopioid derivative ofdoses are given promptly if needed. p-aminophenol (Table 8-1). It is an effective analgesic for mild to moderate pain. Its mechanism of action is unclear and it seems to act only centrally. It has littlePAIN CONSIDERATIONS anti-inﬂammatory effect and few gastrointestinal (GI)The neurophysiology of pain is complex with bio- side effects. It also does not affect platelet aggregation.chemical, neural, cognitive, and emotional components Signiﬁcant hepatotoxicity is known to occur with largethat can affect the patient’s perception of pain and how overdoses.much relief he or she is obtaining. Thus, there is not asingle ‘‘magic bullet’’ that will provide optimal pain PHARMACOLOGY. The mechanism of action of acet-relief in all circumstances. aminophen is poorly understood, but is thought to Multimodal analgesia is an important tool for emer- inhibit the action of prostaglandin synthetase. It acts ongency physicians. Diverse methods of pain control, such the hypothalamus to reduce fever.as positioning for comfort, dimming the lights, distrac-tion (such as television, music, Child Life volunteers) as DOSING.The usual dose of acetaminophen is 325–1,000well as regional nerve blocks or hematoma blocks, can mg every 4–6 hr as needed; the maximum daily dose
Pharmacology of Commonly Utilized Analgesic Agents 45 Table 8-1. Selected nonopioids Type Dose Pediatric dose Toxicity Maximum dose (mg/kg/d) Acetaminophen Not an NSAID. Exact 100 Oral 650 mg to 1 g q4 hr 10–15 mg/kg mechanism unknown. Liver Rectal 1g q6 hr 10–15 mg/kg q4 toxicity possible when 150 mg/kg taken in 24 hr Aspirin 650–975 q4 hr 10–15 mg/kg Reye syndrome in children 60 who subsequently get ﬂu or chickenpox. Tinnitis as dose escalates Toxic dose 150 mg/kg Diﬂunisal 200–500 mg Not approved ASA derivative, q8–12 hr contraindicated in ASA allergy Ibuprofen 400–800 mg 10 mg/kg q 6–8 hr GI irritation 40 q4–6 hr Platelet dysfunction Renal dysfunction Bronchospasm Interacts with protein-bound drugs Naproxen Oral 250–500 mg 5–7 mg/kg q12 hr As for ibuprofen 20 q6–8 hr Indomethacin N/A As for ibuprofen 3 Oral 25–50 q12 hr Rectal 100 q24 Ketorolac IV 30 mg/dose IV 0.5 mg/kg q6 Max As for Ibuprofen ? IM 60 mg/dose 120 mg/d Highest rate of GI bleeding on the NSAIDS Ketoprofen 50–100 mg/dose Not approved As for Ibuprofen 300 mg/d Piroxicam 10–20 mg q 12–24 hr Not approved As for Ibuprofen 40 mg/d Sulindac 150 mg q 12 hr Not approved Pancreatitis, hypersensitivity 400 mg/d Celecoxib 200 po bid Not approved Contraindicated in sulfa ? allergy Meloxicam 7.5–15 mg qd JRA 2yo Not a selective COX-2 7.5 mg 0.125 mg/kg qd inhibitoris 4 g. Children under 12 years of age or less than 30 kg ADVERSE EFFECTS. Acetaminophen is generally wellshould take 10–15 mg/kg every 4–6 hr as needed, maxi- tolerated when used at the recommended doses. Mildmum 75 mg/kg/day. Oral or rectal routes may be used. rashes have been reported, as has bone marrow suppression, as manifested by neutropenia, thrombo-CONTRAINDICATIONS. Acetaminophen should be avoided cytopenia, and agranulocytosis. Hepatotoxicity canin patients who have a known hypersensitivity reaction result from a single toxic ingestion or multiple excessiveto the drug. doses but is rare at therapeutic doses.PRECAUTIONS. Chronic alcoholics who have cirrhosis IMPORTANT DRUG INTERACTIONSmay be at increased risk of hepatotoxicity, and high Anticonvulsants. Many anticonvulsants inducedoses of acetaminophen should not be given to them. hepatic microsomal enzymes, for example, phenytoin,
46 Analgesia for the Emergency Patientbarbiturates, and carbamazepine. Increased conversion COX-1 helps to generate prostacyclin, a vasodilatorof acetaminophen to its toxic metabolite may occur in that increases GI mucosal perfusion. In the stomach,patients who are taking anticonvulsants, and care COX-1 increases bicarbonate and mucus production,should be taken with large and prolonged doses of which are important for protecting the mucosal lining.acetaminophen. Inhibition of COX-1 compromises these protections, Oral anticoagulants. There are reports of a drug in- predisposing patients to ulcerations and bleeding, whichteraction between acetaminophen and warfarin, but are then exacerbated by concomitant NSAID-inducedresults are inconsistent. Hylek et al. reported that platelet dysfunction.patients taking warfarin and high doses of acetamino- COX-1 and COX-2 affect the cardiovascular system byphen (9,100 mg/week) were at much greater risk of blocking the production of endothelial prostacyclinhaving an INR 6. The mechanism of the interaction is (vasodilatory) and thromboxane (platelet aggregation).unknown but may relate to inhibition of the cytochrome These two effects balance each other and can be protec-P-450 microsomal enzyme system by acetaminophen. tive in states of abnormal platelet activation. Inhibition ofHowever, for mild analgesia and fever reduction, acet- COX-1 produces antiplatelet activity that may be cardi-aminophen is still preferable to NSAIDs because of the oprotective by inhibiting thromboxane more than pros-potential for serious bleeding complications in the tacyclin. Inhibition of COX-2 inhibits prostacyclin morecontext of concomitant warfarin and NSAIDs use. than thromboxane and may produce prothrombotic effects, increasing the risk of cardiovascular events.COMMENTS AND CONTROVERSIES. Acetaminophen is a COX-1 produces renal vasodilatory prostaglandinsgood choice for pain management and antipyresis. It is that help maintain the renal blood ﬂow and glomerularthe safest pharmacologic option for pain in children and ﬁltration rate. Inhibition of this effect, especially inadults. It has a high toxic:therapeutic ratio and lacks volume-depleted patients, can result in renal ischemiasigniﬁcant drug interactions as compared with other and even acute renal failure.pain medications and can be used safely even in patientswith most comorbid medical conditions. Nonselective COX inhibitors No particular NSAID has been proven to be superior toNonsteroidal anti-inﬂammatory agents any other for any indication. Drug selection shouldNSAIDs inhibit cyclooxygenase (COX) and, as a result, depend on availability, convenience, and cost.the biosynthesis of prostaglandin, providing decreasedinﬂammation, analgesia, and fever reduction. They are CONTRAINDICATIONS. NSAIDs are contraindicated ininvaluable in the treatment of acute pain syndromes in patients who have known hypersensitivity to NSAIDs.the ED: acute headache, renal or biliary colic, gout, and Patients with asthma and known hypersensitivity to aspirinother painful presentations of musculoskeletal origin. are at particular risk of developing an adverse reaction.NSAIDs have synergistic effects with opioids and canreduce the amount of opioids needed to achieve ADVERSE EFFECTS. The best-documented, serious adversepain relief in a patient. NSAIDs do have some potentially effect of NSAIDs is GI mucosal injury. In 10–60% ofsigniﬁcant adverse effects that can limit their usefulness. patients taking NSAIDs, abdominal pain, dyspepsia, or There are two COX isoenzymes that mediate prosta- nausea will develop (Table 8-2). After 1 year of use, 2–4%glandin synthesis. COX-1 is present in all cells and plays develop symptomatic ulcers. Risk factors include age,an important role in homeostatic functions. COX-2 is concomitant use of warfarin or corticosteroids, conges-induced by injury or inﬂammation and generates pros- tive heart failure, diabetes, and coronary artery disease.taglandins that fuel the inﬂammatory process. Nonse- Histamine-2 receptor antagonists have been shown tolective NSAIDs inhibit both COX-1 and COX-2, giving decrease the incidence of the NSAID-induced PUD.rise to not only multiple beneﬁcial effects (reduction of There is evidence that cytoprotective agents, such asinﬂammation, pain, and fever), but also many undesir- misoprostol and proton pump inhibitors, reduce the riskable effects. more effectively than histamine-2 receptor antagonists.
Pharmacology of Commonly Utilized Analgesic Agents 47 Table 8-2. Risk of GI effects of nonselective ACE inhibitors. Concurrent use of NSAIDs with ACE NSAIDS inhibitors may impair renal function and impair the antihypertensive effects of ACE inhibitors. Lowest risk Ibuprofen 400 mg Diuretics. Avoid using NSAIDs in patients who are Intermediate risk Aspirin, indomethacin, naproxen, sulindac, ibuprofen 800 mg taking diuretics. They have a greater risk of developing High risk Ketorolac, tolmentin, renal failure because of NSAID-mediated, decreased renal ketoprofen, and piroxicam blood ﬂow. Also, the natriuretic response to diuretics depends in part on prostaglandin-mediated vasodilatation. Glucocorticoids. Patients on corticosteroids will have increased risk of PUD. Addition of NSAIDs should be NSAIDs inhibit vasodilatory prostaglandins that used cautiously, if at all.increase renal ﬂow and glomerular ﬁltration rate and Lithium. NSAIDs enhance lithium reabsorption andmay cause renal ischemia and functional damage in may directly reduce lithium excretion, leading tovolume-depleted patients. Sodium and water retention, increased lithium levels. Central nervous system (CNS)hypertension, hyperkalemia, and acute renal failure symptoms (drowsiness, confusion, vertigo, convulsions,may also ensue, especially in patients with congestive or tremors), cardiac dysrhythmias, and QRS wideningheart failure but have otherwise acceptable symptom are warnings of lithium toxicity. The lithium dosagecontrol. should be reduced when adding an NSAID is necessary. Headache, tinnitus, drowsiness, lightheadedness, and Methotrexate. Chronic coadministration of NSAIDsmild dermatologic reactions are among the adverse and methotrexate have resulted in prolonged, elevatedeffects that patients may report. Severe liver problems blood levels of methotrexate, resulting in severe toxicity.and bone marrow suppression have been reported, but A possible mechanism may be the decreased renal per-these occur rarely (Table 8-3). fusion caused by NSAIDs, decreasing the elimination of methotrexate.DRUG INTERACTIONSOral anticoagulants. The antiplatelet effects of NSAIDs COMMENTS AND CONTROVERSIES. NSAIDs combine an-added to the anticoagulant properties of coumadin algesia and anti-inﬂammatory effects with low abusecompound the risk of signiﬁcant bleeding complica- potential and much different side effects than thetions, especially from GI ulcers. Furthermore, NSAIDs opioids. Oral NSAIDs can be as effective as oral opioids.displace protein-bound coumadin and cause subsequent Parenteral NSAIDs have been shown to be as effective asincreases in prothrombin time at a constant coumadin opioids in some settings. However, parenteral NSAIDsdose. Avoid adding NSAIDs to patients on warfarin. do not appear to work better or faster than oral NSAIDs. Table 8-3. Precautions for using nonselective NSAIDS 1. Patients who are dehydrated or hypovolemic are at high risk of acute renal impairment 2. Patients who have impaired renal function, liver disease, or congestive heart failure, in particular, those already taking ACE inhibitors, angiotensin II receptor blockers (ARB), or diuretics 3. Use cautiously in the elderly, who are at greater risk of developing renal toxicity and failure 4. Patients with asthma and known aspirin hypersensitivity are at an increased risk of bronchospasm 5. Third-trimester pregnancy: may prolong gestation or prematurely close the ductus arteriosus (FDA category C) 6. All have the potential for GI side effects 7. They may interfere with the effects of many antihypertensives 8. There is little clinical evidence of individual superiority of any particular NSAID over another 9. The newer agents may cost as much as 50 times more than the older ones
48 Analgesia for the Emergency Patient Different patients respond differently both to the reducing sodium excretion by the same amounteffects and the side effects of different NSAIDs; some (approximately 20%) as do NSAIDs.experimentation may be necessary to determine the best Selectivity. Selectivity of an agent refers to the extentchoice for a particular patient. to which it inhibits COX-2 activity but not COX-1 ac- tivity. In vitro, it would appear that there are very sig-KETOROLAC TROMETHAMINE (TORADOL). Ketorolac is the niﬁcant differences between the different types of agentﬁrst nonopioid analgesic agent available for parenteral (COX-1/COX-2 enzyme activity reduction ratio is 0.1use in the United States. For acute musculoskeletal pain, for indomethacin, as compared with 28,000 for valde-60 mg ketorolac administered intramuscularly (IM) has coxib). In vivo, however, the selectivity does not appearbeen shown to be approximately equivalent in analgesic to signiﬁcantly decrease COX-2 inhibitors’ effects on GIefﬁcacy to 800 mg of ibuprofen given orally. Because mucosa, renal function, and platelets as compared tothe action of ketorolac is due to the inhibition of COX-1 inhibitors.prostaglandin synthesis, its onset is no faster than anequivalent agent given orally. Ketorolac is also 10–35 EFFICACY. No studies on COX-2 inhibitors’ effectivenesstimes more expensive than morphine or ibuprofen. in pain relief have been conducted in ED settings. COX- 2 inhibitors are superior to placebo and equivalent toCOX-2 inhibitors COX-1 inhibitors in acute postoperative dental pain,DESCRIPTION. The discovery of two distinct COX iso- postoperative orthopedic pain, primary dysmenorrheal,enzymes (COX-1 and -2), one (COX-2) associated and osteoarthritis. There are no studies comparingmostly with pain and inﬂammation, raised hope that a COX-2 inhibitors’ efﬁcacy in renal colic, biliary colic,new class of analgesics could be developed. These would acute gout, headache syndromes, sickle cell crisis, orcontrol pain and inﬂammation with fewer adverse acute musculoskeletal or soft-tissue injury. At this point,effects (particularly GI mucosal injury) than traditional there is no evidence that COX-2 inhibitors are signiﬁ-NSAIDs. Unfortunately, the functional distinction cantly more effective than their COX-1 counterparts forbetween the nonselective and COX-2 speciﬁc NSAIDs the management of acute pain in the ED.has proven to be far less pharmacologically useful than ithad seemed at ﬁrst. DRUG INTERACTIONS In the ED, these agents have a limited role in the Nonselective NSAIDs. COX-2 inhibitors should not beinitial management of acute pain. However, they have a combined with NSAIDs because of their similar phar-role in postdischarge use. macological effects. The exception would be ASA for cardioprotection, which is especially important in thePHARMACOLOGY context of possible COX-2 inhibitor-associated cardio-Gastrointestinal. Agents that selectively inhibit COX-2 are vascular events.expected to cause less ulceration and have a lower risk of Interactions that are similar to those of nonselectivebleeding. However, COX-2 has been identiﬁed in normal NSAIDs. COX-2 inhibitors have similar interactions asgastric mucosa, and its possible role in protection and NSAIDs with ACE inhibitors, antihypertensive agents,healing of the gastric mucosa may mean that selective anticoagulants, and lithium (see above).inhibitors may not have any GI-protective advantage. Antacids. Antacids that contain magnesium or alu- Cardiovascular. COX-2 inhibitors may have pro- minum reduce COX-2 inhibitor plasma concentrationsthrombotic effects from greater inhibition of prostacy- and may decrease the agent’s clinical effects.clin than thromboxane, thus increasing the risk of Fluconazole. Fluconazole inhibits cytochrome P450-cardiovascular events. 2C9 isoenzyme and cause increased side effects from Renal. It had been hoped that COX-2 inhibitors COX-2 agents due to decreased metabolism andwould not decrease renal perfusion as much as tradi- increased blood levels of these agents.tional NSAIDs. However, COX-2 inhibitors appear Sulfoamide allergy. Celecoxib has a similar structure toto have no advantage, decreasing renin activity and the sulfonamides, and cross-reactive hypersensitivity
Pharmacology of Commonly Utilized Analgesic Agents 49reactions have occurred in sulfa-allergic patients. Other Table 8-4. Precautions for using COX-2 inhibitorsCOX-2 agents have not been reported to cause the sameproblem. 1. Patients with a history of PUD or GI bleeds 2. Elderly or debilitatedSAFETY AND ADVERSE EFFECTS 3. Volume-depleted patients 4. Patients taking ACE inhibitors or diureticsTolerability. Adverse reactions to COX-2 agents most 5. Patients with renal or hepatic diseaseoften occur in the GI tract, but a few patients report 6. Pregnancy (FDA category C)vague neurological symptoms such as headache and 7. Children under 18dizziness. Otherwise, the rate of adverse reactions is notsigniﬁcantly greater than that seen with placebo or tra-ditional NSAIDs. available in North America. A 20 mg dose has been Endoscopic, clinically asymptomatic ulcers, not as- shown to provide a similar amount and duration ofsociated with bleeding, were found in 7–10% of patients analgesia to ketorolac (30–60 mg) and lasts longer thantaking COX-2 inhibitors as compared with 27–40% of IV morphine (4 mg).patients taking traditional NSAIDs. Signiﬁcant GI effectsoccurred in 1.3% vs 1.8% of patients taking refocoxib vs COMMENTS AND CONTROVERSIES. COX-2 inhibitors havetraditional NSAIDs per year of exposure. not been studied in the ED for use in acute pain syn- The most commonly reported renal events from taking dromes or acute-on-chronic pain exacerbation. Most ofrefocoxib were edema (2.1%), hypertension (0.8%), and the studies describe adverse events that tend to occurexacerbation of preexisting hypertension (0.6%). These after a much longer duration of therapy than is eitherevents were not related to dosage or duration. used in the ED or prescribed upon discharge home. Serious vascular events. COX-2 agents may have a Though evidence suggests that they are as effective inprothrombotic effect based on their greater inhibition of acute pain as traditional NSAIDs and may be betterprostacyclin than of thromboxane. In the VIGOR trial, tolerated, they are generally much more expensive.1.1% of refocoxib patients suffered serious vascular events, The risk of serious cardiovascular events constitutes aas compared with 0.5% of naproxen patients. In the signiﬁcant deterrent to their long-term use.CLASS study, no clear difference in cardiovascular risk wasapparent. Mukherjee et al. suggested that AMI rates in the Opioidstwo studies were higher than the baseline rate in a large Titrated intravenous opioids are the mainstay of phar-meta-analysis and that COX-2 agents, therefore, increased macological management of acute pain. The beneﬁcialthe risk of a cardiovascular event. It is not completely clear effects of opioids have been well documented for cen-that the patient populations were comparable. turies, as have its toxicity and potential for abuse. Fear of Although ED physicians are unlikely to prescribe inducing addition has led to underuse of opioids bylong-term COX-2 inhibitors, they should be aware of many physicians. However, many studies have shownthe potential increase in risk of cardiovascular events that short-term use of opioid analgesics for acute painand ensure that patients who are on COX-2 inhibitors syndromes is not associated with future dependence.are also taking an appropriate antiplatelet agent, if in-dicated (Table 8-4). Pharmacology Opioids bind to several different classes of receptorsSPECIFIC AGENTS. The two COX-2 inhibitors about located throughout the nervous system and suppresswhich we have the most information are celecoxib and neuronal pain transmission peripherally, at the spinalrefocoxib. Valdecoxib and parecoxib are newer, more cord, and in the thalamus. They also act to modify thehighly selective agents that seem to have fewer GI perception of pain at the level of the cortex. There areadverse effects but similar efﬁcacy to NSAIDs. Parecoxib three main opioid receptors: mu, kappa, and delta. Muis a parenterally administered prodrug that is metabo- receptors mediate euphoria, sedation, respiratorylized to valdecoxib. It is the ﬁrst IV/IM COX-2 inhibitor depression, and nausea. Kappa receptors cause spinal
50 Analgesia for the Emergency Patientanalgesia and central sedation; they also produce dys- For a given drug and dosing regimen, maximum painphoria. Delta receptors inhibit pain transmission and control is achieved when serum levels reach a steadymay decrease myocardial and brain oxygen demand. state: requiring ﬁve half-lives. Repeating doses at the Opioids also suppress the medullary cough center and same period as the half-life after initial titration is andecrease the hypercarbic drive. They can activate the effective way to relieve continuous pain. Prescribingchemoreceptor trigger zone causing nausea and vomiting. repeat analgesic doses, rather than ‘‘as needed,’’ is theThey decrease bowel motility and smooth muscle func- most effective way to accomplish pain relief.tion, causing urinary retention and constipation (but can The treatment of pain should start by prescribingbe used to slow diarrhea). Opioids cause mast cell shorter-acting opioids titrated to pain relief, followeddestabilization and subsequent histamine release, pro- by a longer-acting agent and a planned dosing scheduleducing urticaria, pruritus, and orthostatic hypotension. to maintain relief. The use of long acting, delayed Because opioids cause euphoria, they are subject to release, or transdermal formulations to begin painabuse. Patients who use them for prolonged periods will treatment will result in achieving peak serum medica-suppress their production of endogenous opioids and tion levels long after the initiation of therapy, whichdevelop physiologic dependence and subsequently may result in the patients receiving too large a dose inwithdraw if the medication is abruptly stopped. These an attempt to expeditiously achieve pain relief, or toocharacteristics make many physicians and patients small a dose in anticipation of subsequently higherreluctant to use opioid medications, even under ap- levels (see Table 8-5).propriate circumstances. Opioids can relieve any level of pain because they Speciﬁc Agentslack the ‘‘ceiling’’ effect of many other analgesics. They Morphineprovide dose-related analgesia with variable sedation Intravenous morphine is the ﬁrst choice for treatmentand anxiolysis. There is not a standard, ﬁxed, or of acute severe pain in ED patients (Table 8-5). It isweight-related dose necessary to produce a given clinical typically started at 0.1 mg/kg IV and can be repeatedeffect: the dose that produces the desired pain relief is every 5 min at 0.05 mg/kg until pain is relieved. Oralthe correct dose for that particular patient at that par- administration of morphine can be an effective option forticular time. There is no clinically signiﬁcant difference moderate or severe outpatient pain, but only 20% of thebetween the different mu-receptor agonists; any opioid ingested dose reaches the tissues after ﬁrst-pass metabo-can relieve severe pain if its side effects can be tolerated lism, and this delayed onset makes titration difﬁcult.when administered in a dose sufﬁcient to relieve the pain. A common misperception is that morphine causes Opioids should be the ﬁrst-line agents in the man- more smooth muscle spasm than other narcotics andagement of acute severe pain. Morphine, hydro- should be avoided in patients with biliary or renal colic.morphone, hydrocodone, and oxycodone have a short- There is neither any evidence to support this conceptto-intermediate onset and duration of action. The tim- nor any that shows superior efﬁcacy of any other nar-ing of their clinical effects corresponds with their peak cotic over morphine in these situations.serum levels. Maximal analgesia occurs 60–90 min after Morphine is chieﬂy metabolized by conjugation into aoral administration, 30 min after IM injection, and 1–6 three-conjugate and six-conjugate form. The three-min after IV administration. Oral doses have signiﬁcant conjugate form has no opioid analgesic activity and hasﬁrst-pass metabolism and much higher doses are been associated with signiﬁcant CNS side effects (tre-required for an equivalent effect to a parenterally ad- mors, myoclonic jerks, delirium, and seizures) if notministered dose. cleared by the kidneys; this presents a greater risk in Mixed opioid agonist-antagonist antagonists have a elderly patients and those with renal insufﬁciency. The‘‘ceiling’’ beyond which increasing doses do not afford six-conjugate form is made in less abundance than theincreasing pain relief. They also have a high rate of side three-conjugate form and has an opioid analgesiceffects and may cause withdrawal symptoms in patients potency that is much stronger than that of morphine. Italready tolerating large doses of pure agonist opioids. plays an important role in morphine’s efﬁcacy.
Table 8-5. Common opioids and their equipotent doses Generic Oral Intravenous Duration Half-life Comments Precautions Morphine 0.5 mg/kg 0.1 mg/kg 3–4 hr 2–3 hr Standard for comparison Respiratory depression 40–60 mg 10 mg Hypotension Sedation Histamine release Codeine 2.5 mg/kg 1.3 mg/kg 2–4 hr 2–3 hr Poor analgesic Constipation, nausea, and 200 mg 130 mg Excellent cough suppressant vomiting Hydromorphone 0.075 mg/kg 0.015 mg/kg 2–4 hr 2–3 hr Inactive metabolites, less 7.5 mg 1.5 mg accumulation in patients with renal or hepatic disease Hydrocodone 15 mg N/A 3–4 hr 2–3 hr Excellent cough suppressant Fewer side effects than codeine and greater potency Oxycodone 0.125 mg/kg 0.1 mg/kg 3–4 hr 2–3 hr Parenteral form not available Absorbed well in oral form, 12.5 mg 10 mg in US has been associated with High bioavailability relative to most abuse opioids Meperidine 3 mg/kg 0.75 mg/kg 2–3 hr 45–90 min Toxicity from metabolite Avoid with MAOI. Caution (demerol) 300 mg 75 mg normeperidine in renal or hepatic failure Fentanyl 3 lg/kg (transmucosal) 1 lg/kg 0.5–1.5 hr 0.5 hr No histamine release For IV administration, push 300 lg 100 ug Transcutaneous and and ﬂush slowly to avoid transmucosal absorption ‘‘rigid chest’’ syndrome Alfentanil 10 lg/kg 12 min 1.5 hr Duration of action during Muscular rigidity if 1000 lg redistributive phase very administered too quickly short, duration increases with larger doses Oxymorphone 0.1 mg/kg (rectal) 0.01 mg/kg 3–4 hr 2–3 hr Well absorbed rectally 10 mg 1 mg Methadone 0.2 mg/kg 0.1 mg/kg 4–8 hr 15–190 hr Long-acting narcotic used in 20 mg 10 mg opioid addiction treatment and for chronic pain Propoxyphene 1 mg/kg 0.5 mg/kg 2–4 hr 2–3 hr Shown to be inferior to Has little role in the 100 mg 50 mg acetaminophen alone in treatment of pain common oral preparations Heroin 0.5 mg/kg 0.05 mg/kg 3–4 hr 0.5 hr Here for illustrative purposes, 60 mg 5 mg not used medically, common opioid of abuse Tramadol 50–100 mg Selective mu agonist, not May precipitate serotonin51 associated with physiologic syndrome in SSRI patients dependence
52 Analgesia for the Emergency Patient Morphine destabilizes mast cells causing histamine primary indications are in patients who are allergic torelease and can cause pruritus and localized urticaria morphine or have renal or hepatic disease.that can track up the vein after IV administration. This Hydromorphone is available as an injectable solutionis a common phenomenon and does not constitute an and its oral tablets come in 1, 2, 4, and 8 mg strengths.allergic reaction to morphine. Nausea, dizziness, and There is also a 3 mg rectal suppository. Oral doses areconstipation are other common side effects. 4–8 mg PO q3–4 hr; IM doses are 1–2 mg q 3–4 hr, IV When used in combination with acetaminophen, dosing is 0.015 mg/kg mg every 5 min titrated to painpostorthopedic surgery patients used 16% less morphine relief. A sustained release oral hydromorphone formula-in their patient-controlled analgesia and reported lower tion was recently pulled from the market due to reportedpain scores. A multimodal approach can signiﬁcantly overdose potential when combined with alcohol.enhance the delivery of analgesia. FentanylMeperidine Fentanyl is a synthetic opioid that is excellent for rapidMeperidine was one of the most commonly used opioids titration analgesia in acute, severe pain. It is highly li-for the treatment of acute pain in the ED. It is metab- pophilic and produces analgesia within 1–2 min of IVolized by the cytochrome P-450 system to the metabolite infusion. It also redistributes rapidly and its duration ofnormepridine, which has no analgesic effects but potent action is only 30–60 min. It is metabolized by the p-450CNS excitatory effects. Meperidine blocks muscarinic system into inactive metabolites. Drug accumulationreceptors and has signiﬁcant anticholinergic effects, and toxicity may occur after tissue saturation following acausing agitation, delirium, and visual hallucinations. prolonged infusion, but this is unlikely to happen dur- Normeperidine has a half-life of 24–48 hr, as com- ing acute therapy.pared to the 2–3 hr half-life of meperidine. Repeated Fentanyl releases less histamine than morphine anddosing can lead to accumulation of normeperidine and is associated with fewer peripheral effects. It is moreincrease the risk of neurotoxicity. Normeperidine also frequently associated with respiratory depression withblocks the reuptake of serotonin and norepinephrine regular use than morphine, and patients receivingand has been associated with serotonin syndrome. infusions of the drug should be monitored with obser-Normeperidine is not an opioid and is not reversible vation or pulse oximetry. Fentanyl’s short duration ofwith naloxone. action makes it ideal for use in patients who require These diverse adverse effects related to its principal serial examinations.metabolite make meperedine an inferior choice for pain Fentanyl is available in IV form, as well as the raspberry-management compared to most other opioids. It should ﬂavored transmucosal lozenges (200, 400, 600, 800, 1,200,not be used in the management of acute pain. and 1,600 mcg). DuragesicÒ patches are used for sustained release of fentanyl in chronic pain patients, butHydromorphone should not be used in the management of acute pain.Hydromorphone is a semisynthetic derivative of morphinedeveloped in the 1920s. It is the p-450 metabolite of Oxycodonehydrocodone. It is conjugated primarily into several inac- Oxycodone is a strong opioid agonist. It is widelytive metabolites and is, therefore, better tolerated in elderly available in combination with acetaminophen or aspirinpatients and those with renal or hepatic impairment than as well as by itself. It is also available in long-acting oralmorphine. One of its metabolites has been found to be formulations. It has a very high bioavailability relative toexcitatory in rat models and to accumulate in patients who the other opioids and is quickly and efﬁciently absorbed.receive prolonged therapy, but at much lower levels than This has led to an association with abuse. Oxycodone isthe equivalent metabolite in morphine. not available in a parenteral form in the United States, Hydromorphone is similar to oxycodone and mor- although studies have found its IV form to be equia-phine in its analgesic effects and adverse effects. Its nalgesic to morphine.
