CLINICAL EMERGENCY MEDICINE CASEBOOKUnlike the comparatively calm and orderly world of many specialties andsubspecialties in medicine, emergency medicine is not divided into speciﬁcareas of practice. Emergency patients come in all shapes and sizes, at anytime of day or night, with a wide range and acuity of maladies. Emergencyphysicians must become experts in diverse areas of medicine. They arerequired to make prompt, informed and often lifesaving decisions aboutpatient care. A cornerstone of emergency medicine training is the constantstudy of clinical scenarios and simulated cases. This book offers a uniqueyet underutilized strategy for learning: a case-based approach from realpatients and actual events. Each case provides the opportunity for learningessential clinical concepts. Focused exclusively on the needs of emergencyphysicians in training, students and nurses, the book covers more than 100common and unusual emergency medicine case scenarios. The proceduresand learning have been class-tested by the Stanford/Kaiser EM ResidencyProgram and are supplemented with high-quality clinical photographs andimages.Joel T. Levis, M.D., Ph.D., FACEP, FAAEM, is Clinical Instructor ofEmergency Medicine (Surgery) at Stanford University School of Medicineand Senior Emergency Physician for The Permanente Medical Group,Kaiser Santa Clara, California. Dr. Levis is Medical Director, Foothill Col-lege Paramedic Program, Los Altos Hills, California.Gus M. Garmel, M.D., FACEP, FAAEM, is Clinical Associate Profes-sor of Emergency Medicine (Surgery) at Stanford University School ofMedicine and Senior Emergency Physician for The Permanente Medi-cal Group, Kaiser Santa Clara, California. Dr. Garmel is coeditor of AnIntroduction to Clinical Emergency Medicine: Guide for Practitioners in theEmergency Department, published in 2005 by Cambridge University Press,and author of Career Planning Guide for Emergency Medicine, 2nd ed.,published in 2007 by EMRA.
CLINICALEMERGENCYMEDICINECASEBOOK JOEL T. LEVIS, M.D., Ph.D., FACEP, FAAEM Clinical Instructor, Department of Surgery, Division of Emergency Medicine, Stanford University Senior Emergency Physician, The Permanente Medical Group, Kaiser Santa Clara, CA Medical Director, Foothill College Paramedic Program, Los Altos Hills, CA GUS M. GARMEL, M.D., FACEP, FAAEM Co-Program Director, Stanford/Kaiser EM Residency Clinical Associate Professor, Department of Surgery, Division of Emergency Medicine, Stanford University Medical Student Clerkship Director, Emergency Medicine (Surg 313D), Stanford University School of Medicine Director, Emergency Medicine Clerkship for Rotating Interns, Kaiser Santa Clara, CA Senior Emergency Physician, The Permanente Medical Group, Kaiser Santa Clara, CA Senior Editor, The Permanente Journal, Portland, OR
DedicationJoel T. Levis, M.D., Ph.D. Gus M. Garmel, M.D.To my mother, Eileen Levis: For your constant support, To my residents, students and colleagues in emergencyencouragement and sacriﬁces throughout the years. medicine, nursing and other specialties: Because of you, outstanding patient care happens.To my colleagues at Kaiser Santa Clara and StanfordUniversity, and the residents of the Stanford/Kaiser To The Permanente Medical Group, Kaiser Santa Clara, andEmergency Medicine Residency Program: You are all such Stanford University: The organization and institutions thatwonderful clinicians and talented people, and you continue support my academic pursuits and encourage me to excel into inspire me. all aspects of my professional life.To Gus: A superb mentor, phenomenal educator, To Joel, a former resident and chief resident: Yourtremendous clinician and true friend; without your efforts, enthusiasm for our specialty is refreshing, and your workthis textbook would not have happened. ethic unparalleled. I am honored to be your colleague, mentor and friend, and to have collaborated with you on thisAnd to my wife Estelle: For your encouragement and love and prior scholarly projects.that gives me strength to pursue my dreams. Without you,the rewards of life would have little meaning. To my parents, siblings and friends: Thanks for encouraging me to follow my dreams. And to Laura, my true passion in life.
ContentsPreface page xiAcknowledgments xiiiForeword xvI. HEENT (Head, Eyes, Ears, Nose and Throat) 1 Sore throat in a 29-year-old male 3 2 Left eye pain and discharge in a 44-year-old male 5 3 Sudden, monocular vision loss in a 62-year-old female 9 4 Syncope and monocular vision loss in a 76-year-old female 13 5 Eye pain and blurred vision in an 89-year-old female 17II. CARDIOVASCULAR 6 Palpitations and chest heaviness in a 26-year-old female 21 7 Chest pain in a 26-year-old male 25 8 Palpitations in a 36-year-old male 29 9 Chest pressure for two days in a 37-year-old male 33 10 Low back pain and leg weakness in a 40-year-old male 37 11 Acute chest pain in a 42-year-old male 41 12 Rapid heart rate in a 47-year-old male 45 13 Chest pain and syncope in a 48-year-old male 49 14 Syncope and hypotension in a 54-year-old male 53 15 Palpitations and shortness of breath in a 69-year-old male 57 16 Chest pain following emotional stress in a 70-year-old female 61 17 General body weakness and slow heart rate in a 72-year-old male 65 18 Headache, neck pain and chest pain in a 73-year-old male 69 19 Near syncope, tachycardia and chest pain in a 74-year-old female 73 20 Chest pain for 12 hours in a 75-year-old female 79 21 Shortness of breath and cough in an 80-year-old female 83 22 Weakness, fatigue and shortness of breath in an 88-year-old male 87 23 Sudden onset of back pain in a 91-year-old male 91III. PULMONOLOGY 24 Pleuritic chest pain in a 27-year-old male 97 25 Acute onset of shortness of breath in a 30-year-old female 101 26 Recurrent pneumonias in a 37-year-old male 109 27 Hemoptysis in a 47-year-old male 113 28 Cough, fever and shortness of breath in a 62-year-old male 117 vii
viii Contents IV. GASTROENTEROLOGY 29 Abdominal pain and dysuria in a 16-year-old male 123 30 Left upper quadrant abdominal pain in an 18-year-old male 127 31 Abdominal pain and vomiting in a 29-year-old female 131 32 Right lower quadrant abdominal pain and fever in a 36-year-old male 135 33 Abdominal pain and diarrhea in a 64-year-old female 139 34 Rectal and abdominal pain in a 70-year-old male 143 35 Abdominal pain in a 75-year-old male 147 36 Abdominal pain and anorexia in a 77-year-old female 151 37 Sudden onset of back pain in an 84-year-old male 155 38 Intermittent abdominal pain for one day in an 86-year-old female 159 V. GENITOURINARY AND GYNECOLOGY 39 Right ﬂank pain in a 20-year-old female 165 40 Right lower quadrant abdominal pain in a 28-year-old female 169 41 Abdominal pain and vaginal bleeding in a 33-year-old female 173 42 Genital trauma in a 34-year-old male 177 43 Recurrent vaginal bleeding after miscarriage in a 39-year-old female 179 44 Scrotal pain and swelling in a 75-year-old male 183 VI. NEUROLOGY/NEUROSURGERY 45 Left-sided weakness in a 13-year-old male 189 46 Worst headache of life in a 23-year-old female 193 47 Lower extremity weakness in a 26-year-old female 197 48 Headache, neck pain and dizziness in a 35-year-old male 201 49 Low back pain and weakness in a 37-year-old male 205 50 Headache and left arm weakness in a 44-year-old female 209 51 Headache and seizures in a 45-year-old female 213 52 Acute onset of altered consciousness in a 66-year-old male 219 VII. TRAUMA 53 Left upper quadrant abdominal pain following a bicycle collision in a 13-year-old male 225 54 Assault with stab wounds to a 16-year-old male 229 55 Left thigh pain in an 18-year-old male 235 56 Neck pain after a golf swing in a 26-year-old male 239 57 Cardiac arrest in a 29-year-old male 241 58 Right lower quadrant abdominal pain in a 36-year-old female 245 59 Blunt head trauma in a 37-year-old male 247 60 Neck pain after a fall in a 75-year-old female 251 61 Posterior neck pain in a 77-year-old male 255 VIII. ORTHOPEDICS 62 Elbow trauma in a 3-year-old male 261 63 Foot trauma in a 12-year-old male 265 64 Forearm pain and swelling in a 14-year-old male 269
Contents ix 65 Foot pain while playing soccer in a 22-year-old male 273 66 Elbow trauma in a 29-year-old male 275 67 Forearm trauma in a 32-year-old male 279 68 Left knee pain following trauma in a 68-year-old male 283 69 Left hip pain in a 70-year-old male 287 70 Thigh trauma in an 81-year-old female 291IX. HAND 71 Right thumb pain and swelling in a 20-year-old female 297 72 Paint gun injury to the hand in a 22-year-old male 299 73 Finger pain and swelling in a 34-year-old male 303 74 Finger laceration in a 50-year-old female 307 75 Cat bite to the ﬁnger of a 52-year-old male 311X. PEDIATRICS 76 Rapid heart rate in an 8-week-old male 317 77 Cough, fever and poor feeding in a 4-month-old male 321 78 Head trauma in a 5-month-old male 325 79 PEG tube complication in a 7-month-old female 329 80 Cough and fever in a 10-month-old female 333 81 Vomiting in a 21-month-old male 337 82 Choking episode in a 21-month-old male 341 83 Abdominal pain and vomiting in a 23-month-old male 345 84 Vomiting, diarrhea and seizure in a 3-year-old male 349 85 Left arm and leg weakness in a 6-year-old female 353 86 Chest pain in a 9-year-old female 357 87 Headache and vomiting in a 12-year-old female 363XI. INFECTIOUS DISEASE 88 Back pain and fever in a 24-year-old male 369 89 Intermittent fevers, chills and headache in a 26-year-old male 373 90 Fever and rash in a 39-year-old male 379 91 Fever, abdominal pain and diarrhea in a 51-year-old male 383 92 Right groin pain and swelling in a 56-year-old female 387 93 Fatigue, weight loss, intermittent fevers and sweats in a 74-year-old male 391XII. TOXICOLOGY/ENVIRONMENTAL 94 Acute agitation and confusion in a 13-year-old male 397 95 Lethargy and bradycardia in a 14-year-old male 401 96 Acetaminophen overdose in a 17-year-old female 403 97 Headache and rash in a 21-year-old male 407 98 Bilateral foot pain and swelling in a 47-year-old male 411 99 Snakebite in a 55-year-old female 415100 Facial swelling in a 62-year-old female 421101 Intentional alkali ingestion in a 65-year-old female 425102 Symptomatic bradycardia in an 85-year-old female 429
x Contents XIII. MISCELLANEOUS 103 Bilateral leg swelling in a 30-year-old male 435 104 Headache and bruising in a 33-year-old female 437 105 Total body rash in a 33-year-old male 441 106 Bleeding gums and fatigue in a 40-year-old female 445 107 Vomiting and dizziness in a 47-year-old male 449 108 Right leg swelling in a 50-year-old male 453 109 Fever and rash in a 57-year-old male 457 110 Dehydration and general body weakness in a 75-year-old female 461 111 Left arm swelling in a 95-year-old female 465 Answer Index 469 Subject Index 471