Pharmacology of Commonly Utilized Analgesic Agents 53 Similar to the other opioids, the analgesic effects of more nausea and constipation than pain relief. Codeine isoxycodone are dose dependent. A 15 mg dose has a often prescribed for cough suppression.similar efﬁcacy to 10 mg of IV morphine. The onset of Codeine is available as codeine syrup (5 mg/ml),action of oral oxycodone is 20–30 min. Oxycodone, in codeine tablets (15, 30, 60 mg), and as an injection ofcombination with acetaminophen, has similar efﬁcacy to codeine phosphate (15, 30, and 60 mg/ml). Tylenol witha higher dose of oxycodone alone. codeine syrup is also available (12.5 mg codeine with Oxycodone is available in 5 mg tablets and in a 5 mg/ 120 mg acetaminophen per 5 ml).5 ml solution. It also comes in 15 and 30 mg tablets anda concentrate of 20 mg/ml. The controlled release forms Tramadolcome in 10, 20, 40, and 80 mg tablets. Tramadol is a synthetic compound that is a selective mu agonist. It is chemically unrelated to the morphine-likeHydrocodone opioids. It is metabolized in the liver by the cytochromeHydrocodone is metabolized in the liver to hydro- P-450 system. One of its metabolites, M1, has an evenmorphone. It provides greater pain relief when com- greater mu-receptor afﬁnity than tramadol and has anbined with acetaminophen or NSAIDs than either elimination half-life of 9 hr. Tramadol also appears tocomponent does alone. Hydrocodone-acetaminophen have effects on GABA and serotonin receptors and could(5 mg/500 mg) provides comparable analgesia to theoretically precipitate serotonin syndrome if admin-codeine-acetaminophen (30 mg/500 mg) in patients istered with SSRIs.with acute musculoskeletal pain or who have undergone Tramadol, as a selective mu agonist, should not causedental surgery. Hydrocodone causes more drowsiness physiologic dependence as the other opioids do. Since itsand dizziness but less nausea or vomiting. Hydrocodone release, however, it has been associated with abuse andis also used as an antitussive. withdrawal similar to that of other opioids, but at low Hydrocodone-acetaminophen and hydrocodone- enough rate that, after a review in 1998, its status as anibuprofen combinations are available with 5 or 7.5 mg unscheduled drug was maintained.of hydrocodone per tablet, but the dosing of these Tramadol has been found to be an efﬁcacious paincombination drugs is limited by the acetaminophen medication at low doses. At increasing doses, it iscontent as well as the combined adverse effects. associated with nausea and vomiting, limiting its use toHydrocodone itself can be prescribed 5–20 mg PO low doses. Tramadol 37.5 mg combined with acet-every 4–6 hr as needed. The combination tablets should aminophen 325 mg was found to have similar efﬁcacy tobe prescribed as 1–2 tablets every 4 hr as needed for hydrocodone 5 mg combined with acetaminophenpain. 325 mg. Side effects include nausea, vomiting, and dizziness.Codeine In combination with SSRIs or tricyclic antidepressants,Codeine is the most commonly prescribed opioid, tramadol may lower the seizure threshold in patientsusually in combination with acetaminophen with which with epilepsy.it acts synergistically. Codeine is a prodrug with minimal Tramadol is available in oral tablets of 50 mg,analgesic effect until metabolized in the liver to mor- recommended dose is 50–100 mg every 4 hr. It is alsophine and other metabolites. available in combination with acetaminophen, 37.5 mg/ Approximately 10% of the population metabolizes 325 mg.codeine poorly and experiences toxicity (nausea, consti-pation, pruritus) but not pain relief. It is a somewhat FOLLOW-UP/CONSULTATIONeffective analgesic against mild to moderate pain but CONSIDERATIONSfrequently causes GI symptoms (mainly nausea andvomiting) at doses that have limited analgesia or A patient who has received opioid medications for acuteeuphoria. The analgesic effect from codeine is dose pain syndromes should be discharged in the company ofrelated, but doses greater than 60 mg cause incrementally a responsible, competent adult who will provide and
54 Analgesia for the Emergency Patientsupervise transportation home and ensure that there is 3. McEvoy GK. American hospital formulary service. Bethesda, MD: American Society of Health System Pharmacists,someone who will monitor the patient overnight. Close 2000.follow-up with a primary care provider is essential for 4. Hylek EM, Heiman H, Skates SJ, et al. Acetaminophen andongoing pain management. other risk factors for excessive warfarin anticoagulation. Discharge prescriptions should provide sufﬁcient JAMA 1998;279:657–662. 5. Lipsky PE, Brooks P, Crofford LJ, et al. Unresolved issuesamounts of medication to adequately treat the patient in the role of cyclooxygenase–2 in normal physiologicthrough the expected course of the injury or until follow- processes and disease. Arch Intern Med 2000;160:up. Patients receiving courses of narcotics that are 913–920.expected to last longer than 5–7 days should be warned 6. Turturro MA, Paris PM, Seaberg DC. Intramuscular ketorolac versus oral ibuprofen in acute musculoskeletalabout the likelihood of tolerance to the medication and the pain. Ann Emerg Med 1995;26:117–120.possible need for tapering of the medication as the treat- 7. Loewen PS. Review of the selective COX-2 inhibitorsment concludes, and should have close follow-up with a celecoxib and refocoxib: Focus on clinical aspects. Can J Emerg Med 2002;4:268–275.primary care provider to oversee the management of this. 8. Mukherjee D, Nissen SE, Topol E. Risk of cardiovascular events associated with selective COX-2 inhibitors. JAMASUMMARY 2001;286:954–959. 9. Joranson DE, Ryan KM, Gilson AM, et al. Trends inThere is no ‘‘one-size-ﬁts-all’’ approach to managing medical use and abuse of opioid analgesics. JAMA 2000:283(13): 1710–1714.acute or acute-on-chronic pain. If nonpharmacologic 10. Jovey RD. Opioid analgesics. In Managing pain, ed. RDadjuncts are available, such as environmental effects Jovey. Toronto, Canada: Healthcare and Financial Pub-(e.g., dimming the lights), psychological distraction, and lishing, for the Canadian Pain Society, 2002, pp. 47–61.physical modalities (positioning, ice), then these should 11. Latta K, Ginsberg B, Barkin RL. Meperidine: A critical review. Am J Ther 2002;9:53–68.be used. 12. Weiner AL. Meperidine as a potential cause of serotonin Physicians should know the expected effects of anal- syndrome in the emergency department. Acad Emerg Medgesic therapy and monitor patients for side effects from 1999;6:156–158.different analgesic agents. Patient responses to the effects 13. Quigley C. Hydromorphone for acute and chronic pain. Cochrane Database Syst Rev 2002;1:CD003447.or side effects of an analgesic can vary considerably. 14. Edwards JE, Moore RA, McQuay JH. Single dose oxycodone and oxycodone plus acetaminophen for acute postoperative pain. Cochrane Database Syst RevBIBLIOGRAPHY 2000;4: CD002763. 1. Schug SA, Sidebotham DA, McGuinnety M, et al. 15. Turturro MA, Paris PM, Yealy DM, et al. Hydrocodone vs Acetaminophen as an adjunct to morphine by patient- codeine in acute musculoskeletal pain. Ann Emerg Med controlled analgesia in the management of acute post- 1991;20:1100–1103. operative pain. Anesth Analg 1998;87:368–372. 16. Silverstein F, Faich G, Goldstein J, et al. Gastrointestinal 2. Barkin R. Acetaminophen, aspirin or ibuprofen in toxicity with celecoxib versus non-steroidal anti- combination analgesic products. Am J Ther inﬂammatory drugs for osteoarthritis and rheumatoid 2001;8:433–442. arthritis JAMA 2000;234:1247–1255.
9 Patient Assessment: Pain Scales and Observation in Clinical Practice Tania D. Strout and Dawn B. Kendrick SCOPE OF THE PROBLEM CLINICAL ASSESSMENT MEASUREMENT CONCEPTS Reliability Validity Clinical Signiﬁcance vs Statistical Signiﬁcance Unidimensional vs Multidimensional Scales PAIN SCALES Unidimensional Pain Scales NRS VAS Verbal descriptor scale (VDS) The Wong-Baker FACES Pain Scale The FACES Pain Scale Multidimensional Pain Scales The Preverbal, Early Verbal Pediatric Pain Scale The CRIES scale MPQ – Short Form (SF-MPQ) Memorial Pain Assessment Card (MPAC) Brief Pain Inventory – Short Form (BPI-SF) SUMMARY BIBLIOGRAPHYSCOPE OF THE PROBLEM CLINICAL ASSESSMENTThe measurement of a patient’s pain intensity is inher- There are multiple barriers to the clinical assessment ofently complex. The pain experience is unique to each pain, including, but not limited to, provider biases,individual, inﬂuenced by many factors such as medical patient anxiety, family attitudes, cultural beliefs, andcondition, developmental level, emotional and cognitive provider suspicion of ‘‘drug-seeking’’ behavior. Thestate, culture, the hospital environment, family issues and National Institutes of Health has stated that patient self-attitudes, language barriers, and levels of fear and anxiety. report is the most reliable indicator of the existence andThe often chaotic, loud, and hurried emergency depart- intensity of pain. Barriers to pain assessment are greatestment (ED) environment only serves to compound these for those patient populations who cannot self-reportdifﬁculties. It is well documented in scientiﬁc literature their pain experience.that oligoanalgesia is a signiﬁcant issue within emergency Pediatric patients and those with impaired cognitionmedicine. In order to appropriately manage patients’ communicate and display pain in very different ways.pain, we must attempt to accurately assess their pain. Infants and young children often cry or whimper when 55
56 Analgesia for the Emergency Patientthey are in pain. They often cannot localize or describe or equivalence, is the second type of reliability thattheir pain and, therefore, it may be difﬁcult to assess and clinicians should consider when choosing a pain ratingquantify. This may be similar in the elderly patient with tool. This refers to the ability of two independentdementia or other cognitive and communicative observers to use the same scale at the same time toimpairments. In these patients or those with or inability observe the same patient and obtain the same result.to characterize their pain owing to endotracheal intu-bation, it is often useful to observe and assess for Validitychanges in behavior, body language, vocalizations, per- Validity is concerned with the extent to which a toolformance of activities of daily living, and physiologic actually measures what it is intended to measure. Threeparameters. Providers of emergency care must be aware primary types of validity are described in the literature:of these limitations and use available tools and direct content validity, construct validity, and predictiveobservation to ensure the best possible outcomes for validity. Evidence of content validity examines the ex-their patients. tent to which the tool includes the major elements rel- Despite these and other barriers to pain measurement, evant to what is being measured. Construct validity isa vast literature describing a great number of pain concerned with the degree of agreement between ameasurement instruments and their properties exists particular measure and other measures that evaluate thetoday. The utilization of such measurement instruments same concept, for example, the degree of agreementprovides emergency clinicians a common language with between two separate pain scales. Predictive validitywhich to communicate assessment ﬁndings in a con- addresses the ability to predict future outcome on thesistent manner. For patients, these instruments can be a basis of the score provided the given instrument. Here,tool that assists them in better communicating the we would expect that a score would indicate lower painsubjective pain experience to their clinicians. However, intensity after a patient receives pain medication.all scales are not appropriate for all patient populations, Figure 9-1 depicts the relationship between validityand the appropriate instrument should be chosen. and reliability. The image in quadrant A represents aSpeciﬁcally, a patient’s age, cognitive and developmental situation where the measure is both reliable and valid,abilities, and preferences need to be addressed when meaning that the results are consistent and that itchoosing the appropriate tool. measures what it is intended to measure. Quadrant B illustrates a situation of high reliability without validity; the measure is consistently not measuring what it isMEASUREMENT CONCEPTS intended to measure. High validity with low reliability isUnderstanding several concepts central to scale devel- displayed in Quadrant C, where this measure wouldopment is useful in assisting clinicians when choosing a provide a valid, but inconsistent, group estimate. Finally,scale to use with their particular population. Knowledge in Quadrant D there is a situation of both low reliabilityof reliability, validity, and the differences between uni- and validity, meaning that the measure is not consistentdimensional and multidimensional scales can be helpful and does not measure what it should.in ensuring that an appropriate tool is utilized. Clinical Signiﬁcance vs Statistical SigniﬁcanceReliability Recent contributions to the emergency medicine litera-Reliability addresses the consistency of a given measure ture discuss clinically signiﬁcant changes in scoresover time. When evaluating pain measurement instru- obtained with the numerical rating (NRS) and visualments, two types of reliability are of particular interest. analog scales (VAS). When evaluating pain, it is im-The ﬁrst type is termed stability, or test-retest reliability. portant to consider the difference between clinical andHere, the clinician is concerned with the consistency statistical signiﬁcance in pain score changes. Cliniciansof the scale over time. Ideally, a pain scale should give should keep in mind that clinically signiﬁcant changesthe same rating at time a and at time b if the patient’s are those experienced by the patient. A statisticallypain intensity has not changed. Interrater reliability, signiﬁcant change in pain score does not necessarily
Patient Assessment and Pain Scales 57 Validity High Low High Reliability A B Low C D Figure 9-1. Reliability vs validity.indicate a change that is meaningful in the life of a in addition to the sensory dimension. An example of apatient. Additional research in this area is needed to unidimensional scale is the NRS whereas the McGillfurther elucidate the relevance of pain score changes Pain Questionnaire (MPQ) is a multidimensional scaleduring clinical management. measuring all three pain dimensions. Table 9-1 describes Melzack and Casey’s pain dimensions with examples ofUnidimensional vs Multidimensional Scales scale measures.Melzack and Casey have proposed that there are threedistinct dimensions of the pain experience that are PAIN SCALESassessable: the sensory-discriminative dimension, theaffective-motivational dimension, and the cognitive- Unidimensional Pain Scalesevaluative dimension. Unidimensional scales are NRSthose that measure only one of these pain dimensions, NRSs consist of a range of numbers and are mostusually pain intensity as a component of the sensory- frequently a 11-point (0–10) or 101-point (0–100) scale.discriminative dimension. Multidimensional scales With these instruments, a patient is simply told that 0attempt to measure the affective-motivational and represents ‘‘no pain’’ and 10 or 100 represents ‘‘the worstcognitive-evaluative dimensions of the pain experience, possible’’ or ‘‘unbearable’’ pain. The clinician then asks
58 Analgesia for the Emergency Patient Table 9-1. Dimensions of pain Pain dimension Description Example of measures Sensory-discriminative Pain location, intensity, temporal aspects NRS dimension Affective-motivational Emotional aspects, aversion, fear, SF – MPQ: ‘‘Cruel – punishing,’’ ‘‘fear,’’ dimension suffering ‘‘sickening’’ Cognitive-evaluative Patient’s evaluation of the meaning and BPI-SF: ‘‘Normal work,’’ ‘‘walking dimension consequences of pain ability’’ No pain 0 1 2 3 4 5 6 7 8 9 10 Worst possible pain Figure 9-2. NRS. No Worst pain possible pain None Mild Moderate Severe Indicate the severity of your pain on the line above. 0 1 2 3 Place a single mark through the line at the point that best represents your pain. Choose the word that best describes your pain. Figure 9-3. VAS. Figure 9-4. VDS.the patient to choose a number that represents their in the clinical setting, its disadvantages are that it can onlycurrent pain intensity. Many hospitals use the NRS in be used in its written form, it requires two steps to score,rating pain as it offers several advantages including ease of and the tool may be rendered invalid if multiple photo-administration and scoring, multiple response options, copies of it are made. Figure 9-3 represents the VAS.and no reported age-related difﬁculties in its utilization.Although the NRS is commonly administered verbally, it Verbal descriptor scale (VDS)may be administered in written form as well. Figure 9-2 Verbal descriptor or rating scales (VDS or VRS) aredepicts the 11-point NRS in its written format. simple scales made up of a list of phrases or adjectives describing pain intensity, from least to most intense.VAS Each phrase or descriptor is assigned a number andThe VAS is a 10-cm horizontal line anchored with a patients are asked to choose the descriptor that mostwritten pain descriptor at each end. The left-hand end of accurately describes their current pain intensity. Thethe line is labeled ‘‘no pain,’’ whereas the opposing end patient’s pain score is the number associated with theiris labeled ‘‘worst possible pain’’ or ‘‘worst pain imag- chosen descriptor or phrase. Although many verbalinable.’’ Here, a clinician shows the image to the patient scales exist, one of the most common in clinical practiceand asks the patient to make a vertical mark on the line is the four-point scale labeled with the descriptors,at the area that best represents their current pain in- ‘‘none,’’ ‘‘mild,’’ ‘‘moderate,’’ and ‘‘severe.’’ The four-tensity. The clinician then measures the distance from point VDS is displayed in Figure 9-4.the left-hand anchor to the patient’s mark. In addition to describing pain intensity, similar scales Although the VAS has been used extensively in re- may be used to assess a patient’s degree of pain relief,search and has been shown to be both reliable and valid with common descriptors being ‘‘none,’’ ‘‘slight,’’
Patient Assessment and Pain Scales 59 0 1 2 3 4 5 No hurt Hurts Hurts Hurts Hurts Hurts little bit little more even more whole lot worst Figure 9-5. The Wong-Baker FACES Pain Rating Scale. (From Hockenberry MJ, Wilson D, Winkelstein ML. Wong’s essentials ofpediatric nursing, 7th edn. St. Louis, MO: Mosby, 2005, p. 1259. Used with permission. Copyright Mosby.)Instructions: Explain to the person that each face is for a person who feels happy because he has no pain (hurt) or sad because he hassome or a lot of pain. Face 0 is very happy because he doesn’t hurt at all. Face 1 hurts just a little bit. Face 2 hurts a little more. Face 3hurts even more. Face 4 hurts a whole lot. Face 5 hurts as much as you can imagine, although you don’t have to be crying to feel thisbad. Ask the person to choose the face that best describes how he is feeling.Figure 9-6. The FACES Pain Scale. (From Bieri D, Reeve RA, Champion GD, Addicoat L, Ziegler JB. The Faces Pain Scale for the self-assessment of the severity of pain experienced by children: Development, initial validation, and preliminary investigation for ratioscale properties. Pain 1990;41(2):144. Used with permission.)‘‘moderate,’’ ‘‘lots,’’ and ‘‘complete.’’ Although VDSs many different languages including Spanish, French,are simple to administer to patients who are literate and Italian, Portuguese, Romanian, Bosnian, Vietnamese,without cognitive impairment, some researchers believe Japanese, Chinese, and German.that the small number of descriptor choices can limit theprecision of the instrument. The FACES Pain Scale Another commonly employed pictorial scale is theThe Wong-Baker FACES Pain Scale FACES Pain Scale, also referred to as the Bieri Scale. LikeThe Wong-Baker FACES Pain Rating Scale is a pictorial the Wong-Baker FACES Pain Rating Scale, Bieri’s FACESscale consisting of a series of six drawn faces with Scale consists of a series of drawn faces representing theexpressions indicating the range of pain intensity from continuum from no pain to severe pain. Patients areno pain (no hurt) to the worst pain (worst hurt). Each shown the scales faces and are asked to choose the faceface is assigned a number from zero to ﬁve indicating best representing their pain state. One key differenceincreasing pain intensity. between the Wong-Baker and Bieri FACES scales is that A standard set of instructions explaining the meaning the latter includes a neutral face as the ‘‘no pain’’ anchor.of each face is included with the scale, and clinicians are It has been suggested that a smiling face as an anchorasked to read these instructions to the patient. Following could potentially lead to the confusion of pain andthe instructions, the clinician asks the patient to choose happiness. Another key difference is the absence of tearsthe face that best describes how they are feeling. Figure 9-5 on the ‘‘most pain’’ Bieri face. Some have felt that thedisplays the Wong-Baker FACES Pain Rating Scale. presence of tears may introduce bias for people from Originally designed for use with school-aged children, cultures where crying in response to pain is not accept-the FACES Scale has been studied extensively and is now able, or for male patients who may not be comfortableconsidered reliable and valid for toddler through ado- choosing a face with tears to represent their pain.lescent age children. There is evidence to suggest validity Figure 9-6 represents the FACES Pain Scale.in adult, older adult, and cognitively impaired popula- Like the Wong-Baker Scale, the Bieri Scale has beentions. Additionally, this scale has been translated into shown to be reliable and valid in a wide variety of age
60 Analgesia for the Emergency Patientgroups, from toddlers to older adults. The FACES Pain with this age group. The full version of the PEPPS scaleScale has also been used successfully with patients who contains seven assessment categories: heart rate, facial,are cognitively impaired. cry (audible/visible), consolability/state of restfulness, body posture, sociability, and sucking/feeding.Multidimensional Pain Scales The scale authors modiﬁed these original categoriesThe Preverbal, Early Verbal Pediatric Pain Scale for use in the ED by eliminating the heart rate andDesigned speciﬁcally for toddlers who are not yet to be sucking/feeding category as providers of emergency careable to self-report their pain experiences using tools were concerned that elevated heart rate in febrile orsuch as the Wong-Baker FACES Pain Rating Scale, the scared toddlers and no oral intake status or the presenceModiﬁed Pre-Verbal, Early Verbal Pediatric Pain Scale of nausea in emergency patients would erroneously(M-PEPPS) is an important tool for clinicians who work affect pain scores in this population. The modiﬁed Parameter 0 1 2 3 4 Facial Relaxd Grimace, Severe facial brows grimace; expression drawn brows together; lowered, eyes tightly partially drawn closed, together; squinting eyes tightly closed Cry No cry Whimpering, Intermittent Sustained Screaming (Audible/Visual) groaning crying crying Consolability/State Pleasant, Distractible, Able to Unable to of Restfulness well easy to console, console, integrated console, distract with restlessness, intermittent difficulty, sustained fussiness intermittent movement restlessness, irritability Body Posture Body at Clenched Localization Intermittent Sustained rest, fists, curled with or arching, relaxed toes and/or extension or sustained flailing, positioning reaching for, flexion or movement thrashing, touching stiff and with our and/or wound or non-moving without kicking area periods of rigidity Sociability Responds With effort, Absent eye to voice responds to contact, no and/or voice and/or response to touch, touch, voice makes eye makes eye and/or contact contact but touch and/or difficult to smiles, obtain or easy to maintain obtain or maintain; sleeping Total Score: ____________Figure 9-7. M-PEPPSª. (From Schultz AA, Murphy E, Morton J, Stempel A, Messenger-Rioux C, Bennett K. Perverbal, early verbalpediatric pain scale (PEPPSª): Development and early psychometric testing. J Pediatr Nurs 1999;14(1):19–27. Used with permission ofthe author and Elsevier.)
Patient Assessment and Pain Scales 61 CRIES Score Parameter 0 1 2 Crying No High Pitched Inconsolable Requires Oxygen for No 30% 30% Sat 95% Increased Vital Signs HR BR Pre-Op HR or BP ↑ 20% of HR or BP ↑ 20% of Pre-Op Pre-Op Expression None Grimace Grimace/Grunt Sleepless how No Wakes at Frequent Constantly Awake measured during Intervals study Coding Tips for Using CRIES Crying The characteristic cry of pain is high-pitched If no cry or cry which is not high-pitched, score 0 If cry high pitched but baby is easily consoled, score 1 If cry is high pitched and baby is inconsolable, score 2 Requires Look for changes in oxygenation. Babies experiencing pain manifest Oxygen for Sat decreases in oxygenation as measured by TCO2 or oxygen saturation. 95% (Consider other causes of changes in oxygenation: atelectasis, pneumothorax, over sedation, etc.) If no oxygen is required, score 0 If 30% O2 is required, score 1 If 30% O2 is required, score 2 Increased Vital Note: Take BP last as this may wake child causing difficulty with other Signs assessments. Use baseline pre-op parameters from a non-stressed period. Multiply baseline HR x 0.2 then add this to baseline HR to determine HR which is 20% over baseline. Do likewise for BP. Use mean BP. If HR and BP are both unchanged or less than baseline, score 0 If HR or BP are increased by increase is 20% of baseline, score 1 If HR or BP are increased by increase is 20% over baseline, score 2 Expression The facial expression most often associated with pain is a grimace. This may be characterized by: brow lowering, eyes squeezed shut, deepening of the naso-labial furrow, open lips and mouth. If no grimace is present, score 0 If grimace alone is present, score 1 If grimace and non cry vocalization grunt is present, score 2 Sleepless This parameter is scored based upon the infant’s state during the hour preceding this recorded score. If the child has been continuously asleep, score 0 If he/she has awakened at frequent intervals, score 1 If he/she has been awake constantly, score 2 Figure 9-8. The CRIES Scale. (From Krechel SW, Bildner J. CRIES: A new neonatal postoperative pain measurement score. Initialtesting of validity and reliability. Pediatr Anesth 1995;5:53–61. Used with permission of Blackwell Publishing.)version of the scale has been found to be reliable and behavior in each of the ﬁve categories, scoring each categoryvalid in ED pediatric patients. and then summing the categories for a total score. The The M-PEPPS is displayed in Figure 9-7. To score the observation period for the scale varies from patient toM-PEPPS, the emergency clinician observes the patient’s patient, but can typically be accomplished with under
62 Analgesia for the Emergency Patient2 min of observation time. Scores range from 0 to 20 with include the complex nature of the observation and scoringratings of 6 considered indicative of mild to no pain. process and the use of physiologic measures that are known to be inﬂuenced by a great many variables other than pain.The CRIES scale The CRIES instrument is presented in Figure 9-8.The CRIES (crying, requires oxygen for saturation above95%, increased vital signs, expressions, and sleeplessness) MPQ – Short Form (SF-MPQ)was developed to assist in assessing the pain of neonates. Although rarely used in acute care settings, the SF-MPQThis instrument combines the observation of patient be- bears mentioning as it may be appropriate for use withhavior with physiologic parameters to provide a composite some patients. This tool contains both a VAS portion and ascore for the assessment of pain. Clinicians assess three list of pain descriptors, 11 from the sensory-discriminativebehavioral parameters (crying, expression, and sleepless- domain and 4 from the affective-motivational domain.ness), evaluate for an oxygen requirement to maintain To use this tool, the clinician asks the patient tosaturation levels greater than 95%, and evaluate for elevated complete the VAS and to rank each pain descriptor asheart rate and blood pressure. Weaknesses of the scale ‘‘none,’’ ‘‘mild, ’’ ‘‘moderate,’’ or ‘‘severe.’’ These are Check the column to indicate the level of your pain for each word, or leave blank if it does not apply to you.— Mild Moderate Severe 1 Throbbing 2 Shooting 3 Stabbing 4 Sharp 5 Cramping 6 Gnawing 7 Hot-burning 8 Aching 9 Heavy 10 Tender 11 Splitting 12 Tiring-exhausting 13 Sickening Mark or comment on the above figure where you 14 Fearful have your pain or problems 15 Cruel-punishing Indicate on this line how bad your pain is—at the left end of line means no pain at all, at right end means worst pain possible. No Worst possible pain pain S /33 A /12 VAS /10 Figure 9-9. SF-MPQ. (Reproduced with permission of author. Copyright Dr. Ron Melzack.)
Patient Assessment and Pain Scales 63ranked 0 (none) to 3 (severe) and each section of the This tool assesses the presence of pain, pain intensity,tool (sensory, affective, and VAS) is summed to provide pain relief, and mood. The MPAC is quick and simplenumerical scores. This tool can be completed in to use and has been shown to correlate well withapproximately 2–5 min. more complex pain, mood, and anxiety rating scales. This The advantage of using this instrument is that its mul- instrument has not yet been validated in the emergencytidimensional nature provides more insight into the population. The MPAC is displayed in Figure 9-10.patient’s subjective pain experience. Disadvantages includelimited reliability and validity testing and no studies of this Brief Pain Inventory – Short Form (BPI-SF)nature speciﬁc to the emergency patient population. Figure The BPI-SF is another multidimensional assessment tool9-9 illustrates the short form version of the MPQ. with potential application in the emergency population. This questionnaire consists of a series of nine questionsMemorial Pain Assessment Card (MPAC) with numeric scale responses. The questions address theDesigned for the rapid assessment of cancer patients’ sensory-discriminative and affective-motivational omains,pain experience, the MPAC consists of a series of three as well as provide information on physical functional status.VASs and one set of pain intensity descriptors. The The BPI-SF is intended to be self-administered bycard is designed to be printed on one sheet of paper, the patient and is thus limited to those who arefolded, and shown to the patient one section at a time. literate, physically able to use pen and paper, and without Mood scale Moderate Strong Just noticeable Worst Best Mild Excruciating mood mood No pain Severe Weak 4 2 Pain scale Relief scale Least Worst No Complete possible possible relief relief pain pain of pain of pain 1 3Figure 9-10. MPAC. (From Fishman B, Pasternak S, Wallenstein SL, et al. The Memorial Pain Assessment Card: A valid instrument forthe evaluation of cancer pain. Cancer 1987;60:1151–1158. Used with permission.)Note: Card is folded along the dashed line and each measure is shown to the patient separately in the numbered order.
Brief Pain Inventory (Short Form) 1. Throughout our lives, most of us have had pain from time to time (such as minor hedaches, spralns, and toothaches). Have you had pain other than these every day kinds of pain today? Yes No 2. On the diagram, shade in the areas where you feel pain. Put and X on the area that hurts the most. Front Back Right Left Left Right 3. Please rate your pain by marking the box beside the number that best describes your pain at itsworst in the last 24 hours. 0 1 2 3 4 5 6 7 8 9 10 No Pain As Bad As Pain You Can Imagine 4. Please rate your pain by marking the box beside the number that best describes your pain at its least in the last 24 hours. 0 1 2 3 4 5 6 7 8 9 10 No Pain As Bad As Pain You Can Imagine 5. Please rate your pain by marking the box beside the number that best describes your pain on the average 0 1 2 3 4 5 6 7 8 9 10 No Pain As Bad As Pain You Can Imagine 6. Please rate your pain by marking the box beside the number that tolls how much pain you have right now. 0 1 2 3 4 5 6 7 8 9 10 No Pain As Bad As Pain You Can Imagine 7. What treatments or medications are you receiving for your pain? 8. In the last 24 hours, how much relief have pain treaments or medications provided? Please mark the box below the percentage that most shows how much relief you have received. 0% 10% 20% 30% 40% 50% 60% 70% 80% 90% 100% No. Complete relief Relief 9. Mark the box beside the number that describes how, during the past 24 hours, pain has interfered with your: A. General Activity 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes B. Mood 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes C. Walking ability 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes D. Normal Work (includes both work outside the home and housework) 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes E. Relations with other people 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes F. Sleep 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes G. Enjoyment of life 0 1 2 3 4 5 6 7 8 9 10 Does not Completely Interfere Interferes xxxxxxxxxxxxxxxxxxxxxxxxxxx xxxxxxxxxxxxx xxxxxxxxxxxx Figure 9-11. BPI-SF. From The Memorial Pain Assessment Card: A valid instrument for the evaluation of cancer pain. Cancer1987;60:1151–1158. Used with permission.
Patient Assessment and Pain Scales 65 Table 9-2. Summary of pain scale properties Scale Population Reliability Validity Uni- or Use caveats acceptable? acceptable? multidimensional NRS School age Yes Yes Unidimensional Self-report Adolescent Some elders Adult may have difﬁculty Elders Cognitively impaired may have difﬁculty Validated in ED populations VAS School age Yes Yes Unidimensional Self-report Adolescent Some elders Adult may have difﬁculty Elders Cognitively impaired may have difﬁculty Requires pencil/paper Validated in ED populations VDS Toddlers able to Yes Yes Unidimensional Self-report self-report Requires literacy School age Some elders may Adolescent have difﬁculty Adult Cognitively impaired Elders may have difﬁculty Small number of descriptor choices Wong-Baker Verbal toddlers Yes Yes Unidimensional Self-report FACES School age Smiling ‘‘no pain’’ anchor Adolescent may be intrusive Adult Tears on ‘‘most pain’’ Elderly anchor may introduce Cognitively impaired cultural or gender bias FACES (Bieri) Verbal toddlers Yes Yes Unidimensional Self-report School age Adolescent Adult Elderly Cognitively impaired M-PEPPS Preverbal and early Yes Yes Unidimensional Observational verbal toddlers Validated in ED population CRIES Neonates Yes Yes Unidimensional Observational Validated in ICU population SF-MPQ Adult Yes Yes Multidimensional Self-report Requires literacy Lengthy Requires pencil/paper MPAC Adult Yes Yes Multidimensional Self-report Requires pencil/paper BPI-SF Adult Yes Yes Multidimensional Self-report Requires literacy Lengthy Requires pencil/paper
66 Analgesia for the Emergency Patientcognitive impairment. Additionally, this tool has not been 8. McCormack HM, Horne DJ, Sheather S. Clinical applica- tions of visual analog scales: A critical review. Psychol Medvalidated in the ED population. Strengths of the instru- 1998;18(4):1007–1019.ment are relative ease of administration and the addi- 9. Jensen MP, Karoly P, Braver S. The measurement oftional information of function obtained when compared clinical pain intensity: A comparison of six methods. Painto unidimensional measures of pain intensity alone. The 1986;27(1):117–126. 10. Wong DL. Validity of a FACES Pain Rating Scale withBPI-SF is depicted in Figure 9-11. an adult population. Published online March 15, 2002, http://www3.us.elsevierhealth.com/WOW/faces11.html, lastSUMMARY accessed on August 15, 2006. 11. Berg DM. 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10 Pathways and Protocols for the Triage Patient with Acute Pain Paula Tanabe SCOPE OF THE PROBLEM Overcrowding Patient Satisfaction CLINICAL ASSESSMENT PAIN MANAGEMENT Protocols FOLLOW-UP CONSIDERATIONS SUMMARY REFERENCES Elderly patients with hip fractures have been describedSCOPE OF THE PROBLEM as experiencing signiﬁcantly longer time to pain assess-Emergency departments (EDs) face many challenges. ment when the ED is at capacity.Recent data suggest that patient visits in United States Delays associated with overcrowding leave manyEDs have increased 18% over the past 10 years and are patients in the waiting room after the initial triage as-now estimated to approximate 110 million visits annu- sessment by a nurse. Patients with pain are forced toally. Pain is the most common symptom in which wait for physician evaluation and potential pain relief.patients present to the ED. Up to 78% of all patients Patients who must wait for physician evaluation prior topresent to the ED with a chief complaint of pain. receiving any pain relief measures will experience delays Emergency providers have an important opportunity in analgesic administration.to intervene with analgesic agents at triage to provideanalgesia to patients suffering pain. To affect this Patient Satisfactionscheme, there is a need for nurse-driven analgesic pro- EDs are under pressure to meet patient satisfactiontocols at triage. goals. A frequent source of patient dissatisfaction is the initial wait to see the physician. In a recent study, 69%Overcrowding of subjects reported being comfortable receivingED crowding has recently been recognized as a critical analgesics from a nurse prior to physician evaluation.problem by the Institute of Medicine. A national survey Despite patients’ belief that triage pain management isof eight EDs reported experiencing overcrowding 12– important, Stalnikowicz et al. reported that two-thirds73% of the time (mean = 35%). A direct consequence of of ED patients were reluctant to ask for pain medica-ED overcrowding is a prolonged time to evaluation by a tions unless the pain was unbearable. These observationsphysician. demonstrate the responsibility triage nurses have in Variability at individual institutions is common, and initiating analgesic management.data from a prospective study conducted at a single site Providing analgesic interventions at triage provides areports an average time to initial analgesic of 74 min. Time unique opportunity toto pain assessment is also affected by ED overcrowding. provide more timely relief of patients’ pain 67
68 Analgesia for the Emergency Patient • Patients in severe pain • Patients 15 years of age • Patients who are hemodynamically unstable (P100, BP 100 systolic) • Patients with an altered LOC (GCS15) or respiratory rate 12/min • Patients with severe liver impairment • Patients presenting with possible ischemic chest pain • Patients presenting with shortness of breath as a major presenting complaint • Patients presenting with headache • Patients with abdominal pain • The patient must not be allergic to codeine or paracetamol • Patients who have taken a total of 4g or more of Paracetamol in the previous 24 hr • The administering nurse must advise the patient that they must not drive or operate heavy machinery for 3 hours after taking panadeine forteFigure 10-1. Example exclusion criteria for patients treated by triage analgesic protocols. (Reprinted with permission from Fry M,Ryan J, Alexander N. Accident and Emergency Nursing 2004;12(3):136–140, table 1, p. 137, Elsevier.) increase patient satisfaction while waiting for initial ask the patient whether the patient has taken any physician evaluation analgesics or used other methods to decrease pain prior address Joint Commission of the Accreditation of to arrival. Patient exclusion criteria for the speciﬁc triage Healthcare Organization (JCAHO) pain goals. protocols should be queried for each patient encounter Implementation of nurse-driven analgesic protocols (Figure 10.1).at triage is the most effective method to accomplishthese three important goals. ED crowding has led to a PAIN MANAGEMENTdelay in initial analgesic administration for the largenumber of patients that present with pain. Nurse-driven The process of developing and implementing nurse-analgesic protocols that can be implemented at triage driven analgesic protocols at triage has been described inhave been developed and studied. These protocols have the literature. A multidisciplinary team should bebeen found to lead to improved times to provision of formed with considerable time to develop and imple-analgesic agents, as well as reduction in pain scores. ment the protocols. The following elements should be addressed in these protocols: 1. Goal or desired outcomes of the protocol.CLINICAL ASSESSMENT 2. Possible types of chief complaints to be included:The JCAHO mandates assessment of pain for all Anticipation of intravenous catheter insertion,patients. Most hospitals have integrated pain assessment eye pain, absence of trauma history, foreign bodyas a ﬁfth vital sign and documentation of a pain score is sensation, musculoskeletal trauma, lacerations,usually performed at ED triage. headaches, cellulites, back pain of musculoskele- It is also important to assess components of pain tal nature.complaints other than intensity. Location, duration of 3. Possible types of chief complaints to be excluded:pain, aggravating, and alleviating factors can be helpful chest pain, abdominal pain, sickle cell pain crisis,in characterizing patient pain. The triage nurse should severe headaches.
Protocols for Triage Patient 69 4. Speciﬁc nonpharmacologic strategies: ice, eleva- 7. Safeguards if administering controlled substances tion, distraction techniques (music, toys, video at triage. games). 8. Pre- and postpain assessment and documentation. 5. Speciﬁc pharmacologic agents and doses: acet- 9. Availability and proximity of pharmacologic and aminophen, ibuprofen, acetaminophen with nonpharmacologic agents. codeine, hydrocodone, proparacaine, EMLA 10. Instructions for patients that leave without being cream, ELA Max, LET. seen after administration of a pharmacologic 6. Exclusion criteria for speciﬁc pharmacologic agents. agent. I. All patients upon arrival to the ED will have their pain level evaluated and documented at triage. Pain will be evaluated using the numeric 0–10 scale, FLACC infant scale, or Wong-Baker FACES scale as appropriate to patients comprehension or age. • 0 Constitutes no pain • 1–3 Constitutes mild pain • 4–6 Constitutes moderate pain • 7–10 Constitutes severe pain All allergies are assessed as per hospital protocol. No pediatric patient under 6 months old may have Ibuprofen. No female of child-bearing age who could be pregnant will receive Ibuprofen. *Please note whether the patient has been medicated prior to arrival for pain with medication dose and time in triage note. II. 1. Pain medication guidelines related to pain level or complaint 2. Mild pain 1–3/10: Any contusion, sprain, laceration, headache, back pain, etc. (patients with acute pain not likely to require immediate surgical intervention or moderate sedation and no other contraindications). • Acetaminophen: Pediatrics 15 mg/kg PO Adults 650 mg PO • Ibuprofen: Pediatrics 10 mg/kg PO (6 months or older) Adults 400 mg PO 3. Moderate Pain 4–6/10: For musculo skeletal pain related to MVC, possible fracture, etc. • Acetaminophen: Pediatrics 15 mg/kg PO Adults 650 mg–975 mg PO • Ibuprofen: Pediatrics 10 mg/kg PO (6 months or older) Adults 600 mg PO Figure 10-2. Example pediatric ED protocol for analgesic treatment at triage. (Reprinted with permission from Jutun. Andrews@uchospitals.edu, May 15, 2006.)
70 Analgesia for the Emergency Patient 4. Severe Pain 7–10/10: For obvious deformities, chronic back pain, migraines with N/V (any severe pain that should not require immediate surgical intervention or moderate sedation). • Acetaminophen with Codeine Elixir: Pediatrics acetaminophen 120 mg/ 5ml, Codeine 12 mg per 5 ml (Give 1 mg/kg Codeine PO) • Acetaminophen with Codeine Tablets: Adults acetaminophen 300 mg/Codeine 30 mg (Tylenol #3) (Give 1 or 2 tablets PO) • Ibuprofen: Pediatrics 10 mg/kg PO (6 months or older) Adults 800 mg PO For obvious deformities, establish IV access, give morphine sulfate 0.1 mg/kg 5. Eye injuries: Any age child (it is not restricted for adults only) may have Tetracaine 1 to 2 drops in affected eye(s) if patient is not allergic and does not have a globe injury. This may be repeated every 5–10 min up to 3 doses. Patient may not have this medication in their possession. 6. Bugs in ear: Any age patient may have Auralgan drops, 2–4 drops (or enough to fill ear canal) in the affected ear. Contraindicated if there is a possible perforated tempanic membrane or obvious canal trauma/bleeding. 7. Ear pain/sore throat pain: Any age patient may have Tylenol or Motrin per weight appropriate dose for any pain level. 8. Extremity injuries: All patients with extremity injuries (except amputations) will have ice applied and instructed to elevate affected limb. III. 9. These guidelines apply to all triage patients who will not have an immediate room assignment and will have to wait to see a physician. Triage nurse will reassess these patients within 1 hr of pain management intervention for effects of measures taken. Figure 10-2. (continued) 11. Education of all staff including nurses and Triage protocols that do not include opioids often physicians. include nonpharmacologic measures (e.g., ice, elevation, 12. Standing orders. and distraction) and allow for the administration of 13. Documentation tools. acetaminophen and/or ibuprofen. Protocols including 14. Quality improvement monitoring. opioids will most frequently allow the nurse to admin- ister acetaminophen with codeine or oxycodone. OralProtocols opiate protocols have been described in the adult andMany protocols have been developed for the delivery of pediatric medical literature. Intravenous opiate triageanalgesic agents at triage (Figures 10.2 and 10.3). These protocols have also been developed and described in theprotocols often address analgesic management in two literature. These reports have characterized protocols forcategories: (a) over-the-counter, nonopioid medications the administration of morphine and hydromorphoneand (b) opiates. prior to physician evaluation.
Protocols for Triage Patient 71 Protocols for administration of initial medication Purpose: To facilitate patient care in busy environment, promote patient comfort, and minimize patient wait. Subjective data: Early administration of medication will minimize suffering, benefit patient outcomes, and improve customer satisfaction. Expected outcome: The patient will experience less uneasiness, distress, discomfort, and anxiety. Any registered nurse, mid-level provider (MLP: nurse practitioner or physician assistant) may institute the following interventions in order to expedite patient care according to medical protocol orders established by Dr. Nancy Ryan, medical director of Emergency Medicine. Initiation of these orders is based on completion of a patient assessment. The patient will be informed that the medications are being given to promote comfort prior to them being evaluated by the emergency physician. Documentation: Time of administration, name, dose, and route of medication will be documented. “Per protocol” to be documented or “per protocol” box to be checked. Contraindications to Ibuprofen/NSAIDs: Persons with hypersensitivity to NSAIDs, allergy to ibuprofen or aspirin, nasal polyps, asthma, severe renal disease, severe hepatic disease, history of ulcers or GI bleed, other coagulopathies, pregnancy. Contraindications to acetaminophen: Persons with hypersensitivity to acetaminophen, intolerance of yellow dye #4, alcohol, table sugar, Precautions: anemia, hepatic disease, renal disease, alcoholism, pregnancy, elderly. Patient characteristics Medication order Maximum Comments dose Pediatric Inclusion criteria Acetaminophen Acetaminophen Rectal medications, if population 15 mg/kg p.o. or 650 mg dose or available, should be given A pediatric patient with a ibuprofen 10 mg/kg p.o. 75 mg/kg/day when there is vomiting or if (age 3 months temperature of 101 ºF or greater the child may be going to to 17 years) with and: Ibuprofen surgery a fever 800 mg dose or if no medicatons were given 40 mg/kg/day The triage nurse or MLP PTA, administer ibuprofen. must document when the last if acetaminophen was given acetaminophen and/or 1 hr PTA, administer ibuprofen were received and ibuprofen. the allergy status of the child. if ibuprofen was given ½ hr Aspirin should never be PTA, administer acetaminophen administered to a child Exclusion criteria: Contraindications, as listed above Minor Inclusion criteria: Ibuprofen: Acetaminophen Documentation Musculoskeletal All patients with minor 1 g dose or 75 mg/ Document time of Adults: age 65 or trauma musculoskeletal pain associated kg/day pain ratings older: ibuprofen with trauma and pain intensity immobilization, ice 400 mg PO Ibuprofen ratings of Ն 4/10. ibuprofen or Adults: 65 age: 800 mg dose or Hemodynamically stable with no acetaminophen, and dose ibuprofen 800 mg 40 mg/kg/day evidence of respiratory distress or administered PO altered mental status Children: ibuprofen Have not taken ibuprofen, tylenol, 10 mg/kg or other analgesics in the last 4 hr. If the patient meets the Exclusion criteria following criteria, then administer: Contraindication, as listed above Figure 10-3. Example of ED protocol for analgesic treatment at triage. (Permission obtained from Weintraub B, Northwest Community Healthcare, firstname.lastname@example.org, September 7, 2006.)
72 Analgesia for the Emergency Patient Acetaminophen as listed below: Meets contraindications to Ibuprofen Not allergic to acetaminophen No history of liver disease or ETOH abuse Adults: Ն18 years acetaminophen 1 g PO Children: Ն17 years: acetaminophen 15 mg/kg PO, not to exceed 1 g PO Renal Inclusion criteria Administer Toradol Toradol 30 mg IV and Document time of: colic pain, 30 mg IV and Dilaudid 0.5 mg IV pain ratings consistent with Ն18 years old Dilaudid 0.5 mg IV renal colic medication, route, and dose Severe flank pain with possible adminstered radiation to the groins Note: any question regarding Sudden onset of pain exclusion criteria, consult with ED MD required prior to Possible past history of renal administration of medications calculi Exclusion criteria Pain radiating to back Absent pulses Pulsatile abdominal mass History or renal insufficiency Patients greater than 50 years of age Syncope Hypotension Allergy to NSAIDs, morphine, or dilaudid Recent NSAID use Contraindications to NSAIDs (as above) Intracranial lesion or increased ICP Depressed ventilatory function: COPD, emphysema, status asthmaticus Topical Inclusion criteria EMLA Refer to “Topical analgesia Patients assessed for Place a dollop of anesthesia protocol” nonemergent venipuncture and EMLA cream (1/2 of 5 g EMLA cream must be IV insertions require adequate tube) over each of two applied for at least 45 min pain control for the procedure selected sites and cover prior to the start of based on their emotional and with a tegaderm the procedure. It may be left cognitive developmental level dressing in place for up to 3 hr without decreased LET should be applied to ELA-Max ELA-Max effectiveness lacerations/abrasion, which Place a quarter size Not to exceed It is not necessary to cover potentially will need repair or dollop of ELA-Max (5 g 100 cm2 in patient ELA-Max but it may be extensive cleaning tube) at least 2 10 kg patient and coverd if desired. ELA-Max potential IV sites attains effectiveness in 200 cm2 in patients 20–30 min and remains active 10–20 kg up to 3 hr Figure 10-3. (continued)
Protocols for Triage Patient 73 Exclusion criteria Hypersensitivity to any local anesthetics of the amide type or to L.E.T Lidocaine any other components of the Avoid application of EMLA Epinephrine Tetracaine product or ELA-Max to open (LET) cuts/wounds Apply LET directly onto wound. Cover As LET contains with a cotton ball epinephrine, it should not be Lidocaine allergy/sensitivity for applied to areas with a saturated in LET LET administration terminal blood supply (e.g., The area by the fingers/toes, top of nose and medication should ears). extend approximately 1/2 cm beyond the Maximum effectiveness of margin of the wound to LET is achieved in allow proper suture 20–30 min, and it remains placement effective for up to 1 hr RNs will record date, time, and application site on the ED record Ophthalmic Inclusion criteria Proparacaine 2 drops Use caution in patients with pain All ages hydrochloride, 0.5%: cardiac disease or hyperthyroidism Eye pain due to possible foreign 1 drop; may be repeated × 1 body or symptoms suggestive of in 15 min Advise patient not to rub corneal abrasion eyes after instillation of medication Exclusion criteria Suspect globe injury Known hypersensitivity to any component of the solution Consult with physician for eye pain due to exposure from acid or base All other causes; consult with physician required Acute Inclusion criteria Nebulizer: Albuterol One dose Reassessments as per the wheezing due 18 years old 2.5 mg + Ipratropium respiratory assessment to asthma Wheezing, with Hx of asthma bromide 0.5 mg in 3 ml flow sheet normal saline, with Exclusion criteria oxygen at 6 Hypersensitivity to Ipratropium bromide, atropine, or its Liters/min ×1 dose derivatives Caution: In patients with narrow angle glaucoma, prostatic hypertrophy or bladder neck obstruction, cardiovascular disease, convulsive disorder, hyperthyroidism, diabetes Figure 10-3. (continued) team should be held accountable to report outcome dataFOLLOW-UP CONSIDERATIONS on an ongoing basis. Data should be shared with phy-Once education is complete and the protocol is imple- sician and nursing staff, as well as hospital administra-mented, ongoing quality improvement monitoring is tion. Potential outcome measures may includeessential nurse-driven analgesic protocols. A dedicated proportion of analgesics provided to patients who did
74 Analgesia for the Emergency Patientand did not meet criteria, time to initial analgesic, re- in the emergency department. Emerg Med 1999;11(3): 128–132.duction in pain scores, and adverse events. 4. Hwang U, Richardson LD Sonuyi TO et al. The effect of Ongoing education is a critical element of any nurse- emergency department crowding on the management ofdriven analgesic protocol. ED nurse turnover may be pain in older adults with hip fracture. J Am Geriatr Sochigh. Physician providers may also frequently change in 2006;54(2):270–275. 5. Beel TL, Mitchiner JC Frederiksen SM et al. Patientthe ED environment. Therefore, a formal discussion of preferences regarding pain medication in the ED. Am Janalgesic administration policies and procedures should Emerg Med 2000;18(4):376–380.be included as a component of medical provider ongoing 6. Stalnikowicz R, Mahamid R Kaspi S et al. Undertreatmenttraining as well as orientation for all new employees. of acute pain in the emergency department: A challenge. Int J Qual Health Care 2005;17(2):173–176. 7. Tanabe P, Ferket K Thomas R et al. The effect of standardSUMMARY care, ibuprofen, and distraction on pain relief and patient satisfaction in children with musculoskeletal trauma. JThere is a tremendous opportunity to affect patient pain in Emerg Nurs 2002;28(2):118–125.the ED environment. However, current challenges in this 8. Tanabe P, Thomas R Paice J et al. The effect of standard care, ibuprofen, and music on pain relief and patientenvironment, including increasing patient volumes, pa- satisfaction in adults with musculoskeletal trauma. J Emergtient expectations, and ED overcrowding, create signiﬁ- Nurs 2001;27(2):124–131.cant barriers to the timely delivery of analgesic therapy. 9. Larsen D. An investigation into the assessment and Given these challenges, the introduction of nurse-driven management of pain by triage nurses in Greater London AE departments. Emerg Nurs 2000;8(2):18–24.analgesic protocols at triage may affect a number of positive 10. Boyd R, Stuart P. The efﬁcacy of structured assessmentbeneﬁts including time to patient analgesic treatment, pa- and analgesia provision in the paediatric emergencytient satisfaction, and hospital and practice regulatory goals department. Emerg Med J 2005;22:30–32. 11. Campbell P, Dennie M Dougherty K et al. Implementa-for the patient in acute pain. Once implemented, nurse- tion of an ED protocol for pain management at triage atdriven analgesic practices should be accompanied by on- a busy Level I trauma center. J Emerg Nurs 2004;30going quality improvement monitoring and education to (5):431–438.ensure protocol success and patient safety. 12. Seguin D. A nurse-initiated pain management advanced triage protocol for ED patients with an extremity injury at a level I trauma center. J Emerg Nurs 2004;30(4):REFERENCES 330–335. 13. Meunier-Sham J, Ryan K. Reducing pediatric pain during 1. McCaig L, Nawar E. National Hospital Ambulatory Medical ED procedures with a nurse-driven protocol: An urban Care Survey: 2004 emergency department summary. In pediatric emergency department’s experience. J Emerg Centers for Disease Control and Prevention National Center Nurs 2003;29(2):127–132. for Health Statistics, vol. 372, ed. U.S. Department of Health 14. Kelly AM. A process approach to improving pain and Human Services, 2006. management in the emergency department: Development 2. Tanabe P, Buschmann M. A prospective study of ED pain and evaluation. J Accid Emerg Med 2000;17(3):185–187. management practices and the patient’s perspective. J 15. Kelly A, Brumby C, Barnes C. Nurse-initiated, titrated Emerg Nurs 1999;25(3): 171–177. intravenous opioid analgesia reduces time to analgesia for 3. Coman M, Kelly A. Safety of a nurse-managed, titrated selected painful conditions Can J Emerg Med 2005;7 analgesia protocol for the management of severe pain (3):149–154.
11 Patients with Acute Pain: Patient Expectations and Desired Outcomes David E. Fosnocht, Robert L. Stephen, and Eric R. Swanson SCOPE OF THE PPROBLEM CLINICAL ASSESSMENT PAIN/SEDATION CONSIDERATIONS PAIN/SEDATION MANAGEMENT FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY pain relief is similarly complex. At the present time thereSCOPE OF THE PPROBLEM is no widely accepted assessment tool available thatThe concepts of patient expectation and desired out- deﬁnes patient expectations for pain relief or delineatescomes for patients with acute pain in the emergency appropriate outcomes for pain relief.department (ED) are surprisingly simple. Most patientspresent to the ED with pain. Patients with pain expect PAIN/SEDATION CONSIDERATIONSpain relief. The obvious desired outcome is relief ofpain. Our ability to move from this simplistic ideal to In an attempt to meet patient expectations and to beginscientiﬁc, evidence-based solutions that facilitate patient to deﬁne an acceptable outcome for pain relief in the EDexpectations, at the same time deﬁning reasonable out- setting, it is helpful to examine each piece of the con-comes for pain relief, is much more complex. This cepts of patient expectations and desired outcomes in-complexity accounts for a great deal of the continued dividually.problem of inadequate pain management in the ED. The premise that patients present with pain to the ED is well documented, widely accepted, and obvious to any clinician who cares for patients in the ED. It is com-CLINICAL ASSESSMENT monly cited that 70% of ED patients present with pain.The clinical assessment of pain is one of the more A recent, large multicenter study of acute pain in EDchallenging aspects of deﬁning patient expectations and patients found that the median patient pain score wasoutcomes for pain relief. Pain assessment methods have eight on a 0–10 point scale.various advantages and disadvantages in ease of use, Patients with pain expect analgesia for pain relief fromscientiﬁc validity, and practicality for use with different their medical providers. Although this may seem obvious,patient populations. Unfortunately each pain assessment it is certainly less well documented and less accepted thanprocess suffers from the common question of ‘‘What the presence of pain. Practice settings outside of the ED,does a pain score of ‘X’ mean?’’ such as postoperative surgical venues, report low levels of The lack of clinician conﬁdence in pain measurement patient expectations for pain relief. In contrast, EDtranslates to even more confusion in trying to use these patients appear to have high expectations for pain relief.scales to deﬁne pain relief outcomes. The task of de- ED patients report a mean expectation for 72%ﬁning and meeting individual patient expectations for of their pain to be relieved by medical caregivers. 75
76 Analgesia for the Emergency PatientAdditionally, 18% of ED patients with pain expect questions regarding the individual’s expectations forcomplete pain relief. Those with severe pain appear to pain relief may allow unrealistic expectations (com-expect more pain relief (85%) than those with moderate plete pain relief) to be addressed prior to failing topain levels (50%). meet these expectations. Identiﬁcation of the decrease Time to analgesic medication administration has also in pain intensity that the patient expects may provide abeen measured. ED patients have been described as target for pain intensity and a desired outcome vari-expecting to receive medication within a mean of 23 min able. The more intangible concept of expressing con-from their time of arrival at an ED facility. This obser- cern for patients’ pain may be addressed with similarvation is in striking contrast to an actual pain medica- interventions.tion delivery time of 78 min. A decrease in pain intensity of 50% for patients in Expectations for pain relief, time to pain medication, moderate pain and 85% for severe pain is supported byand desire for pain medication have all been measured patient expectations for pain relief in a large multicenterin some fashion. The measurement of pain relief is study of pain in ED patients. No single outcome mea-complex and encompasses many variables including sure has been deﬁned for ED acute pain patients, how-satisfaction with care, relationships with caregivers, and ever. Several versions of the question ‘‘Do you needmeeting the individual patient’s expectations for pain anything else for pain?’’ or ‘‘Have your needs for painrelief. Change in pain scores correlate poorly with pa- relief been met?’’ have been proposed but not validatedtient reported relief of pain, leading some to conclude in medical literature. The phrasing and delivery of suchthat asking patients some form of the question ‘‘Do you questions may bias patient responses to the question andneed anything else for pain?’’ may be the best outcome may result in less than satisfactory outcomes. Thesemeasure available. Patient satisfaction measures have queries remain a reasonable place to begin the process ofalso been found to correlate poorly with initial, dis- improving pain relief.charge, or changes in pain intensity. Finally, a caregiver’sattitude appears to have a substantial effect on patient FOLLOW-UP/CONSULTATIONperceptions. An attitude or expression of caring about CONSIDERATIONSthe patients’ pain may be as meaningful as providingpain medication itself. Deﬁnitions of patient expectations and outcome mea- sures for acute pain patients following discharge from the ED are poorly understood. It is known that patientsPAIN/SEDATION MANAGEMENT with moderate to severe pain are likely to continue toAlthough the ideas of meeting patient expectations and have moderate to severe pain up to 1 week later. Littleproviding the desired outcome of pain relief are simple, evidence is currently available with regard to patientit is clear that there are many complex and difﬁcult expectations or to guide clinical practice.problems to overcome before these concepts can be put The temporal variability in the clinical course of dif-into ED clinical practice. ferent disease processes introduces greater complexity in The use of an 11-point (0–10) scale to measure pain measuring outcomes for acute pain following dischargeintensity is a typical place to initiate the processes of from the ED. However, outcome measures for painmeasuring patient expectations and desired outcomes. management, such as interference with routine dailyPatients with moderate to severe pain (4 or greater on activities, are well established and validated in selectedthe 0–10 scale) should be targeted for interventions to disease processes and settings.decrease pain. Rather than a limited focus on patient expectations Algorithms for speciﬁc pain syndromes have been and outcome at the time of ED discharge, one mightdetailed in the medical literature. Providing analgesic propose that deﬁning patient expectations and outcomemedication is an important component of meeting measures following ED discharge are both more valuablepatient’s expectations for pain relief. More detailed and more practical goals. This view requires looking
Patients with Acute Pain 77 Assess pain intensity with Educate patient and Query patient for numeric or establish goals for Pain 4 pain relief visual analog reasonable pain relief expectations scale (0–10) goals Reassess pain Provide intensity analgesic (goal: decrease medication pain intensity by 75%) Yes “Need anything else for pain?” No Discharge plan for analgesia: medication, activities, and follow-up Figure 11-1. Moderate to severe pain intensity assessment and treatment algorithm.beyond the traditional endpoint of ED discharge. 3. Fosnocht DE, Heaps ND, Swanson ER. Patient expecta- tions for pain relief in the ED. Am J Emerg Med 2004;22However, such an approach may more likely result in (4):286–288.achieving tangible clinical goals of pain control with 4. Fosnocht DE, Swanson ER, Bossart P. Patient expectationsoutcomes directed toward the resumption of normal for pain medication delivery. Am J Emerg Med 2001;19activities. (5):399–402. 5. Fosnocht DE, et al. Correlation of change in visual analog scale with pain relief in the ED. Am J Emerg Med 2005;23SUMMARY (1):55–59. 6. Blank FS, et al. Adequacy of pain assessment and painThe concepts of ED patient acute pain management relief and correlation of patient satisfaction in 68 ED fast- track patients. J Emerg Nurs 2001;27(4):327–334.expectations and desired outcomes are surprisingly 7. Stahmer SA, et al. Do quantitative changes in painsimple (Figure 11-1). Most patients present to the ED intensity correlate with pain relief and satisfaction? Acadwith pain. These patients expect adequate and mean- Emerg Med 1998;5(9):851–857.ingful pain relief. To achieve this expectation, medical 8. Thompson DA, Yarnold PR. Relating patient satisfaction to waiting time perceptions and expectations: Thecaregivers must understand pain assessment and disconﬁrmation paradigm. Acad Emerg Med 1995;2expectations for analgesia as well as the proper treatment (12):1057–1062.of pain in daily medical practice. 9. Ward SE, Gordon DB. Patient satisfaction and pain severity as outcomes in pain management: A longitudinal view of one setting’s experience. J Pain Symptom ManageBIBLIOGRAPHY 1996;11(4):242–251. 10. Bursch B, Beezy J, Shaw R. Emergency department 1. Cordell WH, et al. The high prevalence of pain in satisfaction: What matters most? Ann Emerg Med emergency medical care. Am J Emerg Med 2002;20 1993;22(3):586–591. (3):165–169. 11. Hall MF, Press I. Keys to patient satisfaction in the 2. Kuhn S, et al. Perceptions of pain relief after surgery. BMJ emergency department: Results of a multiple facility study. 1990;300(6741):1687–1690. Hosp Health Serv Adm 1996;41(4):515–532.
78 Analgesia for the Emergency Patient12. Trout A, Magnusson AR, Hedges JR. Patient satisfaction 14. Larsen MJ, Fosnocht DE, Swanson ER. Pain management investigations and the emergency department: What does after discharge from the emergency department. Ann the literature say? [In process citation]. Acad Emerg Med Emerg Med 2004;44(4):S88. 2000;7(6):695–709. 15. Todd KH. Pain and pain-related functional interference13. Yarnold PR, et al. Predicting patient satisfaction: A study among discharged emergency department patients. Ann of two emergency departments. J Behav Med 1998;21 Emerg Med 2004;44(4):s86. (6):545–563.