PrefaceEmergency medicine is a tremendously challenging medical specialty. Fortunately,this ﬁeld is profoundly rewarding. It gives health care professionals the uniqueopportunity to help individuals at their time of greatest need. Sometimes, simplyoffering reassurance, kindness or compassion is all that we can do; the importanceof which should never be underestimated. In emergency medicine, health care professionals assist individuals whose pain,anxiety and stress levels are high. Often, our quick decisions and actions are life-saving. Emergency medicine personnel continuously use their extraordinary skills,knowledge and experience to “make things happen” and “get the job done,” in anattempt to positively impact patients and their families, signiﬁcant others, friendsand persons important to them. In reality, physicians, nurses, mid-level providers, paramedics, residents and med-ical students generally have time to look up information from various sources. Yetemergency personnel have the responsibility to provide services not available toindividuals at that moment anywhere other than an emergency department. There-fore, our purpose is even more vital. Practitioners with the most experience often provide the best care, which sug-gests that lifelong learning and learning from errors is crucial to medical practice(perhaps why it is called “practice”). Educators of and mentors for residents, med-ical students, nurses, mid-level providers, paramedics and support staff recognizethat the amount of knowledge one must possess is overwhelming. Often, knowinghow and where to obtain information at a moment’s notice is critical to successfulpatient care outcomes. With Clinical Emergency Medicine Casebook, we attemptto offer what we consider to be an essential yet underutilized strategy for learning:a case-based approach from real patients and actual events. There is agreement inmedicine that patients teach us a great deal; this textbook will provide the opportu-nity for signiﬁcant learning to occur at one’s leisure. Using carefully selected caseswith key teaching points, each learning opportunity (case) illustrates important clin-ical concepts that can expand even the most sophisticated learner’s knowledge base. Our goal is not to offer a deﬁnitive encyclopedia of emergency medicine (if such abook were possible). Rather, we have produced a unique textbook that gives readersthe chance to intelligently work through cases, rehearsing the approach they mighttake for a similar patient in their clinical setting, and what actions they might initiateto render outstanding patient care. Each case is arranged by organ system or specialcategory and is included because of its educational value and interest to clinicians.These cases are not exclusive to emergency medicine practice, even though eachoccurred at a single high-volume, high-acuity emergency department. The variety xi
xii Preface of cases offered should assist health care professionals in diverse ﬁelds who wish to improve their diagnostic and clinical skills. It is our hope that you, our colleagues, will beneﬁt from our efforts. Without question, future patients will beneﬁt from your efforts. With great admiration and respect for our specialty and those active in its prac- tice, we hope you enjoy Clinical Emergency Medicine Casebook. Gus M. Garmel, M.D. Joel T. Levis, M.D., Ph.D.
AcknowledgmentsJoel T. Levis and Gus M. Garmel wish to express gratitude to their emergencymedicine colleagues at Kaiser Santa Clara, California, for expertly caring for thepatients presented in this unique case-based textbook. We appreciate the assis-tance of several of our specialty colleagues from our medical center, whose inputhelped make this textbook a far superior resource for a much broader audience.Our medical staff colleagues who cared for these patients in the hospital and afterdischarge are to be praised for their efforts. Sonia Y. Johnson, M.D., an emergencymedicine colleague and gifted artist, offered beautiful illustrations that detail keypoints in several cases. Drs. Levis and Garmel are especially grateful to Amal Mattu,M.D., FACEP, FAAEM, Program Director for the Emergency Medicine Resi-dency, Co-Program Director for the Emergency Medicine/Internal Medicine Com-bined Residency and Associate Professor of Emergency Medicine, University ofMaryland School of Medicine. An incredibly talented author and educator himself,his enthusiasm for this project demonstrates his commitment to our specialty and hisrespect for us as leaders in medical education. Thank you, Amal, for your friendship,and for sharing your passion by contributing the foreword to our textbook. Finally,we appreciate the complete conﬁdence that Marc Strauss and the staff at CambridgeUniversity Press had in us and in our emergency medicine case-based resource. xiii
ForewordSir William Osler once said, “He who studies medicine without books sails anuncharted sea, but he who studies medicine without patients does not go to seaat all.” Osler championed the importance of providing clinical correlations to thelearning provided by books. In recent years, medical schools have come to recog-nize the importance of clinical correlations. The majority of medical schools in theUnited States have increased patient interactions for even ﬁrst- and second-yearmedical students. Education has become much more problem-based, using simu-lated cases and case presentations. However, the authors and editors of textbookshave been much slower to adapt to this change. The majority of medical textbooks,including those in the specialty of emergency medicine, remain disease-orientedrather than patient-oriented. In other words, readers are expected to improvetheir practice of medicine by reading about diseases rather than by reading aboutpatients. As a result, most textbooks occupy prominent positions on dusty book-shelves, rarely used, let alone read cover-to-cover. Fortunately, those of us who areteachers and students of emergency medicine are in luck. Two outstanding educa-tors have stepped forward to provide a text that will not be relegated to those dustybookshelves but will instead be relished and appreciated for its ability to help usnavigate those uncharted seas that Osler spoke of many years ago. Drs. Gus Garmel and Joel Levis have been teaching emergency medicine formany years. Both have proven track records of success in medical education.Dr. Garmel has received several prestigious national teaching awards and schol-arships and