12 Analgesia for the Adult and Pediatric Multitrauma Patient Wayne Triner SCOPE OF THE PROBLEM CLINICAL ASSESSMENT OF PAIN AND MANAGEMENT OF THE MULTITRAUMA PATIENT PAIN/SEDATION CONSIDERATIONS PAIN AND SEDATION MANAGEMENT Nonpharmacological Approaches to Analgesia Strategies in the Provision of Analgesic and Sedative Agents Regional and Local Anesthesia SUMMARY BIBLIOGRAPHY humanitarian goals of medical practice, attention toSCOPE OF THE PROBLEM analgesia in the multiply injured patient carries signiﬁ-Multiple trauma is deﬁned as injury to two or more cant importance.organ systems. Without exception, pain is a major The consequences of inappropriate analgesia in mul-consideration in the management of the patient with tiply injured patients are difﬁcult to measure. The psy-multiple injuries. Yet, the often-competing physiological chological outcome of trauma patients hospitalized inand operational demands associated with these patients intensive care units (ICUs) includes nightmares, pho-increase the complexity as well as the risk of meeting bias, recollection of pain and anxiety, and other ele-their analgesic needs. ments of posttraumatic stress disorder. There are few Features such as extremes of age, dementia, neuro- studies, however, that have demonstrated that correct,trauma, neuromuscular blocking agents, and intoxicants over- or underutilization of analgesic or sedative agentsimpair a patient’s ability to express pain and limit inﬂuence these psychological outcomes. Studies thatcaregiver’s clinical assessment of pain. Critical care- have evaluated trauma patient outcomes in relation tobased studies have demonstrated that a high proportion their physiological outcomes have not shown survival orof intubated patients have recollection of discomfort morbidity differences. These investigations have shownand pain during the course of their illness. Furthermore, differences in intermediate outcomes such as interleukinclinicians appear to attach a lower magnitude of pain to levels.patient’s conditions than do the patients themselves. It can be concluded that underutilization of analgesiaNot surprisingly then, physician prescribing behavior to acutely injured patients is inhumane and rendersincludes a tendency toward ineffective analgesia, oli- patient care difﬁcult owing to patient resistance andgoanalgesia, in traumatic conditions. distress. Poorly managed analgesia and sedation may For the year 2004, there were almost 1.4 million also be associated speciﬁc markers of worse patienthospital admissions for traumatic conditions (excluding outcomes including prolonged hospitalizations, hemo-isolated hip fractures). Of these, 176,000 involved chil- dynamic instability, ventilator-associated pneumonia,dren under the age 15. Given this magnitude and the and delirium. 79
80 Analgesia for the Emergency Patient ments that systematically deﬁne pain magnitude in theCLINICAL ASSESSMENT OF PAIN AND communicative patient. The visual analog scale, verbalMANAGEMENT OF THE MULTITRAUMA PATIENT descriptive scale, face scale, Face Legs Activity Cry Con-Patient self-reporting is the most accurate means of solability (FLACC), and modiﬁed FLACC scales have allassessing pain (Figure 12-1). There are several instru- been validated and are commonly available. Primary assessment Physical examination/imaging Intubation: consider induction agent and sedation Treat and stabilize critical injuries Bedside procedure (e.g., tube thoracostomy, major laceration) Consider regional anesthesia Consider sedation/analgesia (depending on hemodynamic status – Figure 12.2) Secondary assessment Physical examination/imaging Treat and Operative intervention (e.g., abdominal injury, head injury) stabilize critical injuries Bedside procedure (e.g., laceration repair, fracture reduction) Regional and/or systemic anesthesia/sedation/analgesia Assessment, stabilization Systemic analgesia: Figure 12.2 Figure 12-1. Trauma patient initial evaluation and sedation/analgesia algorithm.
Analgesia for the Adult and Pediatric Multitrauma Patient 81 Patients suffering multiple injuries are often incapable procedures. This modality is a mathematic index derivedof focused communication. This may be from neuro- from several electroencephalographic features.trauma, facial injuries, intoxicants, distraction, anxiety, The bispectral index has been validated in determin-hypoxia, therapeutically induced sedation, and paralysis. ing depth of sedation and anesthesia in both the oper-In these situations, the clinician’s appreciation of pain ating room and ICU. Its use has also been shown toand its management can be easily overlooked. reduce sedative agent dosing and time to waking fol- Alteration of vital signs is a poor indicator of pain. lowing general anesthesia. The range of the index spansCompensation of hypovolemia, hyperthermia, sympa- 0–100. Zero is electroencephalographic silence and 100thomimetic, or anticholinergic intoxicants all may result is full wakefulness. Levels of 45–60 are typical of generalin tachycardia or hypertension. Conversely, vagal stimu- anesthesia whereas levels of 75–80 have been associatedlation, use of calcium channel, and beta receptor blocking with sedative depths appropriate for procedures andagents, as well as age-related cardiac conduction limita- continuous sedation of injured patients.tions, may limit the capacity for increases in heart rate andblood pressure in traumatized patients with severe pain. PAIN/SEDATION CONSIDERATIONS Patients with traumatic injuries should be consideredto be in pain unless they can explicitly state otherwise. Common to many aspects of medical practice, one isPatients with painful injuries that include alterations of more likely to reach a successful outcome, if the goalstheir mental status or patients who are pharmacologi- are ﬁrst deﬁned and they are realistic. Such is the case incally paralyzed should receive appropriate analgesia. providing analgesia in the face of complexities of theLikewise, anticipation of pain during procedures (e.g., multiply injured patient. To best deﬁne these goals, it iswound repair, tube thoracostomy, fracture reduction, useful to begin with the basic tenets of resuscitation:line insertion) should warrant the anticipatory admin- airway, breathing, circulation, and disability.istration of systemic analgesia or local anesthesia despite Selection of agents and techniques to provide comfortthe lack of response from the patient. can often be done in such a manner that physiological In the patient with altered mental status, there may be risk is minimized or that physiological goals can beseveral indicators of pain, particularly agitation. Agita- reached as a result of analgesic intervention (Table 12-1).tion is a common response to pain and is in part related It is often possible to choose combinations of techniquesto increased catecholamine stimulation. Agitation also and agents that enhance therapeutic efforts or minimizeincreases metabolic demands, increases the likelihood of the risk of physiologic deterioration.the patient harming themselves or others, and renders One caveat of administration of pharmacologic agentsthe provision of care more difﬁcult. for analgesia in patients experiencing multiple trauma is Assessment of the bispectral index can be an adjunct that all medications should be administered parenterally,to clinical examination in intubated patients under the preferably via an intravenous route. This is because GIeffect of neuromuscular blocking agents or sedative motility and absorptive capacity as well as sphlancnic Table 12-1. Sedation and analgesia considerations for the trauma patient 1. Is the patient in pain? 2. What is/are the etiology/etiologies of the pain? 3. Is the patient hemodynamically stable? 4. What form of pain control is appropriate? (regional, systemic, both) 5. Would the patient beneﬁt from anxiolysis or sedation? 6. What form of anxiolysis or sedation is appropriate? (benzodiazepine, neuroleptic, both)
82 Analgesia for the Emergency Patientperfusion may not be predictable. This may also be true reduction of preganglionic adrenergic tone (Figure 12-2,of skeletal muscle and subcutaneous perfusion. Orally Table 12-2). Thus, if there are elements of cardiac pumpadministered analgesic therapy may result in erratic or failure (tension pneumothorax, cardiac tamponade,delayed absorption in these patients. Additionally, the congenital or acquired heart disease) or intravascularspeed of onset and ability to titrate to speciﬁc analgesic volume depletion (blood loss, transudative or exudativeendpoints are enhanced by intravenous administration. ﬂuid losses), hypoperfusion may result.Patients with multiple injuries can have complex altera- Propofol and the ultra–short-acting barbiturates aretions in homeostatic mechanisms. Hemodynamic and the agents most strongly associated with decreases inrespiratory consequences of their injuries are of primary blood pressure. Fentanyl is the opiate that is least likelyimportance in the emergency department setting. Once to potentate hypotension, yet with controlled adminis-the initial resuscitation is complete, mediators of in- tration over 3–4 min, all opiates may be considered safe.ﬂammation, adrenal function, coagulation, and gastro- Etomidate is the least likely of sedative agents tointestinal performance are additional considerations. adversely impact hemodynamic performance. Since all analgesic and sedative agents impart their own The use of ketamine increases sympathetic tone with aalterations in physiology, it is important to anticipate the resulting increase in blood pressure and heart rate. Thisconsequences of pharmacological intervention in indi- can lead to increased metabolic demands, worsening ofvidual patients. All but a few pharmacological agents aortic injuries and clot dislodgement from arterialresult in respiratory suppression and blunting of airway injuries. Additionally, ketamine may be associated withreﬂexes. Once a patient is intubated and mechanically increases of intracranial and intraocular pressures,ventilated, respiratory and airway suppression becomes though this effect has been contested.less of a consideration, but the provision of ongoing Nitrous oxide has been used in many facilities andventilator sedation and analgesia begin to merge. Though prehospital agencies for control of mild to moderateintubated, the provider must always consider the ade- pain. Nitrous oxide is commonly self-administeredquacy of ventilation and the ultimate goal of extubation. through a commercially available blender, which pro- vides a 50% mixture with oxygen through a demandPAIN AND SEDATION MANAGEMENT valve (NitronoxÒ). Its use requires an alert and coop- erative patient. One of the physical properties of nitrousNonpharmacological Approaches to Analgesia oxide is that it is far more tissue soluble than nitrogen.Nonpharmacological means of controlling pain should Therefore, closed gas compartments such as pneu-be employed whenever possible. The advantage to this mothoracies and bowel obstructions can expand as aapproach is that the patient may feel more in control result of nitrous oxide use.and there may be lesser requirements for drugs and their Dexmedetomidine (PrecedexÒ) is a unique agent thatadverse effects. Simple measures such as ice, splinting is classiﬁed as an a2 adrenergic agonist. Its principaland repositioning may have signiﬁcant impact. mechanism of action is to reduce CNS presynaptic Whenever possible, spinal clearance should take place norepinephrine release, thereby resulting in sedation.early in the trauma patient assessment. There is evidence Hypotension and heart block have been associatedthat spinal immobilization enhances pain. Finally, with the use of dexmedetomidine. Dexmedetomidineallowing family at the bedside, when feasible, and talking sedation is unique in that patients experiencing sedationto the patient in a sensitive and reassuring manner may with this drug maintain some degree of wakefulnessrelieve anxiety and thus mitigate the pain experience. (along with the ability to follow commands) when stimulated. Simultaneously, respiratory depression isStrategies in the Provision of Analgesic and minimal allowing patients to sustain respiratory minuteSedative Agents volume and ventilator tolerability. There appears toMany of the agents used to provide analgesia and be limited impact on intracranial pressure associatedsedation have the effect of reducing catecholamine with this agent. It is not approved for sedation longeroutput and consequently vasomotor tone through than 24 hr.
Analgesia for the Adult and Pediatric Multitrauma Patient 83 Multiply injured patient with painful injuries No Mechanically ventilated Yes Requires sedation and analgesia Hemodynamially stable Hemodynamically unstable Hemodynamically stable Hemodynamially unstable Volume resuscitation Volume resuscitation Age 13 Age 13 • Non-pharmacological • Nonpharmacological • Nonpharmacological • Nonpharmacological (positioning, • Fentanyl infusion (positioning, (positioning, reassurance) • Regional anesthesia reassurance) reassurance) • Any opiate infusion • Any opiate infusion • Etomidate* bolus • NSAIDs (avoid in alone or in combination • Fentanyl infusion patients at risk of renal with Propofol or alone or in failure or insult and benzodiazepine infusion combination with, gastritis) • Regional anesthesia benzodiazepine or • Regional anesthesia ketamine* bolus if no brain injury Beware • Regional anesthesia Beware Beware • Oligoanalgesia Beware • Oligoanalgesia • Oligoanalgesia • Oligoanalgesia • Oversedation and • Impaired clearance of • Etomidate in patients hypoventilation agents with increased at risk of sepsis (bowel potential of oversedation injuries, central venous and hypoventilation access, anticipated • Reduction of prolonged ventilator catecholamine output course) with potential of inducing hypoperfusion Age 13 Age 13 • Nonpharmacological • Nonpharmacological • Any opiate infusion alone • Fentanyl infusion alone or in combination with; or in combination with; • Benzodiazapine infusion • Benzodiazapine • Ketamine infusion • Ketamine bolus (not in • Regional anesthesia the head injured) • Etomidate bolus • Regional anesthesia * often used to induce sedation as part of rapid sequence intubation. Note that rapid boluses of opiates, benzodiazapines, and propofol enhance their potential to cause hypotension and respiratory suppression. Figure 12-2. Algorithm for ongoing analgesia in multiply injured patient. The use of dexmedetomidine is reported to reduce the use of this drug in trauma patients, but there appears toamount of opiates employed for analgesia and sedation be potential beneﬁts for selected patient populations.in the ICU setting. Dexmedetomidine has also been Patient-controlled analgesia (PCA) is a commonlydemonstrated to have utility in aiding ventilator wean- employed technique for patients who are awake and caning. It may also be useful for endotracheal intubation manage medication through self-administration. Thiswhen maintenance of spontaneous respirations is strategy is based on the premise that if a patient hasdesirable. Currently there is limited experience with the control over his or her own analgesia delivery, he or she
Table 12-2. Sedative and analgesic agents commonly used in the multiple trauma patient84 Class Agent IV dose bolusa IV infusion rateb Physiologic response Unique considerations Opiates Fentanyl 2–4 mcg/kg 1–4 mcg/kg/hr BP # Rigid chest syndrome in high doses. RR ## Least likely of commonly used ICP$ opiates to result in peripheral vasodilatation Hydromorphone 0.015 mg/kg NA BP## RR# ICP$ Merperidine 0.5–1 mg/kg NA BP## Normeperidine metobolite results in RR# potential for adrenergic crisis in ICP$ patients taking MAOIs, seizure with repeated dosing Morphine 0.1–0.2 mg/kg 0.01 mg/kg/hr BP## Histamine release with urticaria near RR# injection site and hypotension ICP$ Sedative Midazolam 0.05–0.2 mg/kg 0.02–0.1 mg/kg/hr BP# Considerable variation in therapeutic RR## window. Start with lower doses in the ICP# young and elderly Lorazapam 0.05–0.1 mg/kg 0.02–0.03 mg/kg/hr BP# RR## ICP# Propofol 1–2 mg/kg 25–125 mcg/kg/hr BP### Avoid propofol infusions in children less over 1 min RR### than 13 years of age owing to rare but ICP## fatal occurrence of cardiac failure. Venous irritation Etomidate 0.1–0.2 mg/kg BP$ Least destabilizing of sedative agents. over 1 min RR# Myoclonus. Adrenal suppression ICP# following single dose as well as continuous infusions. Shown to have outcome impact in sepsis with no trauma studies to date affecting outcome Dissociative Ketamine 0.5–4 mg/kg 0.3 mg/kg/hr BP Sympathomimetic. Hypersalivation and HR emergence reactions. Sedation is marked by RR$ dissociation. There is often wakefulness ICP during this period. Highly analgesic beyond duration of sedation. Very wide therapeutic window Notes: a All dosing are based on ideal body weight. b Unless otherwise speciﬁed, all of these agents should be administered over 2–4 min.
Analgesia for the Adult and Pediatric Multitrauma Patient 85will experience less breakthrough pain and anxiety. adequate intravascular volume. Additionally, propofol isGenerally, a provider obtains an adequate level of an- an effective anticonvulsant and the least likely to resultalgesia through carefully titrated opioid administration. in vomiting. However, propofol in the hypovolemicThereafter, a continuous basal infusion of an opioid is patient or the patient with limitations of cardiac outputestablished and the patient can deliver supplemental will potentate hypotension. The reduction of CPPboluses of the same opioid with the push of a button however, in the face of propofol-induced hypotension isattached to a delivery pump. not proportional to the reduction of blood pressure due The basal infusion rate, doses of patient administered to the reduction of systemic vascular resistance.boluses, and hourly limits on boluses are programmedinto the delivery pump, which ensures these parameters. Regional and Local AnesthesiaIt is typical that a PCA be initiated following the initial The use of regional anesthesia is often overlooked in theevaluation and management of most injuries. PCA initial management of the multiple trauma patient.management of pain has not been shown to be suitable There are several techniques that are well within theas a means of procedural analgesia or sedation. technical reach of emergency physicians, trauma sur- In the setting of multiple traumatic injuries, particu- geons, and orthopedists. These can greatly enhance thelarly if the patient is being mechanically ventilated, the comfort of patients and avoid or reduce the adverseprovision of analgesia mingles with sedation. There are effects of systemic analgesia. Intercostal and femoralseveral agents, which serve to meet both of these needs. nerve blocks are examples of regional anesthesia that canIt is often desirable to titrate more than one agent to reduce pain and opiate requirements in selectedminimize the deleterious effects of either drug alone. patients. Since the experience of pain includes components of Epidural blocks in the setting of chest trauma haveanxiety, there is often a role for pure sedative agents in been shown to reduce mortality, pneumonia, ventilatorenhancing patient comfort. Therefore, the decision to initiation, and days on a ventilator. Epidural blocks areuse both a benzodiazepine and an opiate continuous contraindicated in cases where clinical examination ofinfusion may reduce the potential for hypotension. the abdomen is required due to anesthesia below theLikewise, addition of an opiate infusion to a propofol level of the block. Generally, an epidural block is initi-infusion to a patient with painful injuries would be ated and maintained by an anesthetist or anesthesiolo-expected to reduce the dosage requirement for both, gist. Epidural catheters may be placed and left inthus reducing the occurrence of hypotension. position for as long as several days. When using regional Traumatic brain injury (TBI) is a common component or local anesthesia for control of pain, long-acting agentsof multiple trauma. Improving the outcome of TBI (bupivucaine) are preferred.patients relies principally upon avoidance or reduction ofsecondary brain injury. The overriding consideration inthe acute management of TBI is maintenance of ventila- SUMMARYtion and cerebral perfusion pressure (CPP). Therefore, The provision of analgesia and sedation are fundamentalhypotension and hypoventilation, based upon the delete- skills in managing the multiply injured patient. Theserious effect on CPP, have been repeatedly associated with patients are complex from many standpoints and theadverse outcomes in patients with severe brain injury. administration of pharmacological agents to manage Several of the agents used to provide analgesia or pain and affect sedation serve to increase their com-sedation can have either positive or negative impact on plexity.CPP depending upon how they are used. Thus, careful To safely and effectively provide sedation and anal-attention to maintenance of blood pressure is a key gesia to the trauma patient, the provider must be able toelement in providing sedation and analgesia to patients identify speciﬁc goals, anticipate the combined physio-with severe head injury. logical effects of the injuries and analgesic modalities Propofol is the prototypical agent shown to maintain employed. There is no single practice or technique thatcerebral blood ﬂow and reduce ICP in the presence of
86 Analgesia for the Emergency Patienthas proven safe or effective in all patients. For any in- pediatric critically ill patients receiving neuromuscular blockade. Chest 2005;128:303–307.dividual, several techniques for providing analgesia and 8. Miner JR, Biros MH, Seigel T, Ross K. The utility of thesedation will be equally safe and effective. bispectral index in procedural sedation with propofol in the emergency department. Acad Emerg Med 2005;12:190– 196.BIBLIOGRAPHY 9. Miner JR, Biros MH, Heegaard W, Plummer D. Bispectral electroencephalographic analysis of patients undergoing 1. van de Leur JP, van der Schans CP, Loef BG, Deelman BG, procedural sedation in the emergency department. Acad Geertzen JH, Zwaveling JH. Discomfort and factual Emerg Med 2003;10:638–643. recollection in intensive care unit patients. Crit Care 10. Kwan I, Bunn F. Effects of prehospital spinal immobiliza- 2004;8:R467–R473. tion: A systematic review of randomized trials on healthy 2. Guru V, Dubinsky I. The patient vs. caregiver perception subjects. Prehosp Disaster Med 2005;20:47–53. of acute pain in the emergency department. J Emerg Med 11. Bourgoin A, Albanese J, Wereszczynski N, et al. Safety of 2000;18:7–12. sedation with ketamine in severe head injury patients: 3. Brown JC, Klein EJ, Lewis CW, Johnston BD, Cummings Comparison with sufentanil. Crit Care Med 2003;31: P. Emergency department analgesia for fracture pain. Ann 711–717. Emerg Med 2003;42:197–205. 12. Avitsian R, Lin J, Lotto M, Ebrahim Z. Dexmedetomidine 4. Moon MR, Luchette FA, Gibson SW, et al. Prospective, and awake ﬁberoptic intubation for possible cervical spine randomized comparison of epidural versus parenteral myelopathy: A clinical series. J Neurosurg Anesthesiol opioid analgesia in thoracic trauma. Ann Surg 2005;17:97–99. 1999;229:684–691. 13. Triner W,Levine J, Lai SY, McErlean M. Femoral nerve 5. Petrack EM, Christopher NC, Kriwinsky J. Pain manage- block for femur fractures. Ann Emerg Med 2005;45:679. ment in the emergency department: Patterns of analgesic 14. Flagel BT, Luchette FA, Reed RL, et al. Half-a-dozen ribs: utilization. Pediatrics 1997;99:711–714. The breakpoint for mortality. Surgery 2005;138:717–723. 6. Young J, Sifﬂeet J, Nikoletti S, Shaw T. Use of a 15. Bulger EM, Edwards T, Klotz P, Jurkovich GJ. Epidural Behavioural Pain Scale to assess pain in ventilated, analgesia improves outcome after multiple rib fractures. unconscious and/or sedated patients. Intensive Crit Care Surgery 2004;136:426–430. Nurs 2006;22:32–9. 16. Green SM, Clark R, Hostetler MA, Cohen M, Carlson D, 7. Trope RM, Silver PC, Sagy M. Concomitant assessment of Rothrock SG. Inadvertent ketamine overdose in children: depth of sedation by changes in bispectral index and Clinical manifestations and outcome. Ann Emerg Med changes in autonomic variables (heart rate and/or BP) in 1999;34:492–497.
13 Analgesia for the Emergency Department Isolated Orthopedic Extremity Trauma Patient Michael A. Turturro SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY life-threatening injuries. Then, a general assessment of theSCOPE OF THE PROBLEM injured part by inspection, palpation, and range ofAcute orthopedic injuries are among the most common motion should be performed to exclude immediate limbconditions seen in the emergency department (ED). In threats (e.g., a fracture dislocation of the ankle with2004, fractures, sprains, strains, and contusions vascular compromise) and to assess for deformity, limi-accounted for 14.3 million of the total 110.2 million ED tation of range of motion, and overlying soft tissuevisits in the United States. Acute orthopedic injuries injuries. The skin examination should focus on thetypically cause acute pain and consequent guarding of detection of abrasions, puncture wounds, and lacerationsthe injured part by the patient in an effort to reduce the that could require repair.pain. Although this innate response prevents further A more thorough examination should be undertakeninjury, appropriate initial management of pain will allow to assess for additional injuries, regardless of severity.more rapid mobilization and return to normal function. Though it is important to thoroughly evaluate areasConversely, uncontrolled pain may lead to adverse obviously injured and areas in which the patient com-physiologic consequences such as prolonged immobili- plains of discomfort, additional injuries could poten-zation increasing the risk of thromboembolic compli- tially be overlooked unless a more thoroughcations, limitation of range of motion, and muscular examination is performed.atrophy. Finally, neurovascular assessment should be under- taken to evaluate for associated nerve or limb-threatening vascular injuries and to recognize signs associated with aCLINICAL ASSESSMENT potential compartment syndrome, in which the mostThe extent of acute orthopedic injury can often be common and earliest sign is pain (Table 13-1).predicted by the mechanism of injury. For example, a Plain ﬁlm radiographs should be ordered if on historyfall on an outstretched hand may indicate a Colle’s, an examination there is concern for either a fracture or ascaphoid, or radial head fracture; a twisting injury to the dislocation. Well-validated clinical decision rules haveknee with an audible pop may indicate a rupture of the been developed and implemented for the appropriate useanterior cruciate ligament. of plain ﬁlm radiography in acute ankle and knee injuries. First and foremost in the examination of acute Since not all fractures are immediately radiographicallyorthopedic injuries is a primary survey to detect potential apparent, if there is a strong clinical suspicion for a 87
88 Analgesia for the Emergency Patient Table 13-1. Clinical signs of compartment syndrome PAIN MANAGEMENT Pain Appropriate analgesia in the acute phase of orthopedic Often out of proportion to physical ﬁndings injuries is essential to proper patient management. As it Severe has been demonstrated that effective preoperative an- Poorly localized algesia by a multimodal approach decreases postopera- Increased with passive movement Swelling tive analgesic requirements, effective analgesia provided Often with tension in the ED may be associated with decreased analgesic Paresthesia requirements postdischarge. Additionally, if there are no Pallor contraindications, analgesia can and should be under- Decreased perfusion (late ﬁnding) Decreased capillary reﬁll taken as soon as possible after patient arrival. In the ED Decreased pulses this could entail the use of standing orders for analgesics and nonanalgesic therapy at triage and/or protocols that allow analgesics to be administered prior to radiographyfracture despite negative plain ﬁlms, the injured part (Figure 13-1).should be splinted and the patient should be referred for One of the ﬁrst and simplest steps in the managementdelayed plain ﬁlms in 7–10 days, computed tomography, of pain from an acuteor magnetic resonance imaging. orthopedic injury is immobilization of the injured part in a position of function. This intervention is thought toPAIN CONSIDERATIONS reduce pain by reducing release of inﬂammatory media- tors when the injured part is manipulated. In the ED, thisAfter local injury, an inﬂammatory cascade occurs in which may initially entail simple techniques such as resting anprostaglandins and kinins are released. These substances in injured extremity in the position of comfort on a pillow.turn lower the threshold for stimulation of C-type ﬁbers of In the case of joint dislocations and fractures, reductionthe surrounding tissues. These ﬁbers terminate in the and realignment followed by immobilization by the use ofdorsal horn of the spinal cord, at which several excitatory splinting will accomplish this goal (Table 13-2).neurotransmitters and substance P are released, stimulating Cryotherapy (the use of ice) is also one of the easiestnociceptive neurons that consequently transmit painful although sometimes ignored techniques that may beimpulses to the central nervous system. used in the ED and in the ﬁrst few days of therapy to Based on these mechanisms, analgesia in the patient reduce the pain associated with acute orthopedic inju-with an acute orthopedic injury can take several forms: ries. Ice causes local vasoconstriction, therefore less 1. Reduction of inﬂammatory mediator release by edema and local inﬂammatory release occur, thereby local measures (e.g., ice, splinting) reducing pain. Compression and elevation also may 2. Inhibition of the local inﬂammatory cascade by reduce local tissue edema, in turn reducing overall pain. the use of systemic anti-inﬂammatory agents. In initiating cryotherapy, to reduce the risk of cold- 3. Nerve blocks of the involved peripheral nerves by related injury (e.g., frostbite), ice should be applied at a local or regional anesthetic techniques using local maximum of 15 min intervals several times a day. anesthetics. Conversely, the use of thermal therapy (i.e., heat) has 4. Intrathecal or epidural administration of local been associated with minor reductions in pain associ- anesthetics or opioids (beyond the scope of the ated with acute and subacute myofascial strains, but it is typical emergency physician’s practice). not ﬁrst-line treatment for the pain of contusions, 5. Modulation of the response to the painful fractures, and dislocations. stimulus within the central nervous system by In the pharmacotherapy of acute orthopedic injuries, the use of systemic opioid analgesics. based on the concept of reducing the release of local 6. A combination of two or more of the above inﬂammatory mediators, analgesia can and should be approaches. initiated with an nonsteroidal anti-inﬂammatory agents
Orthopedic Extremity Trauma Patient 89 Local measures: ice, elevation, rest in Patient arrival/ position of comfort Pain scale triage assessment completed Ibuprofen 800 mg PO or oral opioid Patient to treatment room Consider standing order for Continue local analgesia; morphine sulfate 0.1 measures: ice, mg/kg, repeat q15 min as needed elevation, rest Admit/discharge Continue analgesic therapy with Continue local NSAIDs, opioid supplementation measures: ice, as needed elevation, rest Figure 13-1. Suggested approach to pain management for ED patients with acute musculoskeletal injury. small retrospective studies that have demonstrated Table 13-2. Local techniques to reduce the pain of delayed fracture healing with prolonged NSAID use. A acute orthopedic injuries byproduct of the inﬂammatory cascade is the facilitation Immobilization of healing and osteogenesis, which could theoretically be Compression delayed by the use of NSAIDs. A few prospective, ran- Elevation domized, controlled trials have been conducted to eval- Ice (for fractures and contusions) uate this effect in humans and have not demonstrated Heat therapy (for myofascial strains) that this occurs with any clinical signiﬁcance. However, given that this hypothesis has not been tested in a robust manner, some orthopedists continue to have concerns(NSAID). However, many patients who present to the ED regarding fracture healing with prolonged NSAID use. Itwith acute orthopedic injuries may have already attempted is, therefore, appropriate to prescribe NSAIDs from thethis approach prior to arrival and/or may have moderate to ED only for short-term management of pain, in thesevere pain and need additional analgesia with titrated acute-phase postinjury, with long-term NSAID use un-opioid therapy. Additionally, NSAIDs must be used with dertaken in consultation with the follow-up orthopedist.caution in patients at risk for severe complications, such as Although most emergency physicians utilize regionalthose with a history of known peptic ulcer disease, renal anesthetic techniques for laceration repair or jointinsufﬁciency, concomitant use of anticoagulants, or the reduction, it is important to note that these methods canelderly. Since the mechanism of action of the different be used to manage the acute pain associated with frac-NSAIDs is the same, selection should be made based on tures, contusions, bursitis, acute arthritis, sprains, andtheir duration of action, prevalence of adverse effects strains in many cases.(which does differ between various NSAIDs), availability, Of the pharmacologic agents available for pain asso-and cost. Unless the patient is unable to take oral therapy, ciated with acute orthopedic injuries, none is as effectiveNSAIDs should be given by the oral route, since parenteral as carefully titrated doses of opioid analgesics. CertainNSAIDs are no more effective, are more expensive, and are concepts need to be emphasized in the treatment ofassociated with administration pain when used by the in- acute pain associated with orthopedic injuries:tramuscular route. Controversy exists regarding the use of NSAIDs in the 1. Based on the severity of pain and anticipatedmanagement of acute fracture pain, based on animal and analgesic needs, the emergency physician will need
90 Analgesia for the Emergency Patient minimize the need for a repeat ED visit for analgesia. Table 13-3. Initial opioid analgesic dosing for the patient with acute musculoskeletal injury and no Explicit follow-up instructions regarding splint care, signiﬁcant comorbidity crutches, and weight bearing should be provided. Signs of potential compartment syndrome should be Drug Dose explained to the patient and documented on the follow- up form, with instructions to return as soon as possible Morphine 0.1–0.15 mg/kg IV Fentanyl 1–1.5 mcg/kg IV should any of these signs develop. Meperidine 1–1.5 mg/kg IV Hydromorphone 0.025–0.035 mg/kg IV SUMMARY Acute orthopedic injuries are among the most common conditions seen in the ED. to individualize analgesia to either a single dose of All of these injuries require an assessment for associated an oral agent or titrated intravenous analgesia. In injuries and exclusion of any potential life or limb threats. most cases, emergency physicians should have a Effective analgesia in the ED may reduce analgesic low threshold to institute titrated opioid analgesic requirements after the patient leaves the ED. This is best therapy for patients with acute orthopedic injuries. obtained by a multimodal approach, using local techni- 2. In the acute phase after injury, in an effort to keep ques, regional anesthesia when indicated, and pharmaco- pain under control, opioid analgesics should be therapy with NSAIDs and opioid analgesics. Preemptive prescribed at ﬁxed intervals based on the phar- analgesic techniques should be utilized whenever possible. macokinetics of the analgesics used rather than ‘‘prn’’ dosing. 3. Combination opioid-nonopioid products may be BIBLIOGRAPHY beneﬁcial since a lower dose of each component 1. McCaig LF, Nawar EW. National Hospital Ambulatory could be utilized to achieve adequate analgesia Care Survey: 2004 emergency department summary. U.S. Department of Health and Human Services, 2006. and minimize the risk of side effects. 2. Katz J. Pre-emptive analgesia: Evidence, current status and 4. In patients with acute orthopedic injuries who are future directions. Eur J Anesthesiol 1995;10:8–13. otherwise healthy and young with no signiﬁcant 3. Hubbard TJ, Denegar CR. Does cryotherapy improve comorbidities, reasonably large starting doses of outcomes in soft tissue injury. J Athl Train 2004;39: 278–279. opioid analgesics should be utilized, with addi- 4. French SD, Cameron M, Walker BF, et al. A Cochrane tional boluses every 10–15 min until the pain is review of superﬁcial heat or cold for low back pain. Spine adequately controlled (Figure 13-1, Table 13-3). 2006;31:998–1006. 5. Schwartz NA, Turturro MA, Istvan DJ, Larkin GL. Patients’ perceptions of route of nonsteroidal anti-FOLLOW-UP/CONSULTATION inﬂammatory drug administration and its effect onCONSIDERATIONS analgesia. Acad Emerg Med 2000;7:861–867. 6. Koester MC, Spindler KP. Pharmacologic agents inOrthopedic consultation should be obtained for any fracture healing. Clin Sports Med 2006;25(1):63–73.fracture that will require operative intervention, patients 7. Paice JA, Noskin GA, Vanaqunas A, Shott S. Efﬁcacy and safety of ﬁxed dosing of opioid analgesics: A qualityrequiring admission, or urgent follow-up. An adequate improvement study. J Pain 1995;6:639–643.quantity of analgesics should be prescribed for the 8. Center for Disease Control and Prevention, Nationalinterval between ED visit and anticipated follow-up, to Center for Health Statistics, Adv Data 2006;372:1–29.
14 Analgesia for Selected Emergency Eye and Ear Patients Matthew G. Dunn SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT Otologic Ophthalmic FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY easily injured. The most common and clinically signiﬁ-SCOPE OF THE PROBLEM cant eye injury in patients presenting to the ED is theEye and ear problems are common complaints in the corneal abrasion.emergency department (ED), with corneal abrasion and Although the corneal epithelium heals quickly (usu-acute otitis media (AOM) being the most common di- ally within 24–48 hr), a corneal abrasion can be a de-agnoses. AOM is the most common diagnosis made by bilitating injury. It causes signiﬁcant pain, and a cornealphysicians in the United States in children under 15 years abrasion can affect vision depending on the nature andold, with an estimated incidence in children between 17% location on the corneal surface. Patients often remainand 32% per year. In one study as many as 80% of out of work during the corneal abrasion healing processchildren were diagnosed with AOM by age 3 with 40% of secondary to both visual disturbance and the side effectsthose diagnosed with more than three episodes. Although from narcotic analgesia.AOM is predominantly a childhood illness, it does occurin adults with a much lower incidence. CLINICAL ASSESSMENT Pain is the most common complaint associated withthe diagnosis of AOM in both adults and children. The initial approach in assessing a patient with a com-Recent literature describes the importance of aggressive plaint of ear pain is taking a clinical history. The patientpain management in patients with AOM irrespective of might report any of a multitude of symptoms, includingany decision to treat with antibiotics. Otitis externa is fever, chills, poor appetite, and pulling at the ears. Inanother common complaint associated with ear pain, AOM, there will be acute onset of pain, fever, and signs ofwhich has important diagnostic and treatment differ- middle ear inﬂammation as indicated by either erythemaences, including the management of pain. of the tympanic membrane (TM) or distinct otalgia, as The eye is well protected. Most of the eye lies within well as signs or symptoms of middle ear effusionthe orbit, and its anterior surface has both anatomic and including bulging of the TM, limited or absent TMfunctional protections. The tear response washes away mobility, air-ﬂuid level behind the TM, and otorrhea. Aanything that reaches the eye surface. Eyelashes and deﬁnitive diagnosis of AOM must meet three criteria:eyebrows shield the eyes, and eyelids can rapidly close to rapid onset, middle ear effusion, and middle ear in-protect the eye. Even with all these protections the eye is ﬂammation. 91
92 Analgesia for the Emergency Patient Pain is also a predominant complaint in otitis externa population suffering the most. Treating children early,but, unlike AOM, the pain can be elicited by directly particularly if there is signiﬁcant pain, will help with themanipulating either the tragus or the auricle. On direct exam by decreasing the child’s pain and anxiety over thevisualization the external auditory canal will be ery- exam of a painful ear. Pain medications in the form ofthematous and edematous with an exudate within the drops, for example, AuralganÒ, should be withheld untilcanal. The severity of illness and the need for antibiotics an intact TM can be visualized as they can be damagingshould be determined for each patient. to the middle ear. Paramount to the diagnosis and treatment of both Similar to the ear, examination of the painful eyeAOM and otitis externa is the need for adequate pain often elicits signiﬁcant anxiety. Patients may have sig-control. It is also important to note whether the TM is niﬁcant discomfort even with the simple act of openingintact as this impacts analgesic options and selection. the eyes. Blurry vision, tearing, and photophobia might An interview of the eye pain patient will often reveal a also be present in these patients, further challenging thehistory of recent ocular trauma and subsequent acute clinician. Easing patients’ fears and treating their eyeonset of pain suggestive of a corneal abrasion. The pain early and adequately prior to exam will greatlypatient might also report photophobia, tearing, foreign enhance patient comfort as well as one’s ability to per-body sensation, blurry vision, headache, and pain with form a good physical exam. It should also be noted thatextraocular muscle movement. The patient might not rapidly acting ophthalmic anesthetics do not adverselygive a history of trauma as corneal abrasion can result affect the examination of the eye.from minimal trauma such as eye rubbing. Corneal abrasion is diagnosed by direct visualization PAIN MANAGEMENTof the corneal epithelium using a slit lamp and should beaided by the use of cobalt-blue light and ﬂourescein dye. OtologicCorneal abrasions that involve multiple layers and/or are There are many factors to consider when treating earin the visual axis can lead to visual deﬁcits, making it pain: source of the pain, seriousness of the infection, ageimportant to document visual acuity. Globe penetration of the patient, whether the TM is intact. Treatment ofshould also be considered, especially if the mechanism is ear pain may, and in some circumstances should, beconcerning, that is, high-speed grinding. In this case started even before the examination of the patient withSeidel’s test can be used to aid in the diagnosis. oral pain medications. Ear drops (AuralganÒ/lidocaine) are not appropriate at this stage as they require visual- ization of an intact TM prior to use.PAIN CONSIDERATIONS In several small studies, ibuprofen dosed at 10 mg/kgBoth eye and ear complaints are common in the ED and in the pediatric population has been demonstrated ascan elicit signiﬁcant pain. It is important to recognize superior to acetaminophen in the treatment of painpain early and treat effectively, particularly as exam- associated with AOM. This difference, although small,inations of the eye and ear can worsen a patient’s pain should be considered if choosing a single medication. Ifand anxiety. Children presenting with AOM often have the child is in signiﬁcant pain, a combination of acet-signiﬁcant pain, anxiety, and distress, rendering a good aminophen (15 mg/kg) and ibuprofen should be con-physical examination difﬁcult to perform. sidered. If the pain is severe and particularly difﬁcult to For the treatment of pain associated with AOM, it is control, narcotics should be considered. Codeine elixirbeneﬁcial to begin with oral medications such as acet- has been shown to effectively treat moderate to severeaminophen or ibuprofen in an attempt to reduce a pain associated with AOM in children.child’s pain prior to exam. In practice, these medications If the TM is visualized to be intact, anesthetic drops inare often given after the exam and sometimes only when the form of either AuralganÒ (benzocaine/antipyrine),fever is present. Americaine otic, or 4% lidocaine may be instilled There are many studies suggesting inadequate pain directly into the ear canal. These medications are verycontrol by emergency physicians with the pediatric fast acting and provide excellent pain control. Anesthetic
Analgesia for Eye and Ear Patients 93 Table 14-1. Selected analgesic options for patients with AOM and otitis externa Medication Comments Acetaminophen, Ibuprofen Readily available, effective for mild to moderate pain. Studies suggest ibuprofen achieves better analgesia in AOM Topical agents – if TM is intact Anesthetics Fast acting, excellent pain relief; short AuralganÒ duration Americaine otic Narcotics Effective for moderate to severe pain Codeine, hydrocodone, oxycodone Gastrointestinal upset and constipation are commondrops are particularly helpful during the acute stage of also been demonstrated to have a longer duration ofan AOM infection, as most studies indicate that pain clinical effects.from AOM generally resolves after 48–72 hr. An attempt has been made to buffer both of these If otitis externa is diagnosed, nonsteroidal anti-in- medications, similar to buffering lidocaine beforeﬂammatory agents (NSAIDs) are the treatment of choice injection, to alleviate the pain associated with applica-for pain relief. The treatment for otitis externa involves tion to the eye. This approach appears to result in ele-cleaning the canal if possible and antibiotics as indi- vated pain associated with instillation. With nocated. Cleaning the canal is an important step and signiﬁcant difference in price between the two agents,topical analgesics, such as AuralganÒ, Americaine otic, and with proparacaine associated with both less dis-or 4% lidocaine, can be an important adjunct to relieve comfort during instillation and longer duration ofthe pain associated with this intervention. Prolonged use action, proparacaine would appear to be the moreof topical otic drops is generally contraindicated as otic appropriate choice for most corneal abrasion patients.drops can cause irritation to the raw skin associated with Adequate analgesia for patients following discharge isotitis externa (Table 14-1). important for corneal abrasion patients and can greatly improve patient comfort during their healing. TheOphthalmic mainstays of treatment for these patients are usually oralPatients with corneal abrasions often describe signiﬁcant NSAIDs and narcotics.debilitating pain. Although the pain is generally short Historically, eye patching was used as a means tolived, lasting generally 48 hr, it is often signiﬁcant decrease the pain associated with corneal abrasion. Eyeenough to limit their daily activities. Patients with cor- patching, however, has been demonstrated to confer noneal abrasions will require narcotic analgesia. beneﬁt in the reduction of pain. Patching has also been The issues with analgesia for corneal abrasions address associated with an increased risk of infection followingtwo practical concerns: anesthetics for acute eye pain in corneal abrasion. Eye patching is no longer recom-the ED and discharge analgesia. Anesthetic drops provide mended as a routine intervention for corneal abrasionexcellent anesthesia with rapid onset. Prolonged use of patients.anesthetic drops may cause corneal damage, however. Another option that is emerging as an option for The two most common ophthalmic anesthetic drops in analgesia in corneal abrasion patients is the use ofuse are tetracaine and proparacaine. Both medications NSAID ophthalmic drops. Ketorolac 0.5%, diclofenachave similar rapid onset and initial pain during instilla- 0.1%, and indomethacin 0.1% drops have all been usedtion, though tetracaine has been shown to cause more to treat the pain associated with corneal abrasion.pain with instillation than proparacaine. Proparacaine has Numerous studies, including a recent meta-analysis
94 Analgesia for the Emergency Patient Table 14-2. Selected analgesic options for patients with corneal abrasions Medication Comments Anesthetics Both offer rapid onset of anesthesia Proparacaine Proparacaine causes less pain during instillation and lasts longer than tetracaine Tetracaine Do not discharge the patient with topical anesthetic owing to risk of corneal damage Eye patching No beneﬁt in pain control Might increase risk for subsequent infection NSAID drops Provide analgesia without the need for narcotics Ketorolac 0.5% Relatively expensive Diclofenac 0.1% Indomethacin 0.1% Narcotics Provide excellent analgesia for moderate to severe pain Sedating may cause nausea and constipation Proparacaine – 2 gtts before exam Corneal abrasion Ketorolac – 0.5% 1gtt every 6 hr Diclofenac – 0.1% 1gtt every 6 hr Indomethacin – 0.1% 1gtt every 6 hr For severe/continued pain Ibuprofen 10 mg/kg body weight Acetaminophen 15 mg/kg body weight Hydrocodone/apap – 5/500 mg 1–2 every 4 hr as needed AOM Topical – only if TM is intact Auralgan® 2–4 gtts every 1–2 hr as needed Oxycodone/apap – 5/325 mg 1–2 Americaine otic – 2–4 gtts every 1-2 hr as every 4 hr as needed needed Topical anesthetic – 4 gtts used for initial cleaning Otitis externa Ibuprofen – 600–800 mg every 6 hr as needed Apap = Acetaminophen. Figure 14-1. Summary of the analgesic approach to the patient with AOM, otitis externa, or corneal abrasion.have demonstrated that these medications are effective The caveat to NSAID drop use in the corneal abrasionfor pain management. Initially there was concern patient is the high cost of these medications, generallythat NSAID ophthalmic drops would delay healing ranging from $50 to $60 per bottle. This cost would beowing to a blunting of the inﬂammatory response. prohibitive for patients who do not have insurance andRecent studies have demonstrated no merit to this is difﬁcult to justify when narcotics are inexpensive andconcern. provide excellent analgesia. However, in the patient
Analgesia for Eye and Ear Patients 95scenario where the relatively high expense of ophthalmic BIBLIOGRAPHYdrops is not a concern, these agents represent an 1. Arbour JD, Brunette I, Boisjoly HM, Shi ZH, Dumas J,excellent adjunct or alternative to narcotic analgesia as Guertin C. Should we patch corneal erosions? Archthey have been shown to provide adequate analgesia and Ophthalmol 1997;115:313–317.have no sedating side effects (Table 14-2). 2. Bartﬁeld JM, Holmes TJ, Raccio–Robak N. A comparison of proparacaine and tetracaine eye anesthetics. Acad Emerg Med 1994;1(4):364–367.FOLLOW-UP/CONSULTATION 3. Bertin L, Pons G, d’Athis P et al. A randomized, double-blind,CONSIDERATIONS multicentre controlled trial of ibuprofen versus acetamino- phen and placebo for symptoms of acute otitis media inFor any patient with AOM, otitis externa, or corneal children. Fundam Clin Pharmacol 1996;10: 387–392.abrasion, follow-up to a medical provider or specialist 4. Campanile T M, St Clair D A, Benaim M. The evaluation of eye patching in the treatment of traumatic cornealshould take place if there is no prompt relief of symp- epithelial defects. J Emerg Med 1997;15:769–774.toms in a relatively short period of 24–48 hr. Both AOM 5. Dua H S, Forrester JV. Clinical patterns of cornealand otitis externa generally do well with standard epithelial wound healing. Am J Ophthalmol 1987;104: 481–489.therapy and do not routinely require surgical specialist 6. Flynn CA, D’Amico F, Smith G. Should we patch cornealconsultation. Corneal abrasions, in contrast, should abrasions? A meta-analysis. J Fam Pract 1998;47:264–270.typically follow-up to an ophthalmologist to ensure 7. Hoberman A, Paradise JL, Reynolds EA, Urkin J. Efﬁcacyproper healing. Corneal abrasion patients with injuries of Auralgan for treating ear pain in children with acute otitis media. Arch Pediatr Adolesc Med 1997;151:that involve the visual axis should be seen by an oph- 675–678.thalmologist within 24–48 hr from their initial visit. 8. Le Sage N, Verreault R, Rochette L. Efﬁcacy of eye patching for traumatic corneal abrasions: A controlled clinical trial. Ann Emerg Med 2001;38:129–134.SUMMARY 9. Michael JG, Hug D, Dowd MD. Management of corneal abrasion in children: A randomized clinical trial. AnnMinimizing patient pain and discomfort, both in the ED Emerg Med 2002;40:67–72.and during healing, should be paramount in the treatment 10. Weaver CS, Terrell KM. Evidence-based emergency medicine. Update: Do ophthalmic nonsteroidal anti-of patients with eye and ear emergencies. Many excellent inﬂammatory drugs reduce the pain associated withanalgesic options are available for both ear and eye patients simple corneal abrasion without delaying healing? Annwith good evidence to support their use (Figure 14-1). Emerg Med 2003;41:134–140.
15 Analgesia for the Emergency Headache Patient James Miner SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT FOLLOW-UP CONSIDERATIONS SUMMARY BIBLIOGRAPHY headache subtypes and the evolving nature of the diag-SCOPE OF THE PROBLEM nosis of a patient’s headache pain.Headaches present a frequent diagnostic and therapeutic It has been estimated that 12% of the population haschallenge to emergency physicians. In fact, it is estimated had a migraine headache. Dowson (2002) estimated thatthat patients with the complaint of headache account for if a patient presents with a complaint of headache, there1–2% of all emergency department (ED) visits. Primary is a 94% likelihood that it is migraine. If a patient self-headache, also known as ‘‘benign headache,’’ is a head- reports migraine, it drops to 88%. If a primary careache that is not ‘‘secondary’’ to some identiﬁed discrete provider diagnoses migraine, the likelihood is 98% thatpathology (e.g., meningitis, sinusitis, subarachnoid hem- it is a migraine. If a primary care provider diagnoses aorrhage, toothache, etc.). The ED evaluation of headache nonmigraine headache, there is an 82% chance that it isis twofold: ﬁrst, to determine whether the headache is a migraine. Additionally, if a patient self-reports sinusprimary (Table 15-1) or secondary (Table 15-2), and headache, there is a 90% chance of migraine and if athen, if primary, to relieve the patient’s pain, and if sec- patient self-reports a nonmigraine headache, there is anondary, to treat the underlying condition. 86% chance of migraine. The International Headache Society (IHS) has estab-lished several deﬁnitions for classiﬁcations of primary CLINICAL ASSESSMENTheadaches. Although these remain useful in determininglong-term treatment strategies, most ED patients present Because headache is a common problem and also becausewith undifferentiated headaches. These include many ED patients have not formally been evaluated formigraine, probable migraine, episodic tension type, and headache prior to their ED presentation, the diagnosiscluster headaches. For the practical purpose of ED and treatment of headache can be challenging for emer-evaluation, ED patients with headache may be classiﬁed gency physicians. The ﬁrst priority in the assessment of aas serious or benign after the initial evaluation. The patient with a headache is to rule out a secondary cause ofbenign causes of headache (primary headaches) have the headache. This is most easily done if the history,been reported to account for up to 90% of ambulatory physical, and neurological exam do not suggest anpatients presenting with a complaint of headache. Since organic disorder. This can be an especially difﬁcult eval-the further differentiation of the headache before treat- uation, however, in the case of a ﬁrst time headache.ment is unlikely to occur in the ED setting, treatment There is a paucity of data on which characteristics of astrategies must take into account the full range of headache can be used to rule out a secondary cause of96
Analgesia for Emergency Headache Patient 97 Table 15-1. Primary headache taxonomy using IHS criteria Rule out secondary headache diagnosis History, physical, and neurological examinations do not suggest organic disorder* or History, physical, and neurological examinations do suggest organic disorder, but such a disorder can be ruled out by appropriate investigations or Organic disorder is present, but migraine attacks do not occur for the ﬁrst time in close temporal relation to the disorder Migraine without aura (common migraine) Migraine with aura (classical migraine) At least ﬁve attacks fulﬁlling the following criteria: At least two attacks with three of the following four characteristics: Headache attack lasting 4–72 hr (untreated or unsuccessfully One or more fully reversible aura symptoms indicating focal treated) cerebral cortical and/or brain stem dysfunction Headache characteristics (at least two of the following) At least one aura symptom develops gradually over more than 4 Unilateral location min, or two or more symptoms occur in succession Pulsating quality Moderate or severe intensity (inhibits or prohibits No aura symptom lasts more than 60 min. If more than one daily activities) aura symptom is present, accepted duration is proportionally Aggravated by routine physical activity increased Associated symptoms (at least one of the following) Headache follows aura with a free interval of less than 60 min, Nausea and/or vomiting but may occasionally begin before the aura Photophobia and phonophobia Probable migraine Meets all but one of the above criteria Tension headache At least 10 attacks fulﬁlling the following criteria: Headache attack lasting 30 min to 7 days At least two of the following pain characteristics: Pressing/tightening (non-pulsating) quality Mild or moderate intensity (may inhibit but not prohibit activities) Bilateral location No aggravation by walking stairs or similar routine physical activity Both of the following: No nausea or vomiting Photophobia or phonophobia – only one present or both absent Table 15-2. Secondary causes of headache Posttraumatic Vascular disease Other intracranial pathology (hydrocephalus, neoplasm) Substances or their withdrawal Noncephalic infection CNS infection Homeostatic disorders (hypoxia, thyroid dysfunction) Cervicogenic, eyes, ENT, sinuses, mouth, teeth, TMJ, or other craniofacial disorders Cranial neuralgias/neuropathies Psychiatric
98 Analgesia for the Emergency Patient Table 15-3. Distinguishing primary from secondary headache Primary headache (migraine) Secondary headache History Headache onset precedes Headache onset follows exposure exposure High intensity trigger No Yes Exposure associated No Yes with new type of headache Offset coincides with No Yes eliminationheadache (Table 15-3). If a patient presents with a Pain Pain Migraineheadache that is identical to previous headaches, which expression transmission syndrome system systemwere evaluated and found to be benign during the pre-vious episodes, it is unlikely to be caused by a differentetiology during the current evaluation. If a patient pre- Trigeminovascular Second- and third-ordersents with a headache that is new or different from pre- system neuronsvious headaches, there is very little data that can be used Sensory and limbicto rule out various secondary causes by history alone. In cortexthis case, or when the history or physical suggests a sec- Figure 15-1. Headache pain is perceived and initiated throughondary cause of the headache, a primary headache can be the pain expression system, principally the trigeminovasculardiagnosed when the suggested secondary cause has been system, which in turn activates the pain transmission system, which triggers the symptoms of migraine syndrome.ruled out by the appropriate exam. A primary headache can also be diagnosed when asecondary cause is present but the headache did not occur Pain Pain Migrainein temporal relation to it. If the cause of the headache is expression transmission syndrome system systemfound to be secondary to the headache, the treatmentshould be focused appropriate to the underlying disorder,rather than at the headache itself. In the case of a primary Thresholdheadache, the treatments are unique to headaches relative for activationto other pain treatment strategies. The taxonomies ofprimary headaches are described in Table 15-1. The etiology of primary headache pain is not wellunderstood, although there are many well-described the- Genetic factorsories that seem to vary from decade to decade. The theory Environmental factorschanges each decade, but several facts are accepted: all Figure 15-2. Environmental and genetic factors determine thetypes of primary headaches exist on a continuum, they all variable threshold at which a trigger may initiate a primaryrespond to relatively similar treatments, cortical spreading headache.depression is part of the etiology, there are genetic pre-dispositions, and abnormal thalamic pain modulation a trigger that can be a variable intensity. The threshold ofplays a role. Figures 15-1–15-4 display a theory for pri- activation for this system varies owing to both genetic andmary headache etiology. In this model, the pain expres- environmental factors, which leads to the current difﬁ-sion system (that which makes things hurt) is activated by culty in predicting headache onset after a known trigger.
Analgesia for Emergency Headache Patient 99 Nausea patient to safely leave the ED in a timely fashion, with Nucleus of the Photophobia tractus solitarius Phonophobia little subsequent drowsiness or lethargy. With these characteristics in mind, emergency physicians are often reluctant to use narcotics for headache patients. Fur-Pain Pain Migraineexpression transmission syndrome thermore, narcotics have been recently characterized assystem system poor medications for the treatment of migraine head- aches. Alternatively, droperidol and prochlorperazine Threshold for have been used until recent Food and Drug Adminis- activation tration (FDA) warnings about the risk of QT prolonga- tion with the use of droperidol have limited its use. Sumatriptan has also been shown to be effective in Figure 15-3. Once activated, the pain expression systemactivates the pain transmission system, which leads to symptoms treating the spectrum of primary headaches. Its sideof migraine and serves to further lower the threshold for activation effects include coronary artery spasm and chest pain, butof the pain expression system, allowing the symptoms to these occur very rarely. Sumatriptan likely causes painperpetuate themselves. relief for up to 24 hr after administration. The pain relief from subcutaneous Sumatriptan injections in ED Pain Pain Migraine patients with undifferentiated headache has not been expression transmission syndrome system system speciﬁcally studied. However, the ﬁndings of Lipton et al. with oral Sumatriptan in patients with a variety of Threshold for headaches, and the known efﬁcacy of Sumatriptan, activation suggests that it will likely have similar efﬁcacy for relief of headache pain to droperidol. High-intensity triggers Sumatriptan is currently indicated for the treatment Low-intensity triggers Estrogen withdrawal Sub-arachnoid hemorrhage of acute migraine headaches, rather than the full spec- Chronobiological factors Head trauma trum of primary headaches presenting to the ED. A wide Dietary triggers Carbon monoxide Infection variety of triptans exist, and many have been shown to be effective in the treatment of acute migraine head- Figure 15-4. Headache pain can be triggered by either high-intensity or low-intensity triggers depending on the patient’s aches. Only Sumatriptan has been shown to be effectivecurrent threshold for activation. for all subtypes of primary headaches, but it seems logical to assume that because their mechanisms areThere are also likely multiple triggers that have not yet similar they should all work similarly.been deﬁned. Once the pain expression system has been Headache treatments can target either the painactivated, it activates the pain transmission system, which, expression system to mask the pain of the headache untilamong other things, stimulates the nucleus tractus soli- it resolves or the pain transmission system to block thetarius (NTS), leading to symptoms such as nausea, pho- self-perpetuating cycle of the headache and cause thetophobia, and phonophobia. These NTS-mediated headache to resolve. Drugs that treat the pain transmis-symptoms then serve to further lower the threshold for sion system include the triptans (serotonin agonists),activation of the pain expression system, perpetuating and droperidol, prochlorperazine, depakote, and metaclo-increasing the degree of pain from the headache. pramide. Drugs that treat the pain expression system include nonsteroidal anti-inﬂammatory drugs (NSAIDs), narcotics, and acetaminophen.PAIN CONSIDERATIONSThe pain of primary headaches is usually severe enough PAIN MANAGEMENTto require relief, and the ideal medications for this wouldhave no addictive potential, few unpleasant side effects, Approaches to the treatment of primary headache painact quickly, completely resolve the pain, and allow the in the ED are outlined in Table 15-4. Once a secondary
Table 15-4. Headache analgesia summary100 Medication Dose Comments Side effects Sumatriptan 6 mg sub cu Only indicated in patients with a diagnosis Chest pain, anxiety, not recommended for of migraine; studies have shown it to be patients with cardiac risk factors effective for all types of primary headaches Ellitriptan 20–40 mg PO Similar to sumatriptan, less data available Less prominent than for sumatriptan Naratriptan 2.5 mg PO Best evidence is for headache prophylaxis Less prominent than for sumatriptan Rizatriptan 10 mg PO More effective than oral sumatriptan Less prominent than for sumatriptan Zolmatripan 5 mg PO Less prominent than for sumatriptan Droperidol 2.5 mg IV, 5 mg IM Multiple studies with 70% relief of pain Drowsiness is the most frequent report in studies, from primary headache followed by akathesia. Has a FDA black box warning concerning QT prolongation Prochlorperazine 5 mg IV, 10 mg IM Less effective than droperidol when Similar side effects to droperidol, no black box warning compared (60% relief) Valproic acid 500–1,000 mg/day Little efﬁcacy in pain relief, principally effective for headache prophylaxis Dexamethasone 10 mg IM/IV Not very effective in acute attacks, principally effective against rebound headaches Metaclopramide 10–20 mg IV Not as effective when compared to Similar to prochlorperazine prochlorperazine DHE-45 1 mg IV, 4 mg IN Less effective acutely in pain relief than Similar to the triptans with more pronounced nausea sumatriptan, least frequent recurrent and vomiting headache rate of any drug Gabapentin 900 mg/day start Limited efﬁcacy, principally for headache Few side effects prophylaxis, not as effective as valproic acid Carbemezepine 500 mg Marginal efﬁcacy for headache prophylaxis Amitriptyline 50 mg PO Delayed onset limits effectiveness in ED Magnesium 1 g IV Evidence shows effectiveness only when combined with other agents Vitamin B2 100 mg TID Effective headache prophylaxis, similar to gabapentin Intranasal lidocaine Topically applied 4% Unclear if treating the expression system lidocaine or the transmission system NSAIDS Marginal efﬁcacy in most trials Acetaminophen Marginal efﬁcacy in most trials Not recommended as sole therapy for acute primary headache Narcotics No role in the treatment of chronic primary headaches Highly associated with rebound headache Limited role in the setting of acute headaches when pain Highly associated with pain hypersensitivity transmission modifying drugs have failed in both acute and chronic headache
Analgesia for Emergency Headache Patient 101cause of headache has been ruled out, headache treat- of the headache. If a secondary cause is identiﬁed, thements should start with therapies that treat the pain treatment should be speciﬁc to it. If a primary headachetransmission system, which will abort the headache and is diagnosed, the ﬁrst treatment should focus on ter-terminate the symptoms. All of these therapies have mination of the headache syndrome with medicationsbeen found to have somewhat delayed onsets from 30 that treat the pain transmission system. Second-linemin to 2 hr, likely due to the fact that the expressed pain therapies should focus on the relief of pain using nar-the patient is experiencing is not treated by these med- cotics only when ﬁrst-line treatment has failed. Outpa-ications, and the symptoms of pain do not improve until tient treatment should focus on headache prophylaxisthe headache has begun to resolve. and follow up with a neurologist if the headaches are Droperidol, prochlorperazine, and the triptans all recurrent.have effectiveness ranges from 60% to 80%, with onsetsof 30 min to 2 hr. That means, at best, 20–40% of BIBLIOGRAPHYpatients will not get relief from these drugs at it may bedelayed longer than is reasonable to wait for a patient 1. Silberstein SD, Rosenberg J. Multispecialty consensus on diagnosis and treatment of headache. Neurology 2000;54who is very uncomfortable. Therefore, it is frequently (8):1553.necessary to resort to other medications. 2. International Headache Classiﬁcation (IHC) Committee. Given the limited efﬁcacy of acetaminophen and ICD-10 guide for headaches. Cephalalgia 1997;17(Suppl 19):1–82.NSAIDs, and the fact that patients who do not get relief 3. Lipton RB, Stewart WF, Diamond S, Diamond ML, Reedfrom a ﬁrst abortive therapy are unlikely to get relief M. Prevalence and burden of migraine in the Unitedfrom a second agent, narcotics remain a part of the States: Data from the American Migraine Study II.treatment of primary headaches. Given the high rate of Headache 2001;41(7):646–657. 4. Dowson AJ, Lipscombe S, Sender J, Rees T, Watson D.rebound headaches and problems with hypersensitivity New guidelines for the management of migraine instates associated with them in the setting of primary primary care. Curr Med Res Opin 2002;18(7):414–439.headaches, they should remain a second-line therapy 5. Morgenstern LB, Huber JC, Luna-Gonzales H, et al.and only be initiated after a ﬁrst-line agent (drugs Headache in the emergency department. Headache 2001;41 (6):537–541.affecting the pain transmission system) has failed. When 6. Maizels M, Health resource utilization of the emergencyinitiated, the treatment goal should be relief of current department headache ‘‘repeater.’’ Headache 2002;42headache pain. (8):747–753. 7. Jakubowski M LD, Goor-Aryeh I, Collins B, Bajwa Z, Burstein R. Terminating migraine with allodynia andFOLLOW-UP CONSIDERATIONS ongoing central sensitization using parenteral administra- tion of COX1/COX2 inhibitors. Headache 2005;45(7):850–Once pain is relieved in the ED, patients who have had 861. 8. Colman I, Rothney A, Wright SC, Zilkalns B, Rowe BH.more than one primary headache should be seen by a Use of narcotic analgesics in the emergency departmentneurologist as an outpatient. Patients concerned for treatment of migraine headache. Neurology 2004;62continuing or recurrent headache pain should be treated (10):1695–1700.with either oral triptans or headache prophylactic agents 9. Miner JR, Fish SJ, Smith SW, Biros MH. Droperidol vs. prochlorperazine for benign headaches in the emergency(valproic acid has the best evidence for efﬁcacy, followed department. Acad Emerg Med 2001;8(9):873–879.by amitriptyline). Oral narcotics are not effective agents 10. Richman PB, Reischel U, Ostrow A, et al. Droperidol forfor the ongoing treatment of primary headaches and acute migraine headache. Am J Emerg Med 1999;17should not be used. NSAIDs and acetaminophen have (4):398–400. 11. Wang SJ, Silberstein SD, Young WB. Droperidol treatmentlimited efﬁcacy and are unlikely to be effective. of status migrainosus and refractory migraine. Headache 1997;37(6):377–382. 12. Thomas SH, Stone CK, Ray VG, Whitley TW. Intrave-SUMMARY nous versus rectal prochlorperazine in the treatment of benign vascular or tension headache: A randomized,The principal challenge in the treatment of headaches in prospective, double-blind trial. Ann Emerg Med 1994;24the ED is to differentiate primary and secondary causes (5):923–927.