has published several important textbooks, many book chapters andnumerous articles. Dr. Levis has also been recognized among his peers for his schol-arly activities, including teaching, authorship and research. These dedicated educa-tors have already produced several successful academic collaborations. Congratula-tions to them for having the insight to produce a novel textbook that allows readersto study emergency medicine with the patient in mind. Clinical Emergency Medicine Casebook presents the reader with real-life casepresentations that cover the entire spectrum of the specialty of emergency medicine.These cases are presented in a succinct manner, with just enough information andrelevant visual clues that the patient seems to magically appear from within thepages. The reader is then prompted for a diagnosis and, with a ﬂip of the page,the clinically oriented teaching begins. The authors provide a diagnosis, followedby a concise discussion of the condition, including management plans and a set ofconcluding “Key Teaching Points” that reinforce the essentials of the case. Theirdetailed and thoughtful discussions frequently address myths, pitfalls and risk man-agement pearls useful for readers at every level, from student through experienced xv
xvi Foreword practitioner. Following the discussion and teaching points is a brief set of references and suggestions for further reading. The cases are organized in sections important to clinical practice. Within each section, the randomness of case presentations sim- ulates the randomness of actual emergency medicine practice, forcing readers to remain focused and “stay on their toes.” The quality of the cases selected is a particular strength of the text. Drs. Levis and Garmel have chosen cases that practicing emergency physicians are likely to see in a busy emergency department. Some cases are relatively common; for these, the authors provide critical teaching points that are often not well known. They have also included cases that are less commonly encountered in routine practice yet are equally important because of their likelihood for morbidity or mortality. For these cases, the authors focus on methods to minimize risk and improve patient outcomes. Esoteric cases have been speciﬁcally excluded in favor of maximizing practical teaching. Another obvious strength of the book is the quality of the visuals throughout the text. The electrocardiograms, radiographs, photos and illustrations are crisp and unambiguous in their demonstration of important ﬁndings, a rare quality in most medical texts. The text is therefore incredibly useful for gaining visual diagnosis skills. Overall, students, residents, mid-level providers and experienced emergency physicians will ﬁnd this book useful for improving their clinical practice and practical knowledge base. Kudos to Drs. Levis and Garmel, who have written a special textbook. Clini- cal Emergency Medicine Casebook represents a valuable addition to the emergency medicine literature. Students and clinicians will ﬁnd this unique book practical, easy to read and downright enjoyable. My sincere hope is that this text will serve as a model to other authors regarding the importance of bringing the patient to the reader. Amal Mattu, M.D., FAAEM, FACEP Director, Emergency Medicine Residency Co-Director, Emergency Medicine/Internal Medicine Combined Residency Associate Professor, Department of Emergency Medicine University of Maryland School of Medicine Coauthor, ECGs for the Emergency Physician, Volumes 1 and 2 Coeditor, Electrocardiography in Emergency Medicine Coeditor, Emergency Medicine: Avoiding the Pitfalls and Improving the Outcomes Consulting Editor, Emergency Medicine Clinics of North America
PART IHEENT (HEAD, EYES, EARS,NOSE AND THROAT)
1Sore throat in a 29-year-old maleHISTORY OF PRESENT ILLNESSA 29-year-old male with a medical history signiﬁcant for typeI diabetes presented to the ED complaining of a sore throat,inability to swallow solids and fevers to 103◦ F (39.4◦ C) for twodays. He noted a hoarse voice and was able to tolerate onlysmall sips of liquids. He denied signiﬁcant neck swelling orstiffness, and was able to tolerate his secretions. He had immi-grated to the United States from Mexico as a teenager, and hisimmunization status was unknown.PHYSICAL EXAMGENERAL APPEARANCE: The patient was a well-developed,nontoxic, moderately obese male who appeared slightly dehy-drated, sitting upright and in no acute distress.VITAL SIGNS Temperature 103◦ F (39.4◦ C) Pulse 100 beats/minute Blood pressure 145/85 mmHg Respirations 22 breaths/minute Oxygen saturation 100% on room air Figure 1.1 Soft-tissue lateral radiograph of the neck from a 29-year-HEENT: Oropharynx was pink and moist, no erythema, exu- old male with sore throat and inability to swallow solids.dates, tonsillar or uvular swelling noted.NECK: Supple, anterior cervical lymphadenopathy noted, ten-derness to palpation over cricoid cartilage noted.LUNGS: Clear to auscultation bilaterally.CARDIOVASCULAR: Regular rate and rhythm without rubs,murmurs or gallops.ABDOMEN: Soft, nontender, nondistended.EXTREMITIES: No clubbing, cyanosis or edema.A peripheral intravenous line was placed and blood wasdrawn and sent for laboratory testing. Laboratory tests weresigniﬁcant for a leukocyte count of 24 K/μL (normal 3.5–12.5 K/μL) with 92% neutrophils (normal 50–70%). A soft-tissue lateral neck radiograph was obtained (Figure 1.1). What is your diagnosis? 3
4 HEENT ANSWERThe diagnosis is epiglottitis. The soft-tissue lateral neck radio-graph demonstrates swelling of the epiglottis (“thumbprint”sign, Figure 1.2). The Ear, Nose and Throat (ENT) special-ist was urgently consulted, and bedside nasopharyngoscopydemonstrated a swollen, red epiglottis with 90% obstructionof the upper airway. The patient received ceftriaxone 1 gm anddecadron 10 mg intravenously, normal saline 1 liter IV bolus,and was admitted to the ICU for close monitoring and obser-vation. The patient was discharged on hospital day #4 after hissymptoms had improved. Repeat nasopharyngoscopy demon-strated signiﬁcant improvement of the epiglottic swelling. Hewas continued on cefpodoxime proxetil (VantinTM ) orally forten days following discharge.Epiglottitis in adults Figure 1.2 Soft-tissue lateral radiograph of the neck from a 29-year- old male with epiglottitis, demonstrating “thumbprint” sign (arrow).Acute epiglottitis is a potentially life-threatening condi-tion that results from inﬂammation of the supraglottic acute