102 Analgesia for the Emergency Patient13. Jones J, Sklar D, Dougherty J, White W. Randomized treatment of acute migraine headache. Am J Emerg Med double-blind trial of intravenous prochlorperazine for the 1996;14(3):262–264. treatment of acute headache. JAMA 1989;261(8):1174– 16. Lipton RB, Stewart WF, Cady R, et al. 2000 Wolfe Award. 1176. Sumatriptan for the range of headaches in migraine14. Jones EB, et al. Safety and efﬁcacy of rectal prochlorper- sufferers: Results of the spectrum study. Headache 2000;40 azine for the treatment of migraine in the emergency (10):783–791. department. Ann Emerg Med 1994;24(2):237–241. 17. Smith LA, Oldman AD, McQuay HJ, Moore RA.15. Jones J, Pack S, Chun E. Intramuscular prochlorperazine Eletriptan for acute migraine. Cochrane Database Syst versus metoclopramide as single-agent therapy for the Rev 2001;3:CD003224.
16 Analgesia for the Emergency Chest Pain Patient Carl A. Germann and Andrew D. Perron SCOPE OF THE PROBLEM CLINICAL ASSESSMENT Cardiovascular Etiologies Pulmonary Etiologies Gastrointestinal Musculoskeletal Psychological PAIN CONSIDERATIONS PAIN MANAGEMENT Cardiovascular Etiologies Pulmonary Gastrointestinal Musculoskeletal FOLLOW-UP/CONSULTATION CONSIDERATIONS SUMMARY BIBLIOGRAPHY organ system. As an example, esophageal spasm andSCOPE OF THE PROBLEM cardiac ischemia can present with nearly identical painChest pain is an extremely common complaint in the syndromes. A second challenge to treatment of thisemergency department (ED), accounting for 5% of ED patient population is the fact that neither the locationvisits in the United States, or about 5 million visits an- nor the radiation pattern reliably identiﬁes the speciﬁcnually. Pain in the chest may be caused by a wide variety organ system. As a result, the clinician is frequentlyof disease processes involving the cardiovascular, pul- required to pursue a parallel course of both identiﬁca-monary, musculoskeletal, gastrointestinal, psychiatric, tion of the etiology of the pain and simultaneouslyneurologic, and dermatologic systems (Table 16-1). treating the patient’s pain syndrome. Once a deﬁnitive The differential diagnosis in the patient presenting diagnosis is made, the analgesic regimen can be tailoredwith chest pain is broad and includes both acute, life- to the individual pathologic process (Table 16-2).threatening illnesses and benign conditions. An accuratediagnosis and effective therapeutic strategy may be CLINICAL ASSESSMENTachieved by using a thorough knowledge of functionalanatomy and physiology of the thorax in conjunction The ﬁrst step in assessing a patient with chest painwith a proper history and physical examination. The should always be to evaluate and treat potentially life-emergency physician’s choice of analgesic should be threatening causes of discomfort. In assessing patientsbased upon the known or suspected diagnosis. with chest pain, important characteristics of the pain One of the fundamental challenges in diagnosing and should be elicited. These details would include the speedtreating chest pain lies in the fact that neither the quality of onset, site, radiation, quality, and intensity. Furthernor the intensity of the pain is speciﬁc for any single characterization of the pain should include duration and 103
104 Analgesia for the Emergency Patient Table 16-1. Common causes of acute chest pain Visceral pain Chest wall pain Pleuritic pain Aortic dissection Pneumonia Fibromyalgia Mitral valve prolapse Pleurisy Zoster Esophageal spasm/rupture Pericarditis Slipping rib syndrome Pericarditis Pneumothorax Pulmonary embolism ACSs Costochondritis Angina Myocardial infarction Table 16-2. Analgesic and primary treatment strategies for chest pain patients Etiology Treatment Cardiovascular ACS Aspirin, nitroglycerin, oxygen, beta-blocker, morphine, revascularization strategies Pericarditis NSAIDs, narcotic analgesia Aortic dissection Nitroprusside or labetalol, narcotic analgesia Mitral valve prolapse Beta-blocker Pulmonary Pulmonary embolism Oxygen, NSAIDs, narcotic analgesia, anticoagulation, ﬁbrinolysis, or surgical intervention Pneumothorax Narcotic analgesia, tube thoracotomy Pneumonia NSAIDs, tylenol, antibiotics Gastrointestinal Esophagitis Antacid medications Esophageal spasm/rupture Oxygen, narcotic analgesia Peptic ulcer disease Antacid medications Musculoskeletal Costochondritis NSAIDs Psychological Panic disorder Reassurance, anxiolyticswhether it is episodic or persistent. Patients should also unstable angina have coronary stenosis greater than orbe asked of any aggravating or relieving factors, as well equal to 90% with a small degree of vessel patency.as any associated symptomotology. This information Acute myocardial infarction results from myocardialmay focus the suspected diagnosis to a speciﬁc organ cell death due to persistent ischemia. Myocardialsystem. ischemia produces visceral pain that is felt deep in the chest and is often described as vague, poorly localized,Cardiovascular Etiologies and aching in character – frequently radiating to sitesAnginal discomfort is typically characterized as a ret- outside of the chest. Myocardial ischemia and infarctionrosternal tightness or pressure. Stable and unstable may be clinically silent in up to 25% of patients.angina will usually share similar characteristics except Acute pericarditis is caused by inﬂammation of thethat unstable angina may arise at rest with no change in pericardium and may be due to infection (viral or bac-heart rate or blood pressure. Generally patients with terial), immunological responses, myocardial infarction,
Analgesia for Emergency Chest Pain Patient 105or medications. Discomfort is characterized as sharp pain may also be related to a caustic ingestion or infection.that worsens with supine positioning. Examination may Symptoms are usually due to the contact of stomachreveal a friction rub that is frequently positional as well as acid with inﬂamed esophageal mucosa. The visceraltransitory in nature. pain related to esophagitis and reﬂux disease may be Aortic dissection is described as severe and sharp in indistinguishable from angina or pain owing to myo-75–90% of patients. The pain of aortic dissection is usu- cardial infarction. Discomfort may be described as aally described as maximal at the onset of injury, in dis- pressure, dull ache, or burning sensation located in thetinction to pain related to myocardial ischemia, which is mid-chest. Pain associated with GERD may be maximalmore frequently described as having a slowly building or when the person is supine, bending over, or after eating‘‘crescendo’’ pattern of onset. The pain of dissection may a large meal.migrate from an anterior location to a posterior one as the Esophageal rupture (Boerhaave syndrome) is a rare,dissection evolves. Alternatively, dissection pain may though potentially life-threatening, etiology of chestmigrate from a position high in the thorax to lower in the pain. The classic presentation of spontaneous esophagealchest or even the abdomen. Hypertension is present in 60– rupture is severe vomiting or retching followed by acute,75% of patients suffering from this condition. severe retrosternal or epigastric pain. The presence of The discomfort associated with mitral valve prolapse fever, dysphagia, odynophagia, or dyspnea followingfrequently occurs at rest and is often hard for the patient esophageal instrumentation, caustic injection, or a pre-to characterize. It may be described as sharp, aching, existing upper gastrointestinal pathology should raisepleuritic, or ﬂeeting. It may be associated with dizziness, suspicion for perforation.hyperventilation, anxiety, and palpitations. Peptic ulcer disease is classically described as pre- senting with postprandial, dull, boring pain in the ret-Pulmonary Etiologies rosternal or mid-epigastric area. Pain may be relieved byPulmonary embolism (PE) is a relatively common and eating food, and it frequently awakens the patient atfrequently life-threatening disease process that can present night.with a wide variety of chest pain syndromes. When classicin presentation, PE typically produces an acute-onset chest Musculoskeletalpain syndrome, characterized by sharp, pleuritic chest pain Musculoskeletal conditions account for nearly 10% of allthat cannot be relieved by positioning. Additionally, the cases of chest pain. Although acute tenderness on pal-pain may be described as intermittent or constant. Fol- pation to the site of maximal pain suggests that thelowing chest pain, the most common symptoms associated lesion is muscular or skeletal, clinicians must rememberwith PE are dyspnea and tachypnea. Large pulmonary that 5% of patients with acute coronary syndromeemboli can cause a constant, severe, crushing, visceral pain. (ACS) will also have reproducible chest wall pain. Common causes of spontaneous pneumothorax Costochondral inﬂammation may follow trauma, chestinclude changes to barometric pressure, smoking, use of surgery, persistent coughing, viral infections, or overuseinhaled recreational drugs (e.g., crack cocaine), and activities. Costochondritis often affects a wide portion ofchronic obstructive pulmonary disease with resultant the thoracic cage and may be reproduced with palpationpleural blebs. Patients with spontaneous pneumothorax along multiple portions of this distribution.usually complain of sudden, sharp, lancinating, pleuriticchest pain, and dyspnea. Psychological Pneumonia can also produce sharp, pleuritic chest Panic disorder can present as a chest pain syndrome.pain that is usually associated with fever, cough, and Several ED-based studies have found that between 15%possibly hypoxia. and 30% of all ED cases of chest pain are associated with panic disorder as the primary etiology. Although panicGastrointestinal disorder is a diagnosis of exclusion, the clinician shouldEsophagitis is most commonly caused by gastro- keep this etiology in mind when evaluating the chestesophageal reﬂux disease (GERD); however, GERD pain patient.
106 Analgesia for the Emergency Patient reducing left ventricular wall stress by decreasing after-PAIN CONSIDERATIONS load, and may increase coronary blood ﬂow by dilatationSomatic nerve ﬁbers of the chest innervate the dermis of these vessels. However, unstable angina or pain relatedand parietal pleura. These ﬁbers enter the spinal cord at to myocardial infarction may not be relieved by nitro-speciﬁc levels in a dermatomal pattern. For this reason, glycerin. In addition, nitroglycerin may provide relief ofpain from somatic ﬁbers is usually more accurately noncardiac chest pain owing to its actions as a smoothdescribed by the patient in terms of anatomic location. muscle relaxant. Sublingual nitroglycerin (0.4 mg) is theSomatic nerve irritation is often characterized as a sharp common dosage and may be repeated every 5–10 min.sensation. The duration of action is usually brief, lasting 15–30 min. Visceral nerve ﬁbers are found in the heart, esopha- Beta-blockers should also be administered to thisgus, aorta, lungs, and visceral pleura. These organs are patient population and may reduce myocardial oxygeninnervated by visceral nerves that share the same com- consumption by lowering heart rate and systolic bloodmon pathway within the spinal cord. Thus, the speciﬁc pressure. They are highly effective at reducing the fre-location or cause of pain may be difﬁcult to determine quency and anginal attacks and in improving exercisebecause various lesions or disease processes may elicit tolerance in patients with stable angina. The mostvery similar pain syndromes. For example, patients with common side effects of beta-blockers are fatigue,ACS may describe their pain over a poorly localized, depression, bronchoconstriction, and exacerbation ofwide area of the anterior chest wall. This discomfort may congestive heart failure.radiate to the left or right arm as well as to the neck, jaw, Intravenous morphine sulfate is the analgesic ofand back. Therefore, in order to arrive at an appropriate choice for ischemic chest pain refractory to initial cardiacdiagnosis, further information must be obtained via a medications. After initial intravenous beta-blockade,thorough history and physical examination along with morphine offers more effective pain control than sub-appropriate diagnostic studies. sequent doses of metoprolol. Patients should be given 2–4 mg intravenously followed by 2–8 mg intravenously at 5–15 min intervals. Morphine sulfate works as anPAIN MANAGEMENT anxiolytic and as a venodilator in pulmonary vascularCardiovascular Etiologies beds. No studies have yet demonstrated a mortalityCardiac ischemia-related chest pain represents a spec- beneﬁt from the use of morphine sulfate. Morphine istrum of illness from episodic angina to an acute ST- thought to be a superior analgesic, compared to othersegment elevation infarction. The pain of coronary heart analgesics, including fentanyl, droperidol, and meperi-disease can generally be relieved by medications or re- dine, for coronary ischemia-related pain.vascularization. The treatment of pain in this population Pericarditis, being primarily an inﬂammatory process,is vital as discomfort may induce an increase in blood usually responds well to nonsteroidal anti-inﬂammatorypressure, heart rate, and stroke volume by increasing drugs (NSAIDs). Indomethecin is commonly used and iscirculating catecholamines. dosed 25–75 mg every 6–8 hr; however, any NSAID may Unless contraindicated, patients with discomfort be chosen based on its side-effect proﬁle as well assecondary to cardiac ischemia should be given aspirin, patient or clinician preference. No one NSAID has beennitroglycerin, and supplemental oxygen. These therapies shown to be more efﬁcacious for the treatment ofmay alleviate ischemia thereby potentially reducing pericarditis than any other. For severe or persistent pain,ischemia-related discomfort. Severe coronary lesions narcotic analgesia should be used until relief is achievedmay require thrombolytic medications, percutaneous by anti-inﬂammatory agents.intervention, or surgical revascularization to relieve The emergent medical treatment of aortic dissectionanginal discomfort. is aimed at reduction of aortic pressure to reduce the In typical angina pectoris, pain relief usually occurs likelihood of aortic rupture. Intravenous nitroprussidewithin 2–5 min of taking sublingual nitroglycerin. This or labetalol may be used to reduce blood pressure in themedication reduces myocardial oxygen demand through ED. These patients frequently require narcotic analgesia
Analgesia for Emergency Chest Pain Patient 107due to the severity of their pain. Promptly reducing pain of the NSAID agent should be chosen based on its side-in this patient population will also decrease circulating effect proﬁle as well as patient or clinician preference.catecholamines, further reducing the pressure forces on Severe symptoms may require narcotic analgesia withthe aortic lumen. morphine and hydromorphone representing excellent choices for intravenous management. For outpatientPulmonary management, oxycodone or hydrocodone preparationsIn patients with pulmonary emboli, the mainstay of will be effective for pain in excess of that controlled bytreatment is anticoagulation with or without ﬁbrinolysis NSAID therapy alone.or surgical intervention. Supplemental oxygen is also in-dicated and acts as a pulmonary vasodilator that may FOLLOW-UP/CONSULTATIONreduce pulmonary ischemia and pain. Pain may have both CONSIDERATIONSa visceral and somatic component, depending on the sizeand location of the embolus. Large or peripheral emboli Follow-up and consultation chest pain patients will bewill induce irritation of both the visceral and parietal driven by the etiology of the pain syndrome. Inﬂam-pleura due to release of local cytokines. Because of these matory and musculoskeletal-based chest pain will ofteninﬂammatory mediators, NSAIDs are a good ﬁrst choice last for a period of days to weeks. Patients should receivefor analgesia in cases with mild pain. Persistent or severe treatment strategies anticipating the severity and dura-pain may be managed with intravenous opioid analgesia tion of their illness and analgesic requirements.when monitoring for subsequent hypotension. Morphinesulfate may be given at 4–6 mg every 15–20 min. SUMMARY Chest pain in the ED is a common complaint and mayGastrointestinal be caused by a wide variety of pathological processes. AsGastrointestinal causes of chest pain may include many organ systems may produce similar chest painesophagitis, reﬂux disease, esophageal foreign body, or syndromes, the clinical judgment of the care provideresophageal perforation. Treatment is aimed at the must guide the use of appropriate analgesia. Commonlyspeciﬁc cause of the inﬂammation; that is, antiacid utilized medications for these patients include agentsmedication for reﬂux-induced esophagitis in mild directed at the underlying disorder, including nitrates,cases. Proton pump inhibitors such as omeprazole or oxygen, gastrointestinal acid modifying agents, NSAIDs,lansoprazole may also be used for initial antiacid and for those patients breaking through primary treat-therapy. ment modalities, narcotic analgesics. ED treatment of any patient with suspected esoph-ageal perforation depends on the severity of the injuryand the patient’s hemodynamic stability. Treatment BIBLIOGRAPHYshould include supplemental oxygen and cardiopulmo- 1. Burduk P, Guzik P, Piechocka M, et al. Comparison ofnary monitoring before further treatment is considered. fentanyl and droperidol mixture (neuroleptanalgesia II)Patient discomfort may be signiﬁcant and narcotic an- with morphine on clinical outcomes in unstable angina patients. Cardiovasc Drugs Ther 2000;14:259–269.algesia should be given as needed when closely moni- 2. Evert B, Karlson B, Abdon N J, et al. A comparison oftoring vital signs. Morphine sulfate is often used because metoprolol and morphine in the treatment of chest pain inof its reliability and predictable effects. patients with suspected acute myocardial infarction - the MEMO study. J Intern Med 1999;245:133–141. 3. Everts B, Karlson B W, Wahrborg P, Hedner T, Herlitz J.Musculoskeletal Localization of pain in suspected acute myocardialMusculoskeletal pain of the chest may be related to infarction in relation to ﬁnal diagnosis, age and sex, andtrauma, infection, postsurgical changes, and inﬂamma- site and type of infarction. Heart Lung 1996;25: 430–437.tory processes. Treatment involves reassurance, localized 4. Exhauser A, Andrews RM, Fox SF. Clinical classiﬁcations for health policy research; discharge statistics by principalheat, NSAIDs, and avoidance of any precipatory or ex- diagnosis and procedure. Agency Health Care Policy Resacerbating mechanisms. As noted previously, selection 1993;93: chapter 43.
108 Analgesia for the Emergency Patient5. Gupta M, Tabas JA, Kohn MA. Presenting complaint clinical comparison of morphine, nicomorphine and among patients with myocardial infarction who present to pethidine. Acta Med Scand 1984;215:349–354. an urban, public hospital emergency department. Ann 9. Pollack C V. 2004 American College of Cardiology/ Emerg Med 2002;40:180–186. American Heart Association guidelines for the manage-6. Lee T H, Cook EF, Weisberg M, et al. Acute chest ment of patients with ST-elevation myocardial infarction: pain in the emergency room. Arch Int Med 1985;65: Implications for emergency department practice. Ann 345–352. Emerg Med 2005;45(4):363–376.7. Lee TH, Goldman L, Evaluation of the patient with acute 10. Wulsin L, Liu T, Storrow A, et al. A randomized, chest pain. New Engl J Med 2000;342:1187–1195. controlled trial of panic disorder treatment initiation in8. Nielson JR, Pedersen KE, Dahlstrom CG, et al. Analgesic an emergency department chest pain center. Ann Emerg treatment in acute myocardial infarction. A controlled Med 2002;39:139–143.
17 Analgesia for the Emergency Back Pain Patient Donald Jeanmonod SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT NSAIDs Skeletal Muscle Relaxants Carisprodol Cyclobenzaprine Diazepam Metaxolone Orphenadrine Opiates Steroids Antidepressants Heat/Ice Physical therapy/Exercise therapy/Spinal Manipulation/Acupuncture Facet Injections/Epidural Injections FOLLOW-UP CONSIDERATIONS SUMMARY BIBLIOGRAPHY reason for a physician visit. In 2000, 44 million pre-SCOPE OF THE PROBLEM scriptions were written for low back pain, includingAcute low back pain is a very common problem that prescriptions for nonsteroidal anti-inﬂammatory drugsaffects 60–80% of adults during their lifetimes. Fifty (NSAIDs) (16.5%), COX-2 inhibitors (10%), and musclepercent of working-age adults will have at least one relaxants (18.5%).episode of low back pain during any given year. At any Low back pain accounts for a huge ﬁnancial expen-one point in time, 15–20% of the population will report diture. Although patients who become disabled owing tohaving low back pain, 1% of the population will be low back pain represent less than 5% of those with lowtemporarily disabled, and 1% of the U.S. population will back pain problems, they account for up to 60% of thebe chronically disabled from back pain. This equates to societal costs for this disorder. In 1990, the direct24.5 million adults in the United States reporting back medical costs for treating low back pain exceeded $24pain during the year 2000. Low back pain usually starts billion, and total expenditures of $35–56 billion havebetween age 30 and 50, with the median age of onset at 48 been estimated when disability costs are included.years. Men and women are equally affected by thisproblem and it crosses all social and racial boundaries. CLINICAL ASSESSMENTEpidemiologic studies have shown similar prevalenceworldwide. Low back pain is second only to upper re- The majority of low back pain is due to mechanicalspiratory problems as the most common symptom-related musculo-ligamentous injury. Low back pain may arise 109
110 Analgesia for the Emergency Patient Table 17-1. Differential diagnosis of low back pain Mechanical low back or leg pain Nonmechanical spinal conditions Visceral disease Lumbar strain or sprain Neoplasia Aortic aneurysm Degenerative disk disease Multiple myeloma Gastrointestinal disease Degenerative facet disease Metastatic carcinoma Pancreatitis Herniated disk Lymphoma Cholecystitis Spinal stenosis Leukemia Penetrating ulcer Osteoporetic compression Spinal cord tumors Renal disease fracture Retroperitoneal tumors Nephrolithiasis Spondylolisthesis Primary vertebral Pyelonephritis Traumatic fracture tumors Perinephric abscess Congenital disease Infection Genitourinary disease Kyphosis Osteomyelitis Prostatitis Scoliosis Septic diskitis Endometriosis Transitional vertebrae Paraspinous abscess Pelvic inﬂammatory Spondylolysis Epidural abscess disease Ligamentous instability Shingles Inﬂammatory arthritis Ankylosing spondylitis Psoriatic spondylitis Reiter’s syndrome Inﬂammatory bowel disease Osteochondrosis Paget’s disease Source: Adapted from Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268:760–765.from spinal structures including ligaments, facet joints, Neurologic involvement as a cause of pain is sug-vertebral body periosteum, perivertebral musculature gested by the presence of sciatica, neurogenic claudica-and fascia, blood vessels, the annulus ﬁbrosis, and nerve tion, or symptoms of cauda equina syndrome. Sciatica isroots. However, up to 85% of patients with isolated low a unilateral leg pain that usually extends past the kneeback pain cannot be given a precise neuroanatomical and arises from a lumbar radiculopathy. The absence ofdiagnosis. The remainder of the cases can be roughly sciatica makes the presence of a clinically important discdivided between mechanical, nonmechanical, and vis- herniation unlikely. The presence of sciatica can beceral causes (Table 17-1). conﬁrmed by the reproduction of pain on straight leg The emergency provider’s approach to low back pain raise of less than 60 .is not that different from the general practitioner’s. Neurogenic claudication is the presence of leg pain onBecause the majority of low back pain is self-limiting standing or after walking that mimics claudication, butand lacks a neuroanatomical diagnosis, imaging studies unlike claudication, which improves when a patient restsare usually of little utility. When assessing the patient, (even in an upright posture), neurogenic claudicationthe emergency provider should be vigilant for the ‘‘Red often requires sitting with the back in ﬂexion to relieveFlags’’ that are indicators of a more serious cause of low symptoms. Although the sensitivity of neurogenicback pain (Table 17-2). Although up to a third of patients claudication for the detection of spinal stenosis is onlymay report a red ﬂag symptom, only 1–10% of those will 60%, the speciﬁcity is thought to be quite high. Caudahave potentially serious pathology (Table 17-3). The equina syndrome is suggested by the presence of urinarysensitivities and speciﬁcities of various historical and retention (sensitivity 90%) with overﬂow incontinence,physical exam elements are included in Table 17-4. saddle anesthesia (sensitivity 75%), and bilateral lower
Analgesia for the Emergency Back Pain Patient 111 Table 17-2. Red ﬂag indicators to prompt consideration of radiographic imaging for patients with acute back pain Indicators of cancer History of cancer Unexplained weight loss Unrelenting night pain or pain at rest Age 70 Duration greater than 6 weeks Indicators of infection Unexplained fever greater than 38 C (100.4 F) for greater than 48 hr IV drug use Immunosuppression Indicators of fracture Recent signiﬁcant trauma or milder trauma, age 50 Prolonged use of oral corticosteroids Osteoporosis Indicators of cauda equina syndrome Loss of bowel or bladder control Saddle anesthesia Symmetric distal numbness or leg weakness Other Clinical suspicion of ankylosing spondylitis Progressive neurological dysfunction extremity weakness, pain, or sensory abnormalities (sensitivity 80%). Table 17-3. Prevalence of potentially severe causes Because 95% of disk herniations involve the L5 or S1 of acute low back pain in nerve roots, the physical exam should focus on the distal primary care sensory and motor exam (Table 17-5). The most com- mon impairments are weakness of ankle and great toe Etiology Prevalence (%) dorisﬂexion (L5), loss of sensation on the foot (L5, S1), Compression fracture 4 and loss of ankle reﬂex (S1). Although ankle plantar Spondylolisthesis 3 ﬂexion is a function of the S1 nerve root, only severe Herniated disk 1–3 impairments can be detected. Pin prick should be tested Neoplasia 0.7 bilaterally for symmetry along the medial (L4), dorsal Ankylosing spondylitis 0.3 Cauda equine syndrome 0.04 (L5), and lateral (S1) aspects of the feet, as this is more Infection 0.01 accurate than light touch or temperature. Spinal stenosis Unknown In the absence of ﬁndings suggestive of systemic disease Source: Adapted from Deyo RA, Rainville J, Kent DL. What can or cauda equina syndrome, imaging is rarely needed the history and physical examination tell us about low back pain? unless patients have failed 6 weeks of conservative ther- JAMA 1992;268:760–765. apy. Plain radiographs can be used to identify fractures, but are not able to adequately date compression fractures.
112 Analgesia for the Emergency Patient Table 17-4. Sensitivity and speciﬁcity of history and physical exam for disease processes Disease to detect Historical or physical exam ﬁnding Sensitivity (%) Speciﬁcity (%) Cancer Age ! 50 years old 77 71 Previous history of cancer 31 98 Unexplained weight loss 15 94 Failure to improve after 1 month 31 90 No relief with bed rest 90 46 Duration of pain 1 month 50 81 Age ! 50 or hx of CA or unexplained 100 60 Weight loss or failure to improve w/Rx Osteomyelitis IVDA, UTI, or skin infection 40 – Spinal infection Fever 27–83 – Tenderness to percussion 86 60 Compression Fx Age ! 50 years old 84 61 Age ! 70 years old 22 96 Trauma 30 85 Corticosteroid use 6 99 Herniated disk Sciatica 95 88 Ipsilateral straight leg raise 80 40 Contralateral straight leg raise 25 90 Weakness on ankle dorsiﬂexion 35 70 Weakness on ankle plantar ﬂexion 6 95 Weakness on great toe dorsiﬂexion 50 70 Impaired ankle reﬂex 50 60 Sensory loss 50 50 Spinal stenosis Neurogenic claudication 60 – Age ! 50 years old 90 70 Ankylosing spondylitis Age 40 years old 100 7 Pain not relieved supine 80 49 Morning back pain 64 59 Pain duration ! 3 months 71 54 Note: ca, cancer; IVDA, intravenous drug abuse; UTI, urinary tract infection. Source: Adapted from Deyo RA, Rainville J, Kent DL. What can the history and physical examination tell us about low back pain? JAMA 1992;268:760–765. Table 17-5. Physical examination ﬁndings for speciﬁc nerve roots Nerve root Strength Sensory Reﬂex L2 Iliopsoas Anterior thigh, groin None L3 Quadriceps Anterior/lateral thigh Patella L4 Quadriceps and ankle Medial ankle/foot Patella dorsiﬂexion L5 Great toe dorsiﬂexion Dorsum of foot None S1 Ankle plantar ﬂexion Lateral plantar foot AchillesPatients with a high pretest probability for other serious sensitivity as magnetic resonance imaging (MRI) indiseases will require additional imaging, as plain radio- detecting herniated disks and central stenosis. CT cangraphs are not sufﬁciently sensitive to detect other serious detect pathology at the foraminal and extraforaminal nervepathology. Computed tomography (CT) has the same root, but is not effective for evaluating the intrathecal
Analgesia for the Emergency Back Pain Patient 113nerve root. MRI appears to be the superior modality for mine, and opioid receptors prior to effecting a response.imaging the spine. NSAIDs and muscle relaxants, epidural and facet blocks, and exercise, physical therapy, and osteopathic manip- ulation modify the pain response at the level of thePAIN CONSIDERATIONS peripheral nerve. Opiates and transcutaneous electricalThe vast majority of patients will not have a readily nerve stimulators have analgesic efﬁcacy at the spinalidentiﬁed neuroanatomical diagnosis for their low back level, and opiates, antidepressants, neuroleptics, andpain. Expectations of an exact diagnosis, disease-speciﬁc neurostimulants have efﬁcacy at the cortical level. Paintreatment, and complete relief of pain lead patients to should be initially managed with NSAIDs, musclebelieve that their pathology has been missed or that their relaxants, and/or analgesics, with additional optionssymptoms are doubted by the medical practitioner. considered if pain continues.Unsuccessful treatments reinforce a patient’s belief thatthe cause of their pain is not known, further adding to PAIN MANAGEMENTthe psychological distress of chronic pain. Given that 90% of individuals will have resolution of NSAIDspain by 6 weeks, initial therapy should be tailored to U.S. guidelines on the treatment of low back pain statesupport patients through this initial period of pain. The that there is good evidence for the use of NSAID med-patient should be encouraged to remain active during ications for short-term symptom control (Figure 17-1,this period of time, being reassured that the pain asso- Table 17-7). The majority of randomized, controlledciated with physical activity is not causing further NSAID trials for acute low back pain have demonstrateddamage to the spine. This avoids the impairment that the superior efﬁcacy of NSAIDs over placebo, but nonefrequently accompanies chronic low back pain. Patients has demonstrated that one NSAID is superior to another.should be informed that up to 50% of those presenting NSAIDs do not appear to be as effective in acute low backwith acute low back pain will have at least one recur- pain accompanied by the neurologic symptoms of sciaticarence in the ﬁrst 12 months. or radiculopathy. There is conﬂicting evidence regarding Further complicating the expression as well as the the effectiveness of NSAIDs over acetaminophen, whereperception of pain are a number of psychosocial factors neither has proven to be superior in the treatment ofincluding depression, anxiety, job satisfaction, and the acute low back pain. Similarly, there is no evidence thatmonetary reimbursement that may accompany disability NSAIDs are superior to muscle relaxants or opiates forfrom low back pain. Waddell has described a number of the treatment of acute low back pain.criteria on examination that might lead one to believe that NSAIDs tend to be well tolerated in the short-terma patient’s back pain is of nonorganic etiology (Table 17-6). treatment of back pain patients, with withdrawal rates of Understanding the pain pathway helps one under- 2–13% secondary to side effects. Side effects are typicallystand the treatment of low back pain. In the periphery, gastrointestinal, including abdominal pain and diarrhea,injury directly stimulates peripheral nerves or causes but can also include edema, dry mouth, rash, dizziness,release of inﬂammatory mediators that stimulate noci- headache, and fatigue. Adverse effects of NSAIDs includeceptors. The pain stimulus is transmitted to the spinal gastrointestinal bleeding, nephropathy, and worsening ofcord by fast-conducting, myelinated delta ﬁbers and heart failure and hypertension. There is no reported dif-slow-conducting, unmyelinated C ﬁbers. In the dorsal ference in the number or severity of adverse eventshorn of the spinal cord, pain transmission is modulated among trials of different NSAIDs.by opioid receptors. Once a pain stimulus has become severe enough to Skeletal Muscle Relaxantsresult in central transmission, the signal is carried by the One commonly proposed mechanism of low back painspinothalamic tracts to the medulla and thalamus and is the spasm-pain-spasm cycle. According to this theory,eventually to the cerebral cortex. The signal is once again muscle spasm activates afferent pain ﬁbers, whichmodiﬁed by serotonin, norepinephrine, GABA, dopa- stimulate the anterior horn cells, causing increased
114 Analgesia for the Emergency Patient Table 17-6. Waddell’s test Having three or more of the following ﬁve criteria is a strong indicator of a nonorganic cause of low back pain. Refer to the appropriate mental health individual if appropriate. 1. Superﬁcial or nonanatomic tenderness a. Cutaneous hyperesthesia b. Pain on gently rolling the skin 2. Pain on simulated maneuvers a. Axial loading on the top of the head in upright individuals b. Pain on passive range of motion of the shoulder and hip in the same direction in the standing individual 3. Straight leg raising discrepancy a. Lying and sitting straight leg disparity b. Normal sitting straight leg raise with distraction 4. Nonphysiologic distal examination a. Stocking glove sensory distribution b. Pseudocogwheeling – voluntary muscle contraction with recurrent giving way 5. Overreaction Low back pain History and physical exam Uncomplicated low Uncomplicated Suspect major Suspect major Suspect infection back pain sciatica mechanical injury neurological injury NSAID Immobilize Labs and MRI ± muscle relaxant imaging + early return to activity/work Positive Negative No X-ray Consult improvement Positive Consult Negative Negative Add opiate Consider antidepressant Consider physical modalities Figure 17-1.Algorithm for evaluation of acute low back pain.
Analgesia for the Emergency Back Pain Patient 115 Table 17-7. Medications for analgesia in acute back pain patients Generic name Brand name Dose Timing Metabolism Acetaminophen Tylenol 650–1,000 mg q4–6 hr Hepatic Ibuprofen Motrin, Advil 400–800 mg q6 hr Renal Ketorolac Toradol 30–60 mg IM, 30 mg IV q6 hr Renal Muscle relaxantss Baclofen Lioresal 5–20 mg q8 hr Renal Carisoprodol Soma 350 mg q6–8 hr Hepatic/renal Chlorzoxazone Parafon 500–750 mg q6–8 hr Hepatic Cyclobenzaprine Flexeril 5–20 mg q8 hr Renal Diazepam Valium 2–10 mg q6–8 hr Hepatic/renal Metaxalone Skelaxin 800 mg q6–8 hr Hepatic Methocarbamol Robaxin 1,500 mg, 1,000 mg IV/IM q6–8 hr Hepatic Orphenadrine Norﬂex 100 mg, 60 mg IV/IM q12 hr Hepatic Tizanidine Zanaﬂex 4–8 mg q6–8 hr Hepatic Opiates Codeine/APAP Tylenol #3, #4 30/300 mg, 60/300 mg q4–6 hr Hepatic/renal Hydrocodone/APAP Lortab, Vicodin 2.5–10/500 mg q4–6 hr Hepatic/renal Oxycodone/APAP Percocet, Roxicet, Tylox 2.5–10/325–650 mg Hepatic Propoxyphene/APAP Darvocet 100/650 mg q4 hr Hepatic Fentanyl Duragesic 1–2 mcg/kg Titrate Hepatic Hydromorphone Dilaudid 0.015 mg/kg Titrate Hepatic Morphine 0.1–0.2 mg/kg Titrate Hepatic/renalmuscle contraction. For this reason, muscle relaxants system (CNS) effects, including headache, drowsiness,would be expected to have a signiﬁcant affect, breaking and dizziness, and GI effects, including nausea, vomiting,the spasm-pain-spasm cycle. However, clinical and and anorexia. After prolonged administration of musclephysiologic studies, including electromyogram (EMG) relaxants, withdrawal symptoms may occur on abruptstudies, have failed to support this hypothesis. The term cessation. Few studies have compared the various skeletal‘‘skeletal muscle relaxant’’ is a misnomer because at the muscle relaxants for the management of acute back pain.usual prescribed doses, skeletal muscle relaxants do notdepress neuronal conduction, neuromuscular transmis- Carisprodolsion, or muscle excitability and do not appear to relax Carisprodol is prescribed as 350 mg QID. Head-to-headskeletal muscle to a signiﬁcant degree. studies of cyclobenzaprine and carisprodol demon- Oral muscle relaxants have been shown to improve strated equal effectiveness and similar side-effect proﬁlespain to a greater degree than placebo. A systematic re- except for autonomic side effects, which were moreview of the literature looking at 40 trials demonstrated prevalent in cyclobenzeprine. Comparative studies ofthat skeletal muscle relaxants are as effective as NSAIDs carisprodol to diazepam have demonstrated improvedfor the treatment of acute low back pain, but found little efﬁcacy of carisprodol in relieving muscle stiffness,beneﬁt in the treatment of chronic low back pain. muscle tension, and activity impairment with less sideComparisons of combination therapy of a NSAID plus a effects than diazepam therapy.muscle relaxant compared to NSAID therapy alone have The major concern for carisprodol use is its potentialyielded conﬂicting results in comparative trials. for abuse. Meprobamate, a metabolite of carisprodol, is The major side effects of skeletal muscle relaxants are classiﬁed by the Food and Drug Administration (FDA) assimilar for all the medications in this class, although there a schedule IV controlled substance. Although carisprodolare some less common side effects that are unique to each does not carry this classiﬁcation by the FDA, many statesagent. The primary side effects include central nervous have assigned it their own schedule IV classiﬁcation
116 Analgesia for the Emergency Patient quality study demonstrated that a single intravenousCyclobenzaprine dose produced signiﬁcant relief in 45 min when com-Cyclobenzaprine is prescribed in 5 or 10 mg tablets TID. pared to placebo.A large, randomized controlled trial comparing cyclo-benzaprine at multiple doses to placebo demonstrated Opiatesthat cyclobenzaprine recipients had signiﬁcant im- Narcotic analgesics are commonly prescribed for backprovement in all primary efﬁcacy variables, including a pain. There are few studies in the literature evaluating30% reduction in time to complete resolution of the effectiveness of opiates in the treatment of acutesymptoms. A meta-analysis of 14 randomized controlled back pain, but a wealth of clinical experience suggeststrials demonstrated that patients treated with cyclo- that they are efﬁcacious for pain syndromes.benzaprine were ﬁve times more likely to have symptom A few principles should be considered in prescribingimprovement at day 14. Adverse events in these trials narcotics. In treating an acute episode in the emergencywere more common with the 10 mg dose than the 5 mg department, opiate options include oral therapy or in-dose. Somnolence is reported in 18–38% of patients and travenous therapy. Intramuscular (IM) and subcutane-dry mouth in 21–32%. ous (SC) injections have unreliable and erratic drugDiazepam absorption, and it is difﬁcult to give repeated dosesDiazepam in 5–10 mg doses is often prescribed as a muscle secondary to patient discomfort. Because IM and SCrelaxant. A single study of 50 patients comparing diazepam delivery routes have an onset of action that approx-to placebo failed to identify any beneﬁt of diazepam for the imates that of oral agents, there is no beneﬁt to thesetreatment of acute low back pain, but demonstrated methods. The maximum dose of oral analgesics com-increased CNS side effects. Two studies of tetrazepam use bined with acetaminophen or ibuprofen is limited by thein chronic low back pain have demonstrated superiority presence of the nonnarcotic portion of the medication.over placebo in treating chronic low back pain. Although Codeine, propoxyphene, hydrocodone, and oxycodonethere may be some beneﬁt of benzodiazepines for the are common narcotic preparations in this class.treatment of acute low back pain, appropriate evidence is Studies have demonstrated that physicians routinelycurrently lacking in the medical literature. ineffectively treat pain with intravenous opiates. The typical dose of morphine is 0.1–0.15 mg/kg, with similarMetaxolone equipotent dosing of hydromorphone as 0.015 mg/kg,The recommended dose of metaxolone is 800 mg TID. and fentanyl as 1–2 mcg/kg.Although no quality trials of metaxolone have been Side effects of narcotics include CNS depression,published, the low incidence of sedation and short nausea mediated by histamine release, gastroparesis,elimination half-life suggest that metaxolone may be a constipation, and hypotension.muscle relaxant with less likelihood of the typical sideeffects of this group of medications. The only random- Steroidsized controlled trials in the literature evaluating Steroids are occasionally used by practitioners for themetaxolone include studies used for FDA approval from treatment of acute low back pain, particularly in thosethe 1960s and 1970s, where metaxolone demonstrated patients with a radicular component. Data regarding thesuperiority to placebo in the treatment of acute low back utility of treating acute low back pain with steroids arepain or acute exacerbations of chronic low back pain. lacking.The majority of adverse events reported with its use A single study comparing systemic steroids to placeboinclude gastrointestinal effects. for the treatment of acute low back pain did not dem- onstrate any beneﬁt of a dexamethasone taper whenOrphenadrine compared to placebo with pain assessments at 7 days,Few studies have addressed the use of orphenadrine. The less than 1 year, and greater than 1 year. A more recentbeneﬁt of this medication includes its ability to be used article evaluating large dose IV corticosteroids foras an intravenous or intramuscular injection. A high sciatica demonstrated a statistically signiﬁcant, but
Analgesia for the Emergency Back Pain Patient 117clinically irrelevant decrease in pain at 3 days, but no compared to sham treatment, the analgesic differencelasting effect (see reference 10). between groups did not reach statistical signiﬁcance. There is no evidence in the medical literature to supportAntidepressants the use of spinal manipulation for chronic low backThere is no available evidence to support the use of pain. When compared to other accepted therapies forantidepressants for acute low back pain management. low back pain, of both acute and chronic duration,However, there is evidence that antidepressants effective spinal manipulation does not appear to provide signif-in blocking norepinephrine reuptake (tricyclics and icant pain relief or functional improvement.tetracyclics) are mildly to moderately effective in de- A Cochrane review of 35 randomized controlled trialscreasing chronic low back pain. of acupuncture vs placebo or sham treatment for low back pain was only able to identify three relevant trials.Heat/Ice These studies were of small sample size and poorA Cochrane review evaluating data through 2005 found methodological quality, preventing decisive conclusions.that heated wraps applied to the low back provided short-term pain relief and improvement in disability when Facet Injections/Epidural Injectionscompared to placebo tablets or nonheated wraps. One A Cochrane review to determine the effectiveness of in-study comparing heat to ibuprofen or acetaminophen jection therapy in the treatment of acute and chronic lowfound that a heated back wrap provided signiﬁcantly back pain found, on pooled analysis of the four ran-better relief than ibuprofen or acetaminophen at 1 and 4 domized, placebo-controlled trials, no signiﬁcant beneﬁtdays of therapy. Likewise, heat has compared favorably to to epidural corticosteroid injections. It is difﬁcult to drawboth exercise and educational booklets. Studies of heat vs conclusions from these trials secondary to the degree ofcold, cold vs placebo, or cold vs other interventions have heterogeneity in patients, medications, injection techni-been few and of poor methodological quality. ques, small sample sizes, and the signiﬁcant effects of placebo (20–30% recovery in the placebo group).Physical therapy/Exercise therapy/SpinalManipulation/Acupuncture FOLLOW-UP CONSIDERATIONSA recent meta-analysis reviewed 11 of the highest quality Patients evaluated for acute low back pain should bestudies of the MacKenzie technique of physical therapy treated with NSAIDs with or without a muscle relaxantfor low back pain. Although there was a statistical and referred to a primary care physician for continuedbeneﬁt to physical therapy for low back pain, the dif- treatment. Although 79% of back pain patients see only theference between physical therapy and other techniques is initial physician who began their care for low back pain,probably not clinically meaningful. a substantial minority (21%) will see multiple providers. A meta-analysis identifying 11 trials of exercise ther- The suggestion of disc herniation (symptoms of sciatica)apy for acute low back pain found no beneﬁt over no should not rule out a course of conservative therapy.treatment or other conservative therapies. There was Ultimately, the decision to pursue a more aggressivemoderate evidence to suggest that exercise is effective in surgical approach is based on clinical factors, not radio-the care of subacute and chronic low back pain. For graphic studies. This decision is also typically based onyears, bed rest had been advocated based on the obser- the presence of severe, uncontrolled pain, profound orvation that certain types of back pain get better with rest. progressive neurologic symptoms, or failure to respond toStudies have demonstrated that prolonged immobiliza- conservative therapy (Table 17-8).tion with back rest can actually be harmful in thetreatment of acute low back pain. SUMMARY A Cochrane review of studies comparing spinal ma-nipulation versus sham treatments for acute low back Most acute low back pain is self-limited, does notpain demonstrated that although patients receiving require radiographic evaluation, and will resolve in 6spinal manipulation had a clinically signiﬁcant response weeks. After the initial health-care provider has ruled
118 Analgesia for the Emergency Patient 7. Schnitzer TJ, Ferraro A, Hunsche E Kong SX. A Table 17-8. Indications for surgical referral of the comprehensive review of clinical trials on the efﬁcacy back pain patient and safety of drugs for the treatment of low back pain. J Pain Symptom Manage 2004;28:72–95. Symptoms of cauda equina syndrome (loss of 8. Koes BW, Sholten RJ, Mans JM, Boeter LM. Efﬁcacy of bowel/bladder function, saddle anesthesia, non-steroidal anti-inﬂammatory drugs for low back pain: A systemic review of randomized clinical trials. Ann bilateral lower extremity weakness, pain, and Rheum Dis 1997;56:214–223. numbness) 9. van Tulder MW, Sholten RJ, Koes BW, Deyo RA. Non- Progressive or severe neurologic deﬁcit steroidal anti-inﬂammatory drugs for low back pain. A systematic review within the framework of the Persistent neuromotor deﬁcit after 6 weeks of Cochrane Collaboration Back Review Group. Spine conservative therapy 2000;21:2501–2513. Persistent sciatica after 6 weeks of conservative 10. Haimovic IC, Beresford HR. Dexamethasone is not therapy superior to placebo for treating lumbosacral radicular pain. Neurology 1986;36(12):1593–1594. Persistent and disabling low back and leg pain 11. Beebe FA, Barkin RL, Barkin S. A clinical and pharmaco- from spinal stenosis logic review of skeletal muscle relaxants for musculoskele- tal conditions. Am J Ther 2005;12:151–171. 12. van Tulder MW, Koes BW, Bouter LM. Conservative treatment of acute and chronic nonspeciﬁc low back pain: A systematic review of randomized controlled trials of theout potentially serious causes of low back pain, treat- most common interventions. Spine 1997;22:2128–2156.ment should emphasize NSAID therapy. 13. van Tudler MW, Touray T, Furlan AD, Solway S, Bouter Opiates and skeletal muscle relaxants can be added to LM. Muscle relaxants for nonspeciﬁc low back pain: A systematic review with the framework of thethe pain medication regimen for more severe pain at the Cochrane Collaboration Back Review Group. Spinecost of added CNS side effects. Patients should be 2003;28:1978–1992.encouraged not to use bed rest for prolonged periods of 14. Toth PP, Urtis J. Commonly used muscle relaxant therapies for acute low back pain: A review of carisoprodol,time and should be referred to a primary care physician for cyclobenzoprine hydrochloride, and metaxalone. Clin Therreevaluation and further treatment if the back pain persists. 2004;26:1355–1367. 15. Browning R, Jackson JL, O’Malley PG. CyclobenzoprineBIBLIOGRAPHY and low back pain. A meta-analysis. Arch Intern Med 2001;161:1613–1620. 1. Bigos S, Bowyer O, Braen G, et al. Acute low back problems 16. Borenstein DG, Korn S. Efﬁcacy of a low-dose regimen of in adults. Clinical practice guideline no. 14. AHCPR Publ cyclobenzoprine hydrochloride in acute muscle spasm: no. 95-0642. Rockville, MD: Agency for Health Care Policy Results of two placebo controlled trials. Clin Ther and Research, December 1994. 2003;25:1056–1073. 2. Liu X, Pietrobon R, Curtis LH, Hey LA. Prescription of 17. O’Connor AB, Lang VJ, Quill TE. Underdosing of nonsteroidal anti-inﬂammatory medications and muscle morphine compared to other parenteral opiates in an relaxants for low back pain in the United States. Spine acute hospital: A quality of care challenge. Pain Med 2004;29(23):E531–E537. 2006;7:299–307. 3. Deyo RA, Weinstein JN. Low back pain. N Engl J Med 18. Finckh A, Zufferey P, Schurch MA, Balague F, Waldburger 2001;344:363–370. M So AK. Short-term efﬁcacy of intravenous pulse 4. Spengler DM, Bigos SJ, Martin NA, Zeh J, Fisher L, glucocorticoids in acute discogenic sciatica. A randomized Nachemson A. Back injuries in industry: A retrospective controlled trial. Spine 2006;31:377–381. study. I. Overview and cost analysis. Spine 1986;11 19. Staiger TO, Gaster B, Sullivan MD, Deyo RA. Systematic (3):241–256. review of anti-depressants in the treatment of chronic low 5. O’Malley AS, DiGiuseppi C. Counseling to prevent low back back pain. Spine 2003;28:2540–2545. pain. U.S. Preventive Services Task Force. Guide to Clinical 20. French SD, Cameron M, Walker BF, Reggars JW, Ester- Preventive Services, 2nd edn, chapter 60. Washington, DC: man AJ. Superﬁcial heat or cold for low back pain. A U.S. Department of Health and Human Services, Ofﬁce of Cochrane review. Cochrane Libr 2006;4750:3. Disease Prevention and Health Promotion, 1996. 21. Machado LA de Souza MS, Ferreira PH, Ferreira ML. The 6. Deyo RA, Rainville J, Kent DL. What can the history and McKenzie method for low back pain: A systematic review physical examination tell us about low back pain? JAMA of the literature with a meta-analysis approach. Spine 1992;268:760–765. 2006;31:E254–E262.
Analgesia for the Emergency Back Pain Patient 11922. Hayden JA van Tulder MW, Malmivaara AV, Koes BW. 24. Assendelft, WJJ, Morton, SC, Yu Emily, I, Suttorp, MJ, Meta-analysis: Exercise therapy for nonspeciﬁc low back Shekelle, PG. Spinal manipulative therapy for low-back pain. Ann Intern Med 2005;142:765–775. pain. A Cochrane review. Cochrane Libr 2006;447:3.23. Hagen KB, Jamtvedt G, Hilde G, Winnem MF. The 25. Nelemans PJ, diBie RA, deVet HC, Sturmans F. Injection updated Cochrane review of bed rest for low back pain and therapy for subacute and chronic benign low back pain. sciatica. Spine 2005;30:542–546. Spine 2001;26:501–515.
18 Analgesia for the Acute Abdomen Patient Martha L. Neighbor SCOPE OF PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT DYSPEPSIA FOLLOW-UP CONSIDERATIONS SUMMARY BIBLIOGRAPHY laboratory tests, and perhaps plain radiographs. DuringSCOPE OF PROBLEM their ED stay these patients were kept NPO in case theyAccording to the 2004 National Hospital Ambulatory might require emergent surgery, and were rarely givenMedical Care Survey, abdominal pain accounts for more analgesic medications prior to evaluation by a surgeon.that 7.5 million annual patient visits to emergency Those without worrisome ﬁndings were dischargeddepartments (ED) throughout the United States. Ab- home (usually without analgesics), and those withdominal pain is the most frequently reported principal concerning ﬁndings were kept in the ED or hospitalizedreason given by patients for visiting the ED, accounting for continued observation and reexamination.for almost 7% of all ED visits. It is also the leading Pundits have traced the dictum for withholdingdischarge diagnosis in patients aged 22–49 years. analgesia in these patients to the surgical teachings of Abdominal pain constitutes a very diverse group of Zachary Cope who, in the classical medical text, Thediagnoses ranging from benign and self-limited condi- early diagnosis of the acute abdomen, warned that ad-tions, such as gastroenteritis, to acute and life-threat- ministration of analgesics might mask symptom pro-ening diseases, such as ischemic bowel or ruptured gression or alter physical ﬁndings and thereby lead toaortic aneurysms. The challenge for emergency physi- misdiagnosis, delayed surgical intervention, and unfa-cians is to correctly differentiate those patients whose vorable outcomes. Although this has been the standardabdominal condition may be imminently life threaten- of care for the last 100 years, a very dramatic changeing or require surgery, from those who require a more appears to be taking place in how we evaluate andextended evaluation and treatment or may be dis- treat patients with acute abdominal pain in the EDcharged. The ultimate challenge is to safely accomplish (Figure 18-1).this and at the same time providing the patient maxi-mum comfort. PAIN CONSIDERATIONS In the past two decades, following the publication ofCLINICAL ASSESSMENT several small ED clinical studies, the traditionalUntil recently, patients presenting to the ED with ab- approach of withholding analgesics in patients withdominal pain underwent a clinical evaluation consisting abdominal pain has become controversial amongof a routine history and physical examination, a panel of emergency physicians and surgeons alike. Though there120
Analgesia for Acute Abdomen Patient 121 History and physical exam Alternative approaches Fentanyl 1.5 mg/kg Morphine 0.1 mg/kg 0.5 mg/kg q3 min until pain free Repeat exam after pain treatment Repeat exam after pain treatment Repeat exam at 30–60 min Follow exam for changes until diagnosis made Repeat pain treatment with subsequent exam until diagnosis made Specific therapy initiated after diagnosis made Figure 18-1. Pain treatment in undifferentiated abdominal pain.is still no consensus as to whether opioids are completely Another study by Attard et al. in 1992 compared asafe in this setting, it appears that a paradigm shift single IM injection of ‘‘up to’’ 20 mg papaveretumtoward more aggressive use of analgesia is indeed hap- (equipotent to about 12.5 mg of morphine) to placebopening. in 100 patients with abdominal pain hospitalized on a How did this evolution in practice come about? Is this surgical service. They reported that those who receivednew practice based on good scientiﬁc evidence? Or, as some a single IM injection of ‘‘up to’’ 20 mg papaveretum hadexperts purport, is it based on studies with such severe a signiﬁcant reduction in pain and tenderness comparedmethodological problems and limitations that we should with those who received placebo, but there were noquestion the wisdom of changing traditional practice? signiﬁcant differences in the accuracy of diagnoses or An early pivotal study challenging the use of analgesia management decisions between the two groups. Un-in patients with acute abdominal was published in 1986 fortunately, the dose of the opioid used was not con-by Zolti and Cust, who compared sublingual bupre- trolled (the dose varied) and the surgeons making thenorphine (equivalent to about 6.6 mg of IV morphine) treatment decisions were not blinded to the patients thatvs placebo in a prospective double-blind trial of 288 received opioids. Furthermore, as in Zolti’s study, thishospitalized patients with acute abdominal pain, and trial was limited to patients sufﬁciently ill to be hospi-reported no effect on clinical diagnosis. Critics of the talized, thus limiting applicability to patients in the EDstudy, however, note that the buprenorphine dose was setting.no more effective in reducing pain than the placebo and In 1996, Pace and Burke compared the effects ofargue that it should, therefore, not be surprising that it morphine vs saline administration in 71 patients withwas not found to interfere with clinical diagnosis. abdominal pain in the ED. They reported signiﬁcant
122 Analgesia for the Emergency Patientpain relief in patients who received morphine, but found These authors cited examples from their personalno differences between the groups in provisional diag- experiences in which opioid analgesia administration lednostic accuracy or ﬁnal disposition. Criticism of this to ‘‘misses’’ or ‘‘near misses’’ in the proper diagnosisstudy included the small sample size, the variable dose of and subsequent management of patients with acutemorphine allowed, the lack of speciﬁcally deﬁned cri- abdominal pain and argued that analgesia should beteria of whether peritoneal signs were resolved, and the used ‘‘far more judiciously’’ and ‘‘cannot be undertakenlack of effective double blinding of the ED physicians to with any certainty of safety.’’ A ﬂurry of letters followedpatients receiving morphine. in which surgeons cited personal experiences of In 1997 LoVecchio et al. reported that 50% of adult analgesics masking peritoneal signs, and emergencypatients with acute abdominal pain, whose management physicians argued that anecdotal cases were not per-plan had already been determined, had changes in their suasive arguments against the conclusions of the studies,abdominal exam in terms of tenderness or location in even if these studies were ﬂawed.response to either 5 or 10 mg of morphine, but only 6% Increasingly, the dialogue focused on three issues.of patients who received saline had such changes. Sig- First, does analgesia improve a patient’s subjectiveniﬁcantly, neither group differed in either adverse events complaint of pain? The studies suggest that it does.nor delayed diagnosis, and the authors proposed that Second, does analgesia alter physical examination ﬁnd-early analgesia actually allowed for a more detailed ex- ings? Here the studies are contradictory with someamination of localized tenderness. Traditionalists dis- showing no signiﬁcant change and others showingputed their conclusion, however, and argued that the alteration in the physical examination. Third, does an-study in fact supported the concern that crucial physical algesia alter diagnostic accuracy? On this last issue, theﬁndings may be changed by opioid analgesia adminis- answer may depend upon the source of the abdominaltration. pain. Based on these four small studies, emergency medi- Geiderman and Silka in 2000 argued that patientscine experts began espousing the beneﬁts and safety of experiencing diseases characterized by visceral and pa-analgesia administration to patients with abdominal rietal peritoneum inﬂammation (e.g., more advancedpain in the ED. Many emergency physicians and appendicitis, cholecystitis, salpingitis) will havesurgeons, however, continued to be ambivalent about improvement of their pain with opioid analgesia, but arethe liberalization of analgesia use in acute abdominal unlikely to have complete elimination of localizingpain. physical ﬁndings. In contrast, patients with disease Over the next several years, studies purporting the processes not characterized by inﬂammation of theefﬁcacy and safety of analgesia in abdominal pain visceral peritoneum (e.g., pancreatitis, ischemic bowel,became highly scrutinized and criticized by surgeons. bowel obstruction), may not have ‘‘clinically helpful’’Thomas and Silen (see reference 12) cited disparity in well-localized physical examination ﬁndings of tender-trial design and ‘‘insufﬁcient enrollment to address with ness, but rather more diffuse tenderness. Elimination ofany ﬁnality the issue of outcomes.’’ Nissman, Kaplan, these patients’ subjective pain with opioid analgesia mayand Mann further expounded upon these studies’ result in misdiagnosis, delayed diagnosis, or delayednumerous signiﬁcant limitations and design ﬂaws and treatment.concluded that the trials were so problematic that they A universal criticism of the literature published toshould not support the practice of administering anal- date is the small sample size. This is a signiﬁcantgesia prior to surgical evaluation. They argued that the problem because most undifferentiated abdominal painstudies in fact show that analgesia may alter the sub- resolves spontaneously without complications. The lowjective and objective clinical examination, that this event rate of complications thus necessitates large groupblunting of signs and symptoms may be dangerous, and sizes to adequately address the inﬂuence of analgesia onthat it is the surgeon’s interpretation of the degree of outcomes.tenderness and guarding that determines whether a Lukens et al. reported that almost 88% of patientspatient needs rapid operative intervention. with undifferentiated abdominal pain in the ED were
Analgesia for Acute Abdomen Patient 123pain free or improved 3 weeks later, and only 3% remains unclear. There are few studies examining thisrequired hospitalization. Lee et al., on the other hand, issue in children, and those that have been reported havefound in a prospective observational study of 860 ED signiﬁcant limitations. Most studies have been restrictedabdominal pain patients that 8% had an adverse outcome to a small sample of school-aged children.(deﬁned as obstruction, perforation, ischemia, hemor- As with adult patients, the necessary large, multicenterrhage, peritonitis, sepsis, or death) after 3 weeks, but studies are unlikely to be performed in children to de-12.7% of the patients who received opioids had an ﬁnitively answer the many questions regarding analgesicadverse outcome. Using this adverse outcome rate, Lee use in abdominal pain, thus leaving providers to makecalculated that a randomized clinical trial of sufﬁcient size difﬁcult clinical decisions in the absence of adequateto establish the equivalent adverse outcome rate of opioid data.analgesia administration vs placebo would require theenrollment of 1,500 patients. This is clearly far more PAIN MANAGEMENTpatients than all the existing studies combined to date. Most recently, Gallagher et al. reported on the largest What conclusions can be drawn from the nearly twoclinical trail to date of opioid use in adult ED patients decades of study and debate? First, it must bewith undifferentiated abdominal pain. In this random- acknowledged that much of the literature supporting theized placebo-controlled study, 153 patients with ab- use of opioids in undifferentiated abdominal pain hasdominal pain received 0.1 mg/kg IV morphine or signiﬁcant ﬂaws and limitations. Second, it is unlikelyplacebo. The endpoint was not change in their physical that a study of sufﬁcient size to answer all the necessaryexamination, but diagnostic accuracy based on physical questions will be conducted in the near future.examination. In this study, IV morphine signiﬁcantly Conclusions are difﬁcult to draw, and a lack of con-reduced pain severity but did not impact clinical diag- sensus among emergency physicians and surgeons isnostic accuracy. likely to persist for some time. It must also be recognized A potentially important variable when considering that there is much suggestive evidence, perhaps even aanalgesia administration in patients with abdominal preponderance of evidence, supporting the practice ofpain is the wide availability and increasing use of com- ‘‘judicious’’ use of opioid analgesia in ED patients withputed tomography (CT) scanning and ultrasonography. acute undifferentiated abdominal pain.Although it has been argued that the physical exami- Perhaps the more relevant discussion and debatenation is paramount in determining the need for sur- should now be directed toward determining whatgery, CT scanning and ultrasound imaging are now used ‘‘judicious’’ means. Certainly a careful and thoroughfrequently to help determine not only the underlying history and physical examination must be performed oncause of a patient’s abdominal pain, but also the urgency all patients with acute abdominal pain. The morphineand type of surgical intervention that may be needed. dose of 0.1 mg/kg does not appear to mask physical Neighbor et al. in 2005 reported that in an urban ﬁndings, and although it has been shown to be some-teaching ED, the percentage of patients with right lower times an ineffective dose for pain relief, it likely repre-quadrant (RLQ) abdominal pain receiving a CT doubled sents a ‘‘judicious’’ dose. Alternatively, short-actingbetween 1998 and 2003 and the percentage of patients agents, such as IV fentanyl, allow for serial examsreceiving opioid analgesia for their RLQ abdominal pain between doses in the absence of opioid effect, over amore than doubled. Their data suggested that the shorter period than longer acting opioids (Table 18-1).observed increased analgesia use was not directly the The relative safety and efﬁcacy of a low-dose strategy vsresult of the increased utilization of CT scanning, and a short-acting medication and allowing the pain tomay rather reﬂect a paradigm shift toward increasing return has not been determined.use of opioid analgesia in the ED. In patients whose pain is severe enough to warrant the Although analgesic use in adults with abdominal pain administration of high doses of opioid analgesia, it mayis controversial and yet becoming more accepted, anal- be prudent to utilize ancillary imaging such as CTgesic administration in children with abdominal pain scanning or ultrasonography to facilitate diagnosis or
124 Analgesia for the Emergency Patient Table 18-1. Pain treatments in acute abdominal pain Medication Dose Comments Acetaminophen 10–15 mg/kg PO dosing may be contraindicated in patients 500–1,000 mg with potential surgical disease NSAIDs Association with GI bleeding and gastritis make NSAID use in undifferentiated abdominal pain difﬁcult Morphine 0.1 mg/kg IV This dose will not relieve pain sufﬁciently in all patients, but is not typically associated with changes in the physical exam Fentanyl 1–2 lg/kg 30–60 min duration of action will allow for serial exams in opioid-free state, but allows for complete return of the patient’s painpossible need for surgery. Alternatively, in patients who lidocaine, but may also include an anticholinergic ordo not need ancillary imaging, but do require opioid ‘‘antispasmodic’’ agent such as DonnatalÒ. Currentanalgesia, it is important that their subjective complaints evidence, however, suggests that utilization of the GIand physical ﬁndings be carefully monitored over time, cocktail as a diagnostic aid is risky, and its efﬁcacy as aand in the absence of opioid effect prior to discharge therapeutic agent is uncertain.from the ED. Wrenn et al. in 1995 (cited in reference 23) reported that though 50% of his study patients received the GI cocktail for a chief complaint of abdominal pain, 41% ofDYSPEPSIA them had a chief complaint of chest pain. He addi-Dyspepsia, which can be loosely deﬁned as ‘‘persistent or tionally found that two-thirds of the patients receivingrecurrent abdominal pain or abdominal discomfort the GI cocktail also had administered at least one othercentered in the upper abdomen,’’ is a very common drug (most commonly a narcotic, nitroglycerine, anpresenting complaint in the ED. The possible gastro- antiemetic, or a H2-blocker) within 10 min of receivingenterological etiologies are numerous and include peptic the GI cocktail. This practice is problematic in that if theor gastric ulcer disease, gastroesophageal reﬂux disease, GI cocktail is being administered as a diagnostic aid, theesophagitis, duodenitis, gastric stasis, intestinal dysmo- coadministration of other medications makes it difﬁculttility, lactose intolerance, irritable bowel, gallstone dis- to differentiate the effects of the cocktail from those ofease, pancreatitis, or malignancy. the other medications. Determining the speciﬁc GI etiology of dyspepsia in The dangers inherent in using the GI cocktail to dif-the ED is difﬁcult. Non-GI etiologies mimicking dys- ferentiate between GI and cardiac causes of dyspepsiapepsia include such potentially life-threatening pro- have been illustrated in several case series that describeblems as myocardial ischemia or infarction and aortic patients who were ultimately found to have acute myo-aneurysm or dissection. The challenge for emergency cardial infarctions, but whose pain responded partially orphysicians is to rule out potentially serious causes of this completely to a GI cocktail. Indeed, no data on the sen-often vague symptom complex and to provide effective sitivity and speciﬁcity of the GI cocktail in differentiatingsymptomatic treatment for patients. benign from serious causes of dyspepsia exists. Traditionally, in an attempt to either diagnose or treat Providers should never administer the GI cocktail fordyspepsia (or both), many ED physicians have used the the purpose of making a diagnosis. A thorough history,‘‘GI cocktail,’’ a mixture of a variety of medications that physical examination, and appropriate ancillary studies,typically includes not only a liquid antacid and viscous including an EKG are the most crucial components for
Analgesia for Acute Abdomen Patient 125arriving at a correct diagnosis, not a patient’s response to Table 18-2. Treatment of dyspepsiaa GI cocktail. Very few studies exist supporting the therapeutic ef- Inpatientﬁcacy of GI cocktails. A recent study by Bowman and Liquid antacids (do not use as a diagnostic aid)Jones found no difference in pain relief with antacid Outpatientused alone when compared to the addition of H2 blockers Proton pump inhibitorsDonnatalÒ or DonnatalÒ and lidocaine. A 2006 reviewby Bowman and Jones concludes that the ‘‘clinicalbottom line is that antacid alone should be used as thepreferred treatment for dyspepsia.’’ The most common cause of dyspepsia is probably gas- There are other reasons to avoid using drugs such as troesophageal reﬂux disease, and the most appropriateDonnatal to treat dyspepsia. Donnatal is a drug combi- treatment is empiric acid inhibition (Table 18-2). In thenation that contains the sedative phenobarbital and sev- ED this may be initially accomplished with liquid anta-eral anticholinergic medications. These drugs have cids, but for outpatient management, treatment shouldunproven treatment efﬁcacy and also possess potential be with H2 blockers or proton pump inhibitors.adverse side effects (e.g., sedation, urinary retention, drymouth). Furthermore, the anticholinergic component of FOLLOW-UP CONSIDERATIONSDonnatal that purportedly works by relaxing intestinal All patients upon discharge should be advised as to thesmooth muscle, thereby decreasing GI motility and symptoms and signs to look out for that should promptreducing pain-inducing GI ‘‘spasm,’’ may in some their return to a physician or ED for reassessment.patients be contraindicated. Studies suggest that a signiﬁcant number of patients(30–80%) with dyspepsia have a gastrointestinal motility SUMMARYdisorder causing their symptoms, and further inhibition Abdominal pain is a very common complaint of patientsof motility is best avoided. Although ‘‘prokinetic’’ agents presenting to the ED. Although most patients withsuch as metaclopramide may be effective in the treat- abdominal pain have benign conditions that will allowment of patients with symptoms of dysmotility-like them to be discharged home, those with more danger-dyspepsia, determining which patients in the ED might ous problems will be correctly diagnosed based upon abeneﬁt from this class of drugs is impossible. careful history and physical examination, laboratory, To determine which drugs are most effective in and ancillary radiographic studies.treating nonulcer dyspepsia, a 2006 Cochrane Database Most of these patients can have their pain successfullySystematic Review was conducted comparing antacids, managed with oral or parenteral analgesics with nohistamine H2 antagonists, proton pump inhibitors, substantive threat to the physician’s diagnostic accuracy.prokinetics, mucosal protecting agents, and anti- Low doses of opioids do not change a patient’s physicalmuscarinics. This review concluded that antisecretory exam, but may not relieve pain sufﬁciently. A short-therapy is effective, but that the efﬁcacy of prokinetic acting opioid provides patient comfort during the initialtherapy is still unclear. Given that the most predominant ED evaluation and enables reassessment in an opioid-cause of dyspeptic complaints in patients may be gas- free state prior to their discharge home, but allows for atroesophageal reﬂux, empiric acid inhibition with H2 return of the patient’s pain.antagonists or proton pump inhibitors is probably themost reasonable approach in the ED. BIBLIOGRAPHY The symptom complex of dyspepsia has many etiol-ogies. In the ED setting, potentially serious causes must 1. Cope Z. The early diagnosis of the acute abdomen. New York: Oxford University Press, 1921.be ruled out with a careful history, physical examination, 2. Attard AR, Corlett MJ, Kidner NJ, et al. Safety of earlyand appropriate ancillary testing. Use of the traditional pain relief for acute abdominal pain. BMJ 1992;305:GI cocktail as a diagnostic aid should be discontinued. 554–556.