epiglottitis, although no randomized trials to date sup-structures.1,2 Commonly considered a pediatric disease, the port this practice.6current incidence of epiglottitis in adults is 1 to 2 casesper 100,000, which is presently 2.5 times the incidence in KEY TEACHING POINTSchildren.1 Epiglottitis occurs most frequently in men in theﬁfth decade; the disease is more common in countries that do 1. Acute epiglottitis is a potentially life-threatening conditionnot immunize against Haemophilus inﬂuenzae type B. Cur- resulting from inﬂammation of the supraglottic structures,rently, the most common cause of epiglottitis is infection, with a current incidence of 1 to 2 cases per 100,000 adultsalthough sources such as crack cocaine use have also been in the United States.implicated.1 Common pathogens include H. inﬂuenzae (Hib), 2. Sore throat is the chief complaint in 75–94% of cases ofβ-hemolytic streptococci and viruses. adult epiglottitis, whereas odynophagia may be present in The clinical presentation of adult epiglottitis may differ sig- as many as 94% of cases.niﬁcantly from that of the classic drooling child seated in a 3. Soft-tissue lateral neck radiography, which may show antripod position. The most common symptoms in adults are enlarged, misshapen epiglottis (“thumbprint” sign), has asore throat, odynophagia and mufﬂed voice.3 Sore throat is sensitivity of 88% in establishing the diagnosis.the chief complaint in 75–94% of cases, whereas odynopha- 4. The deﬁnitive diagnosis is made through direct laryngo-gia may be present in as many as 94% of cases.4 The pres- scopic visualization of an enlarged, inﬂamed epiglottis.ence of stridor signiﬁcantly increases the need for emergent 5. Treatment of epiglottitis includes intravenous antibioticsairway intervention.5 Unlike children with epiglottitis, where and close airway monitoring in an ICU setting. Most clini-emergency airway management is essential, most cases of cians treat acute cases with intravenous steroids.adult epiglottitis do not require acute airway intervention dueto the greater diameter of the adult airway. REFERENCES The leukocyte count is greater than 10,000 in 80% of  Belleza WG, Kalman S. Otolaryngologic emergencies in thecases of adult epiglottitis. Soft-tissue lateral neck radiog- outpatient setting. Med Clin N Am 2006;90:329–53.raphy, which may show an enlarged, misshapen epiglottis  Berger G, Landau T, Berger S, et al. The rising incidence of(“thumbprint” sign), has a sensitivity of 88% in establish- adult acute epiglottitis and epiglottic abscess. Am J Otolaryn-ing the diagnosis.3 Patients who appear ill or are in extremis gol 2003;24:374–83.should not leave the ED for radiographs, and airway manage-  Tan C-K, Chan K-S, Cheng K-C. Adult epiglottitis (Clinical Vistas Briefs). CMAJ 2007;176:602.ment in patients in extremis should be the ﬁrst and foremost  Bitner MD, Capes JP, Houry DE. Images in emer-responsibility. Direct laryngoscopy is the most accurate inves- gency medicine: adult epiglottitis. Ann Emerg Med 2007;tigation to establish a diagnosis of epiglottitis.3 Management 49:560,563.focuses on two important aspects: close monitoring of the air-  Katori H, Tsukuda M. Acute epiglottitis: analysis of fac-way with intubation (if necessary) and treatment with intra- tors associated with airway intevention. J Laryngol Otolvenous antibiotics.6 Antibiotics should be directed against 2005;119:967–72.Hib in every patient, regardless of immunization status. Cefo-  Alcaide ML, Bisno AL. Phayrngitis and epiglottitis. Infecttaxime, ceftriaxone or ampicillin/sulbactam are appropriate Dis Clin N Am 2007;21:449–69.choices. Steroids are commonly used in the management of
2Left eye pain and discharge in a 44-year-old maleHISTORY OF PRESENT ILLNESSA 44-year-old male with no signiﬁcant medical history pre-sented to the ED with several days of worsening left eye pain,discharge and decreased vision, as well as swelling and rednessto the eyelid and surrounding tissue. He did not wear contactlenses or eyeglasses. The patient currently could not see fromhis left eye. He denied fevers, headaches or recent trauma tothe eye, although he did report a foreign body sensation tothe eye several days prior to the onset of these symptoms. Hedenied experiencing similar symptoms in the past.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient appeared to be in no acutediscomfort.VITAL SIGNS Figure 2.1 A 44-year-old male with several days of swelling, redness Temperature 98.1◦ F (36.7◦ C) and exudate of his left eye. Pulse 75 beats/minute Blood pressure 135/85 mmHg Respirations 22 breaths/minute Oxygen saturation 100% on room airEYES: The visual acuity of the right eye was 20/40; the rightpupil was round and reactive to light. No vision or light per-ception was elicited from the left eye. The left upper and lowereyelids were swollen and erythematous. A thick yellow-greendischarge exuded from the left orbit; the pupil could not beexamined secondary to the thickness and adherence of theexudates. The left eye was proptotic (Figure 2.1). What is your diagnosis? 5
6 HEENT ANSWERThe diagnosis is endophthalmitis and orbital cellulitis of theleft eye. A CT scan of the orbits revealed a markedly proptoticleft ocular globe, as well as a markedly distended left anteriorchamber with mild posterior displacement of the hyperdenselens (Figure 2.2). The CT also demonstrated enhancing inﬁl-trate of the preseptal and periorbital soft tissues associatedwith the left orbit, consistent with orbital cellulitis. It was sur-mised that the patient had recently incurred a penetratinginjury to the globe, which resulted in endophthalmitis withextension to orbital cellulitis. The patient was started on intravenous antibiotics (ceftri-axone 1 gm q12 h and vancomycin 1 gm q12 h), as well asantibiotic eye drops (cefazolin and tobramycin, one drop eachq1 h) and aggressive lubrication of the eye. He was admittedto the medical service with close ophthalmology involvement.By hospital day #10, no improvement in the patient’s symp-toms occurred despite aggressive antibiotic therapy, and thedecision was made to surgically enucleate the left eye. Figure 2.2 CT of the orbits of a 44-year-old male demonstratingPeriorbital cellulitis, orbital cellulitis and endophthalmitis a markedly proptotic left ocular globe (dark arrow), as well as a markedly distended left anterior chamber with mild posterior dis-Periorbital cellulitis (also called preseptal cellulitis) is an infec- placement of the hyperdense lens (white arrow).tion that occurs anterior to the orbital septum. The orbital sep-tum is a layer of ﬁbrous tissue arising from the periosteumof the skull and continues into the eyelids. Because this layer intraocular surgery, penetrating trauma, or contiguous spreadprovides an effective barrier against the spread of infection from adjacent tissues. Endogenous endophthalmitis occursfrom the preseptal tissues into the orbit, periorbital celluli- when infectious agents are hematogenously disseminated intotis does not progress to orbital cellulitis.1 Periorbital tissue the eye from a distant focus of infection.6 Progressive vitri-may become infected either by trauma or due to primary bac- tis is a hallmark of any form of endophthalmitis. Histologi-teremia, which is especially common in young children at high cally, there is massive inﬁltration of the vitreous cavity withrisk for pneumococcal bacteremia.1 inﬂammatory cells, primarily neutrophils.5 In most instances, Orbital cellulitis is post-septal, with involvement of the vitreous inﬁltration is accompanied by progressive intraoc-orbit itself. It is most commonly the result of a complication ular inﬂammation associated with loss of vision, pain, andof ethmoid sinusitis, which accounts for more than 90% of hypopyon. Further progression may lead to panophthalmi-all cases.2 Orbital cellulitis can also be caused by the direct tis, corneal inﬁltration and perforation, orbital cellulitis, andextension of infection from the globe, eyelids, ocular adnexae phthisis bulbi (atrophy and degeneration of a blind eye).5and other periocular tissues, in addition to the sinuses. Orbital Decreased vision and permanent loss of vision are commoncellulitis is more common in children but can also occur in complications of endophthalmitis. Patients may require enu-adults.3 Along with eyelid edema and erythema seen in peri- cleation to eliminate a blind and painful eye. The most impor-orbital cellulitis, patients with orbital cellulitis have proptosis, tant laboratory studies are Gram stain and culture of the aque-chemosis (edema of the bulbar conjunctiva), impairment of ous and vitreous humor.6and pain with extraocular movements, and decreased extraoc- Diagnostic testing for orbital cellulitis starts with contrast-ular movements.1–4 The presence of fever, systemic signs, and enhanced CT imaging of the orbits.3 Findings on CT indicatingtoxicity is variable in patients with orbital cellulitis.4 Bacterial orbital cellulitis include any of the following: proptosis, inﬂam-causes of orbital cellulitis are most commonly Streptococcus mation of the ocular muscles, subperiosteal abscess or frankspecies, Staph aureus and Haemophilus inﬂuenzae Type B.2 orbital abscess.1 Ipsilateral (or bilateral) sinusitis should alsoPseudomonas, Klebsiella, Eikenella and Enterococcus are less be evident (except in cases where orbital cellulitis is causedcommon culprits. Polymicrobial infections with aerobic and by extension of endophthalmitis). Sinus disease is importantanaerobic bacteria are more common in patients 16 years or in the pathogenesis of orbital cellulitis but not of periorbitalolder.2 cellulitis.1 Purulent material from the nose should be col- Endophthalmitis is a serious intraocular inﬂammatory dis- lected with cotton or calcium alginate swabs and submitted fororder resulting from infection of the vitreous cavity.5 Ex- Gram stain and culture on aerobic and anaerobic media; anyogenous endophthalmitis occurs when infecting organisms material obtained from the sinuses or directly from an orbitalgain entry into the eye by direct inoculation, such as from abscess should be assessed in the same manner.2
Left eye pain and discharge in a 44-year-old male 7 Uncomplicated post-traumatic periorbital cellulitis can 2. The diagnostic test of choice for orbital cellulitis is agenerally be treated with oral antimicrobials directed against contrast-enhanced CT scan of the orbits, demonstratingGram-positive bacteria (e.g., cephalexin, dicloxacillin or proptosis, inﬂammation of the ocular muscles, and sub-clindamycin).1 The patient with orbital cellulitis should be periosteal or orbital abscess.promptly hospitalized for treatment, with ophthalmology and 3. Treatment of orbital cellulitis includes administration ofinfectious disease consultations. Historically, the presence of broad-spectrum intravenous antibiotics with close ophthal-subperiosteal or intraorbital abscess was an indication for mology involvement.surgical drainage in addition to antibiotic therapy; however, 4. Endophthalmitis, a serious intraocular inﬂammatory dis-medical management alone is successful in many cases.2 Intra- order resulting from infection of the vitreous cavity, mayvenous broad-spectrum antibiotics (e.g., second- and third- progress to orbital cellulitis.generation cephalosporins or ampicillin/sulbactam) should 5. Treatment of traumatic endophthalmitis includes hospitalbe started immediately until antibiotics can be tailored to admission and administration of intravenous, topical andpathogens identiﬁed on culture.2,3 Typically, intravenous intravitreal antibiotics.antibiotic therapy should be continued for 1 to 2 weeks, fol-lowed by oral antibiotics for an additional 2 to 3 weeks.1–3 Treatment of traumatic endophthalmitis includes admis- REFERENCESsion to the hospital with ophthalmologic consultation, intra-  Givner LB. Periorbital versus orbital cellulitis. Pediatr Infectvenous antibiotics (including vancomycin and an aminoglyco- Dis J 2002;21:1157–8.side or third-generation cephalosporin) and topical fortiﬁed  Harrington JN. Cellulitis, orbital. eMedicine Web site. Avail-antibiotics.6 Intravitreal antibiotics should be administered able at http://www.emedicine.com/oph/topic205.htm. Acces-by an ophthalmologist, with consideration for pars plana sed June 21, 2008.vitrectomy.5,6 Tetanus immunization is necessary if immuniza-  Pasternak A, Irish B. Ophthalmologic infections in primary care. Clin Fam Pract 2004;6:19–33.tion is not current.  Wald ER. Periorbital and orbital infections. Infect Dis Clin N Am 2007;21:393–408.KEY TEACHING POINTS  Lemley CA, Han DP. Endophthalmitis: a review of current evaluation and management. Retina 2007;27:662–80.1. Clinical signs and symptoms of orbital cellulitis include  Peters JR, Egan DJ. Endophthalmitis. eMedicine Web eyelid edema and erythema, proptosis, chemosis, pain with site. Available at http://www.emedicine.com/emerg/topic880. extraocular movements and ophthalmoplegia. htm. Accessed June 21, 2008.