126 Analgesia for the Emergency Patient 3. Pace S, Burke TF. Intravenous morphine for early pain 17. Neighbor ML, Baird CH, Kohn MA. Changing opioid relief in patients with acute abdominal pain. Acad Emerg use for right lower quadrant abdominal pain in the Med 1996;3:1086–1092. emergency department. Acad Emerg Med 2005;12(12): 4. LoVecchio F, Oster N, Sturmann K, Nelson LS, Flasher S. 1216–1220. The use of analgesics in patients with acute abdominal 18. Kim MK, Strait RT, Sato TT, Hennes HM. A randomized pain. J Emerg Med 1997;15:775–779. clinical trial of analgesia in children with acute abdominal 5. Jones P. Early analgesia for acute abdominal pain (letter). pain. Acad Emerg Med 2002;9:281–287. BMJ 1992;305:1020–1021. 19. Bulloch RB, Kabani A, Hancock BJ, Tenenbein M. Early 6. Quinn J. Debunking the myths about analgesia (letter). analgesia for children with acute abdominal pain. Pediat- CMAJ 1994:151:914–915. rics 2005;116(4):978–983. 7. Brewster GS, Herbert ME, Hoffman JR. Medical myth: 20. Servi RJ Skiendzielewski JJ. Relief of myocardial ischemia Analgesia should not be given to patients with an acute pain with a gastrointestinal cocktail. Am J Emerg Med abdomen because it obscures the diagnosis. West J Med 1985;3(3):208–209. 2000;172:209–210. 21. Dickinson MW. The ‘‘GI Cocktail’’ in the evaluation of 8. American College of Emergency Physicians. Clinical policy: chest pain in the emergency department. J Emerg Med Critical issues for the initial evaluation and management of 1996;14(2):245–246. patients presenting with a chief complaint of nontraumatic 22. Welling LR, Watson WA. The emergency department acute abdominal pain. Ann Emerg Med 2000;36:406–415. treatment of dyspepsia with antacids and oral lidocaine. 9. McHale P, LoVecchio F. Narcotic analgesia in the acute Ann Emerg Med 1990;19(7):785–788. abdomen – A review of prospective trials. Eur J Emerg Med 23. Berman DA, Porter RS, Graber M. The GI Cocktail is no 2001;8:131–136. more effective than plain liquid antacid: A randomized,10. Birnbaumer DM. Pain meds for abdominal pain: Even the double blind clinical trial. J Emerg Med 2003;25(3): surgeons say yes! J Watch 2003;717–718. 239–244.11. Bouchard M. Axiom: Never withhold analgesia I patients 24. Quartero AO, de Wit NJ, Lodder AC, Numans ME, Smout with acute abdominal pain. Emerg Med News 1999; AJ, Hoes AW. Abstract disturbed solid-phase gastric (November):32–34. emptying in functional dyspepsia: A meta-analysis. Dig12. Thomas SH, Silen W, Cheema F, et al. Effects of morphine Dis Sci 1998;43(9):2028–2033. analgesia on diagnostic accuracy in emergency department 25. Archimandritis A, Tzivras M, Fertakis A, et al. Cisapride, patients with abdominal pain: A prospective, randomized metoclopramide, and ranitidine in the treatment of severe trial. J Am Coll Surg 2003;196:18–31. nonulcer dyspepsia. Clin Ther 1992;14(4):553–561.13. Nissman SA, Kaplan LJ, Mann BD. Critically reappraising 26. Moayyedi P, Soo S, Deeks J, Delaney B, Innes M, Forman the literature-driven practice of analgesia administration D. Pharmacological interventions for non-ulcer dyspepsia. for acute abdominal pain in the emergency room prior to Cochrane Database Syst Rev 2006;18(4):CD001960. surgical evaluation. Am J Surg 2003;185:291–296. 27. Bytzer P. Diagnostic approach to dyspepsia. Best Pract Res14. Lukens TW, Emerman C, Effroon D. The natural history Clin Gastroenterol 2004;18(4):681–693. and clinical ﬁndings in undifferentiated abdominal pain. 28. Zolti N Cust M. Analgesia in the acute abdomen. Ann R Ann Emerg Med 1993;22:690–696. Coll Surg Engl 1986;68(4):209–210.15. Lee JS, Stiell IG, Wells GA, Elder BR, Vandemheen K, 29. Geiderman J, Silka P. Analgesia in patients with acute Shapiro S. Adverse outcomes and opioid analgesic abdomen West J Med 2000;173(1):13. administration in acute abdominal pain. Acad Emerg 30. Bowman J Jones J. Towards evidence-based emergency Med 2000;7(9):980–987. medicine: Best BETs from the Manchester Royal Inﬁrma-16. Gallagher EJ, Esses D, Lee C, Lahn M, Bijur PE. ry. Use of lidocaine in the gastrointestinal cocktail for Randomized clinical trial of morphine in acute abdominal the treatment of dyspepsia. Emerg Med J 2006;23(11): pain. Ann Emerg Med 2006;48(2):150–160. 873–874.
19 Analgesia for the Renal Colic Patient Allan B. Wolfson and David H. Newman SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT FOLLOW-UP/CONSULTATION SUMMARY BIBLIOGRAPHY patients with a suspected initial episode of renal colicSCOPE OF THE PROBLEM (Figure 19-1).Kidney stones occur in an estimated 5% of the popu-lation at any given time. The estimated lifetime risk for PAIN CONSIDERATIONSthe passage of a renal stone is approximately 10%. Afterhaving one episode of renal colic, an estimated 50% of It is believed that the pain of renal colic is largelyindividuals will suffer a recurrence. It is not surprising, mediated by the synthesis of prostaglandin E2 in thetherefore, that there are more than 1 million visits to renal medulla, leading to increased ﬂow through theU.S. emergency departments (EDs) each year because of afferent arterioles and increased renal pelvis pressure.renal colic. Ureteral smooth muscle spasm may also be a factor. It is believed (though supporting evidence is weak) that the location of renal colic pain may be a predictorCLINICAL ASSESSMENT of the location of the obstructing or partially obstructingSeveral studies have assessed the accuracy of the diag- calculus. Proximally located ureteral stones are thoughtnosis of renal colic based on clinical presentation. Al- to cause superior ﬂank pain, with more distally locatedthough the constellation of ﬂank pain, nausea and stones tending to cause pain radiating from the groin tovomiting, and hematuria has appeared to be reasonably the abdomen and ﬂank.speciﬁc in the classical approach to these patients, morerecent investigations have suggested that when com- PAIN MANAGEMENTputed tomography (CT) scanning of the abdomen andpelvis is performed in the acute setting, important al- Renal colic has been studied more rigorously than bili-ternate diagnoses are identiﬁed relatively frequently. ary colic, particularly with regard to analgesia. Although In one study of subjects who were thought by the desmopressin, topical warming measures, acupuncture,treating physician to have a 90–100% likelihood of and antispasmodic agents have all been studied assuffering a ﬁrst episode of renal colic, 17% were found treatments for acute renal colic pain, nonsteroidal anti-to have alternate signiﬁcant pathology. It, therefore, inﬂammatory drugs (NSAIDs) and opioid analgesicsseems prudent to consider imaging in the majority of remain the mainstays of treatment. 127
128 Analgesia for the Emergency Patient Suspected renal colic Flank pain Nausea/vomiting Hematuria No prior renal colic diagnosis or diagnosis uncertain? Symptom management and All patients analgesia: Yes Do not delay 1. IV line placement analgesia during 2. IV fluid bolus workup if colic 3. Ketorolac 30 mg IV* suspected 4. Morphine sulfate 0.1 Renal colic imaging study: mg/kg or Hydromorphone noncontrast CT 0.5–1.0 mg IV scan 5. IV Antiemetic therapy if needed Repeat: IV morphine sulfate 0.05–0.1 mg/kg or IV hydromorphone 0.5–1.0 mg as needed for analgesia Discharge patient to follow-up: 1. Oxycodone or hydrocodone alone or combination therapy with NSAID or acetaminophen 2. Consider Tamsulosin 0.4 mg q day ϫ 10 days or until passage of stone 3. Return for severe pain or symptoms *NSAID therapy should be used with caution in patients with known or suspected renal dysfunction. Figure 19-1. Management algorithm for the suspected renal colic patient. The Cochrane Collaboration has addressed renal colic the methods are rigorous and the conclusions havepain in two separate reviews, one addressing NSAIDs vs potentially important implications for ED managementopiates and one addressing the utility of intravenous decisions.ﬂuid or diuretics during renal colic pain. Other reviews Recommendations for pain management in acutehave also addressed these issues and have reviewed renal colic, as derived from these reviews and the studyand summarized the available literature on the use of by Safdar et al., can be summarized (Table 19-1). In EDmedications designed to facilitate stone passage, a po- patients, the intravenous route of administration istentially useful adjunct for decreasing the duration of preferred for both NSAIDs and opioid preparations.pain. A recent narrative review of renal colic addresses Intravenous dosing allows for rapid titration to analgesicthe issue of pain relief in the acute phase. effect and, with standard monitoring techniques, poses A recent randomized controlled trial by Safdar et al. minimal risk to the patient.compared the combination of NSAIDs and opioids with NSAIDs are effective in reducing renal colic pain andthe use of either one alone. Although this trial are arguably slightly more effective than narcotics.was limited by a rather small sample size (n = 130), NSAIDs appear to be associated with fewer side effects,
Analgesia for Renal Colic Patient 129 Table 19-1. Treatment recommendations for acute renal colic analgesia. 1. Intravenous therapy is the preferred route for analgesia and symptom management 2. NSAIDs should be considered ﬁrst-line analgesic therapy. NSAIDs should be used with caution in patients with known or suspected impaired renal function 3. Opiate therapy (morphine sulfate, hydromorphone) should be titrated to effective analgesia levels when monitoring patients for opiate-related side effects 4. Combination therapy with NSAID and opiate analgesia appears to be more effective than either class of analgesia alone 5. The impact of intravenous ﬂuid therapy on reduction of pain and stone passage remains unproven 6. Alpha-blocking agents should be considered for outpatient and follow-up patient care to enhance the likelihood of stone passageparticularly vomiting. In the setting of conﬁrmed or time to stone passage, in addition to the likelihood ofhighly suspected renal colic, NSAIDs are a reasonable stone passage, by approximately 30%. Though this effectﬁrst-line analgesic agent. NSAIDs should be avoided or is not a direct analgesic action, a reduction in the du-used with caution in the older patient and individuals ration of pain is a signiﬁcant indirect contribution forwith known or suspected reduced renal function. outpatient pain management. Opioids are effective and safe for renal colic patientsand should be titrated to effective analgesia with careful FOLLOW-UP/CONSULTATIONmonitoring for side effects associated with opiate therapy.Respiratory depression due to opiate administration is Assuming that acute relief of pain is adequate, patientsrare and is most often associated with large doses given in with conﬁrmed ureteral colic can be followed as out-close succession. Although vomiting, drowsiness, and patients by a primary care physician or urologist. Renalother less worrisome side effects occur more often than stones 6 mm in diameter can be expected to passwith NSAID agents, opioids reduce pain rapidly and spontaneously in up to 90% of cases, whereas thosesafely. The combination of NSAID’s and narcotics 6 mm in diameter commonly require urologic inter-appears to be more effective than either agent alone. vention (up to 50% of the time). Thus, the size of the Fluid administration, with isotonic saline or Ringer’s stone may be helpful in guiding follow-up decisions andlactate solution, or the induction of diuresis in the setting the choice of initial conservative vs invasive manage-of acute renal colic remains somewhat controversial. A ment strategies. Consideration may be given to admin-small comparative trial showed no demonstrable impact istration of agents that may act to decrease the time toof either intravenous ﬂuid administration or induction of stone passage, including alpha-blocking agents and cal-diuresis. Given that the purpose of NSAID administration cium channel blockers.is to decrease ureteral and renal pelvic pressure owing to Consultation or follow-up with an urologist is ad-the action of prostaglandin E2, aggressive administration visable in many patients, particularly those with no priorof intravenous ﬂuids might be expected to override the history of nephrolithiasis. All patients should be offeredeffect of NSAID agents. However, there is little data in outpatient analgesic therapy with an appropriate opiatehumans to support either view. agent, typically hydrocodone or oxycodone, and an Alpha-blocking agents, such as tamsulosin, are a re- appropriate duration of therapy for the time to stonecent addition to the management of renal colic. Al- passage or follow-up physician visit.though these agents do not appear to have a role in theinitial, acute management of the renal colic patient, SUMMARYthere does appear to be substantial evidence to supportthe use of these agents in follow-up. The current liter- Pain from renal colic is a common presenting complaintature supports the view that these agents decrease the for emergency patients. A number of medications can
130 Analgesia for the Emergency Patientprovide rapid and substantial analgesic relief to these 6. Portis AJ, Sundaram CP. Diagnosis and initial management of kidney stones. Am Fam Physician 2001;63(7):1329–1338.patients, including NSAID and opiate agents. Patients 7. Lee Y-H, Lee W-C, Chen M-T, Huang J-K, Chung C,who are undergoing a diagnostic evaluation for renal Chang LS. Acupuncture in the treatment of renal colic.colic should not experience a delay to analgesia during J Urol 1992;147:16–18.their workup. Effective analgesic and adjunctive therapy 8. Jones JB, Dula DJ. The efﬁcacy of sublingual hyoscyamine sulfate and intravenous ketorolac tromethamine in theshould be given to all patients for outpatient manage- relief of ureteral colic. Am J Emerg Med 1998;16ment of the symptoms of renal colic. (6):557–559. 9. Holdgate, A, Pollock T. Nonsteroidal anti-inﬂammatory drugs (NSAIDS) versus opioids for acute renal colic.BIBLIOGRAPHY Cochrane Renal Group, Cochrane Database Syst Rev 2006;4: 1. Brown J. Diagnostic and treatment patterns for renal 10. Worster A, Richards C. Fluids and diuretics for acute colic in US emergency departments. Intern J Urol Nephr ureteric colic. Cochrane Renal Group. Cochrane Database 2006;38(1):87–92. Syst Rev 2006;4: 2. Eskelinen M, Ikonen J, Lipponen P. Usefulness of history- 11. Review: Medical therapy with calcium-channel blockers or taking, physical examination and diagnostic scoring in alpha-blockers helps patients to pass urinary stones. ACP J acute renal colic. Eur Urol 1998;34:467–473. Club 2007;v146(1):22. 3. Ha M, MacDonald RD. Impact of CT scan in patients with 12. Teichman TE. Clinical practice acute renal colic from ﬁrst episode of suspected nephrolithiasis J Emerg Med ureteral calculus. N Engl J Med 2004;350(7):684–693. 2004;27(3):225–231. 13. Safdar B, Degutis LC, Landry K, et al. Intravenous 4. Hoppe H, Studer R, Kessler TM, et al. Alternate or morphine plus ketorolac is superior to either drug alone additional ﬁndings to stone disease on unenhanced for treatment of acute renal colic. Ann Emerg Med 2006; computerized tomography for acute ﬂank pain can impact 48(2):173–180. management. J Urol 2006;175:1725–1730. 14. Segura JW, Preminger GM, Assimos DG, et al. Ureteral 5. Nishikawa K, Morrison A, Needleman P. Exaggerated stones clinical guidelines panel summary report on prostaglandin biosynthesis and its inﬂuence on renal the management of ureteral calculi. J Urol 1997;158: resistance in the isolated hydronephrotic rabbit kidney. 1915–1921. J Clin Invest 1977;59:1143–1150.
20 Analgesia for the Biliary Colic Patient Allan B. Wolfson and David H. Newman SCOPE OF THE PROBLEM CLINICAL ASSESSMENT PAIN CONSIDERATIONS PAIN MANAGEMENT FOLLOW-UP/CONSULTATION SUMMARY BIBLIOGRAPHY colic pain due to obstruction alone is not generally as-SCOPE OF THE PROBLEM sociated with abdominal tenderness.Painful biliary tract dysfunction is common. It is esti-mated that more than 20 million people in the UnitedStates have been treated for gall bladder disease, in- PAIN CONSIDERATIONScluding 9 million who have undergone cholecystectomy. As with most abdominal processes that are evaluatedThe overwhelming majority of these procedures (98%) and treated in the emergency department (ED), the di-are related to cholelithiasis, a condition that has also agnosis of biliary tract disease is often unclear on initialbeen reported to be present in 15% of asymptomatic presentation. It is, therefore, worth noting that patientsadults. with undifferentiated abdominal pain may be treated with judicious intravenous narcotics, an intervention that has been well studied and ﬁrmly established as safe.CLINICAL ASSESSMENT When used judiciously, analgesia administration toBiliary colic, a term used to refer to noninﬂammatory, acute abdominal pain patients has been shown to benoninfectious gall bladder pain, is believed to arise from very unlikely to interfere with the clinical diagnosticoutﬂow tract obstruction leading to increased prosta- process.cyclin and prostaglandin elaboration. This process may Though often mentioned, spasm of the sphincter ofresult in muscular spasm of the gall bladder wall, caus- Oddi due to narcotic medication is likely to be sub-ing both viscerally and somatically mediated pain. clinical and is, therefore, not a reason to withhold nar- Typically, biliary pain is experienced in the epigastric cotics. Should this unusual cause of pain be suspected, itand right upper quadrant regions of the abdomen and appears that the narcotic antagonist naloxone is likely tomay radiate to the back. In contrast to classic descrip- be effective in quickly relieving the pain.tions of colic in which minutes-long spasms of pain are In individuals with an established diagnosis of cho-considered characteristic, biliary ‘‘colic’’ frequently lelithiasis who experience characteristic pain, or in thoseremains constant and severe for 2–3 hr or more. with pain that is known to be of biliary origin, imme- Pain in biliary tract disease also often arises in asso- diate treatment is generally directed at relieving painciation with prandial stimulation and may be associated through smooth muscle relaxation. This mechanismwith nausea, emesis, chest pain, and diaphoresis. Biliary may also have the beneﬁt of allowing the passage of 131
132 Analgesia for the Emergency Patient Table 20-1. Treatment recommendations for acute biliary colic analgesia 1. Intravenous therapy is the preferred route for analgesia and symptom management 2. NSAIDs should be considered ﬁrst-line analgesic therapy. NSAIDs should be used with caution in imminent surgical patients or patients in whom transient platelet dysfunction or impaired renal function would be a concern 3. Opiate therapy (morphine sulfate, hydromorphone) should be titrated to effective analgesia levels when monitoring patients for opiate-related side effectsimpacted stones and, therefore, preventing progression dose of 30 mg of intravenous ketorolac appears to beto inﬂammation and cholecystitis. effective and safe for biliary colic patents. The NSAID dose may be repeated at least once if pain is still unre- lieved after 30 min. Adjunctive intravenous narcoticsPAIN MANAGEMENT should also be considered at any point in the course ofThe effectiveness of nonsteroidal anti-inﬂammatory drugs treatment. Intravenous morphine sulfate in 0.05–0.1(NSAIDs) for the treatment of the biliary colic patient has mg/kg boluses every 15 min is a reasonable choice untilbeen documented in multiple small- to medium-sized pain is adequately controlled, at the same time observingrandomized controlled studies of varying quality (Table for opiate side effects.20-1). These trials have shown beneﬁt not only in terms ofpain control, but also occasionally in the prevention (or FOLLOW-UP/CONSULTATIONperhaps delay) of progression to cholecystitis. Both intravenous and oral analgesic NSAIDs have Follow-up options for biliary colic patients should focusbeen utilized successfully for biliary pain, including on arranging surgical evaluation at the same time alsodiclofenac, indomethacin, and ketorolac. Drugs within anticipating the likelihood of further pain. Oral NSAIDthe NSAID class appear to have relatively comparable preparations and oral narcotics may both be utilized forefﬁcacy for these patients. outpatient pain. Medications outside of the NSAID class, including Given the frequency of nausea and emesis with biliaryanticholinergic and antispasmodic agents, have also colic, it may be wise to recommend scheduled dosingbeen studied and have yielded mixed results for anal- rather than as-needed dosing of NSAID therapy, andgesia. These agents include opiates, glycopyrrolate, at- emphasis should be placed on the need for the patient toropine, propinox, hyoscine, glucagon, cerulein, and return to the physician or ED for fever, inability to takecholecystokinin inhibitors. ﬂuids by mouth, or increasing or uncontrolled pain. For patients with active (and established) biliary colicin the emergent setting, an intravenous NSAID appears SUMMARYto be an appropriate initial therapy (Figure 20-1). Thepropensity of biliary pain to be associated with nausea Pain from biliary colic is a common presenting com-and emesis, and the rapid onset of effect, make intra- plaint for emergency patients. A number of medicationsvenous dosing more desirable. can provide rapid and substantial analgesic relief to For patients in whom imminent operative manage- these patients, including NSAID and opiate agents.ment remains a possibility (those with possible chole- Patients who are undergoing a diagnostic evaluation forcystitis or other nonbiliary conditions), surgical biliary colic should not experience a delay to analgesiaconsultation prior to drug administration may be war- during their workup. Analgesic treatment strategiesranted based on local preferences and if there is concern should consider the potential for operative managementon the part of the surgeon regarding the implications of for the individual patient as well as surgical consultanttransient antiplatelet effects of NSAID agents. An initial preferences for the population as a whole.
Analgesia for Biliary Colic Patient 133 Suspected biliary colic Right upper quadrant or mid-epigastric pain nausea/vomiting No prior biliary colic diagnosis or diagnosis uncertain? Symptom management and analgesia All patients Yes Do not delay 1. IV line placement analgesia during 2. IV fluid bolus for workup if colic hydration suspected 3. Ketorolac 30 mg IV* Biliary imaging and/or Morphine sulfate study: 0.1 mg/kg ultrasound or 4. IV Antiemetic therapy if HIDA scan needed Repeat: IV morphine sulfate 0.05–0.1 mg/kg as needed for analgesia Surgical consultation or discharge patient to follow-up 1. Oxycodone or hydrocodone alone or combination therapy with NSAID or acetaminophen 2. Return for severe pain, fever, or symptoms *NSAID therapy should be used with caution in patients with known or suspected renal dysfunction or patients who are imminent surgical candidates. Figure 20-1. Management algorithm for the suspected biliary colic patient. 5. Murphy P, Solomon J, Roseman DL. Narcotic analgesicBIBLIOGRAPHY drugs: Their effect on biliary dynamics. Arch Surg 1. Everhart JE. Khare M, Hill M. et al. Prevalence and ethnic 1980;115:710–711. differences in gallbladder disease in the United States. 6. Lang DW, Pilon RN. Naloxone reversal of morphine- Gastroenterology 117(3):632–639. induced biliary colic. Anesth Analg 1980;59:619–620. 2. Ko CW. Epidemiology and natural history of commo