3Sudden, monocular vision loss in a 62-year-old femaleHISTORY OF PRESENT ILLNESSA 62-year-old female with no signiﬁcant medical history pre-sented to the ED complaining of seeing “ﬂoaters” and ﬂash-ing lights in her right eye associated with loss of vision in theright inferolateral visual ﬁeld (affecting only her right eye) forthe past three days. She did not wear eyeglasses or contactlenses, and denied pain, redness or discharge from the eye.She denied trauma to the eye or headaches.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient appeared well developedand in no acute discomfort.VITAL SIGNS Temperature 98.6◦ F (37◦ C) Pulse 80 beats/minute Figure 3.1 Ultrasound image of the right eye from a 62-year-old female with 3 days of ﬂoaters and an inferolateral visual ﬁeld deﬁcit Blood pressure 135/85 mmHg of the right eye. Respirations 20 breaths/minute Oxygen saturation 100% on room air Visual acuity OD 20/100 OS 20/20 OU 20/40EYES: PERRL, EOMI and no afferent pupillary defect. Lids,lashes and lacrimal glands normal, no conjunctival or scleralinjections, no ocular discharge. The cornea was clear, withoutedema, ﬂuorescein uptake or cloudiness. No cell or ﬂare onslit lamp examination. Right inferolateral visual ﬁeld deﬁcitaffecting the right eye only. Retinal examination of both undi-lated eyes was normal. Intraocular pressures were 12 mmHgOD and 16 mmHg OS, respectively. A linear, 10-MHz ultrasound probe was gently placed overthe closed right eye using a small amount of water-soluble gel(Figure 3.1). What is your diagnosis? 9
10 HEENT ANSWERThe diagnosis is retinal detachment. The ultrasound imagedemonstrates an inferolateral detachment of the retina(arrow, Figure 3.2). The ophthalmologist was urgently con-sulted, and conﬁrmed the presence of retinal detachmentupon dilated retinal examination of the right eye. The patientunderwent microsurgical repair of the retinal detachment,regaining normal vision of her right eye.Retinal detachmentRetinal detachment (RD) involves separation of the retinafrom the underlying retinal epithelium (Figure 3.3). It affectsapproximately 2 in 10,000 people per year.1 Risk factors Figure 3.3 Retinal detachment.for the development of RD include increasing age, previ-ous cataract surgery, focal retinal atrophy, myopia, trauma,diabetic retinopathy, family history of RD, uveitis, and emergency physicians.4–8 The diagnosis of retinal detach-prematurity.1 Patients complain of new ﬂoaters, squiggly lines ment can be made using almost any ultrasonographic probe,or cobwebs that appear abruptly, associated with visual ﬁeld although a linear probe such as the 7.5- to 10-MHz probe isloss.2 Over time, the patient may report a shadow in the preferred. The patient is asked to look straight ahead withperipheral visual ﬁeld, which, if ignored, may spread to involve closed, but not clenched, eyelids. The probe is placed perpen-the entire visual ﬁeld in a matter of days.3 Vision loss may be dicular to the orbit, using conduction gel and minimal pres-ﬁlmy, cloudy, irregular or curtain-like. sure to obtain the image.5 Care should be taken to avoid plac- Examination of the eyes should begin with an assessment ing excessive pressure on the globe while performing the scan,of the visual acuity. The external eye examination should particularly if there is concern for globe rupture (in the settinginclude inspection for any signs of trauma and confrontational of trauma).visual ﬁeld testing; the latter can assist in isolating the loca- RD requires urgent consultation with an ophthalmologist.tion of the RD.3 Pupillary reaction should be checked, and Surgical repair of retinal detachments, typically performeda slit lamp biomicroscopy performed. Intraocular pressures by a retinal specialist, has a high success rate.1 More inva-should be measured in both eyes, as hypotony of more than sive therapies, such as scleral buckling and posterior vitrec-4–5 mmHg less than the unaffected eye is common in RD.3 tomy, have success rates of nearly 90%, whereas less invasiveFinally, a funduscopic examination with ophthalmoscopy is therapies, such as pneumatic retinopexy, may be performedrequired. This examination may not reveal the RD, particu- in an ofﬁce setting in select cases. If the repair is technicallylarly in an undilated eye, as the detachment may be at the successful, visual acuity is often restored to predetachmentperiphery of the retina where the retina is the thinnest.2 levels.1 Patients with new onset visual loss can be rapidly assessedfor RD using bedside ultrasound, readily performed by KEY TEACHING POINTS 1. Retinal detachment (RD) involves separation of the retina from the underlying retinal epithelium, and affects approx- imately 2 in 10,000 people per year. 2. RD is an ophthalmologic emergency, requiring urgent oph- thalmology consultation. 3. Patients with RD complain of new ﬂoaters, squiggly lines or cobwebs that appear abruptly, associated with visual ﬁeld loss. 4. Key components of the ocular examination include visual acuity testing, gross and slit lamp inspection of both eyes, visual ﬁeld confrontation and extraocular movement as- sessment, pupillary response to light and accommodation, testing of intraocular pressures, and fundoscopic examina- tion (best performed on a dilated eye).Figure 3.2 Ultrasound image of right eye from a 62-year-old female 5. Bedside ultrasound is a useful and readily available tool fordemonstrating inferolateral retinal detachment (arrow). making the diagnosis of RD in the emergency department.
Sudden, monocular vision loss in a 62-year-old female 11  Lewin RM, Williams SR, Ahuja Y. Ultrasonographic diagno-REFERENCES sis of retinal detachment in the emergency department. Ann Vortmann M, Schneider JI. Acute monocular visual loss. Emerg Med 2005;45:97–8. Emerg Med Clin N Am 2008;26:73–96.  Kahn An, Kahn Am, Corinaldi C. Retinal detachment diag- Magauran B. Conditions requiring emergency ophthalmo- nosed by bedside ultrasound in the emergency department. logic consultation. Emerg Med Clin N Am 2008;26:233–8. West J Emerg Med 2005;6:47–51. Larkin GL. Retinal detachment. eMedicine Web site. Avail-  Babineau MR, Sanchez LD. Ophthalmologic procedures able at http://www.emedicine.com/EMERG/topic504.htm. in the emergency department. Emerg Med Clin N Am Accessed July 10, 2008. 2008;26:17–34. Blaivas M, Theodoro DL, Sierzenski PR. A study of bedside  Shinar Z. Images in emergency medicine: Retinal detach- ocular ultrasonography in the emergency department. Acad ment. West J Emerg Med 2008;9:54. Emerg Med 2002;9:462b–3b.
4Syncope and monocular vision loss ina 76-year-old femaleHISTORY OF PRESENT ILLNESSA 76-year-old female with a medical history signiﬁcant forhypertension, hypothyroidism, hyperlipidemia and chronicrenal insufﬁciency presented to the ED after fainting whileshopping. She reported feeling lightheaded and dizzy whilewalking in a grocery store, at which time she experienced abrief loss of consciousness. She fell to the ﬂoor, bystanderscalled emergency services but she quickly regained conscious-ness. She denied head trauma or neck pain after the fall. Shealso denied chest pain but had been experiencing some short-ness of breath with exertion over the past several weeks, as Figure 4.1 Noncontrast CT of the brain from a 76-year-old femalewell as low back pain and bilateral thigh pain worse in the with syncope and monocular vision loss.morning. She also noted gradually worsening vision in herright eye over the past week, increasing redness to that eye,and a mild, right-sided headache; her vision prior to this had CARDIOVASCULAR: Bradycardic rate, regular rhythm withoutbeen normal. Upon presentation to the ED, she could per- rubs, murmurs or gallops.ceive light and vague shapes with the right eye. Her med- LUNGS: Clear to auscultation bilaterally.ications included metoprolol, hydrochlorothiazide, Cozaar,levothyroxine, lovastatin and ibuprofen 400 mg orally twice ABDOMEN: Soft, nontender, nondistended.daily for low back pain. She denied tobacco use, drank alcohol RECTAL: Normal tone, brown stool, hemoccult negative.occasionally, lived alone and drove a car for transportation. EXTREMITIES: No clubbing, cyanosis or edema.PHYSICAL EXAMINATION NEUROLOGIC: Visual acuity deﬁcit of right eye (cranial nerveGENERAL APPEARANCE: The patient appeared well hydrated II) as described; remaining neurologic examination nonfocal.and well nourished, and in no acute discomfort.VITAL SIGNS A peripheral intravenous line was placed and blood was Temperature ◦ ◦ 98 F (36.6 C) drawn and sent for laboratory testing. A 12-lead ECG demon- Pulse 54 beats/minute strated sinus bradycardia, rate 56, without the presence of ST- Blood pressure 138/53 mmHg T wave changes. A noncontrast CT of the brain was obtained Respirations 22 breaths/minute (Figure 4.1). Laboratory tests were signiﬁcant for a leuko- Oxygen saturation 98% on room air cyte count of 12.6 K/μL (normal 3.5–12.5 K/μL) with 81% Visual acuity OS 20/50 neutrophils (normal 50–70%), hematocrit of 27% (normal OD light perception and hand 34–46%), creatinine of 1.7 mg/dL (normal < 1.1 mg/dL), ery- motion only (unable to count throcyte sedimentation rate (ESR) of 120 mm/hr (normal ﬁngers) 0–20 mm/hr) and C-reactive protein (CRP) of 18.2 mg/dL (normal < 0.9 mg/dL). The electrolytes, glucose and troponinHEENT: Atraumatic, normocephalic, PERRL, EOMI, no I were within normal limits, and a urinalysis did not show signsafferent pupillary defect. Sclera of the right eye red and of infection.injected, no discharge. Tenderness to palpation over rightforehead. No facial lesions or asymmetry noted. What is your diagnosis?NECK: Supple, no jugular venous distension. 13
14 HEENT the most common dreaded complication if temporal arteritis is ANSWER left untreated or inadequately treated. This complication mayThe diagnosis is temporal arteritis and normochromic, normo- be seen in up to half of patients.5 Affected patients typicallycytic anemia. The CT scan of her brain was normal. Her syn- report partially-obscured vision (“a shade covering one eye”),cope was attributed to her anemia. The patient was admit- which may progress to total blindness.4 If untreated, the otherted to the medicine service and transfused with two units eye is likely to become affected within 1 to 2 weeks. Onceof packed red blood cells. Her post-transfusion hematocrit established, visual impairment is usually permanent. Blurring,improved to 33%. Ophthalmology was urgently consulted and diplopia or amaurosis fugax occurs in 65% of patients beforethe patient was started on oral prednisone 50 mg per day, the development of permanent visual loss.2 The progressionwith the ﬁrst dose given in the ED. She was discharged on to permanent visual loss occurs an average of 8.5 days afterhospital day #2 without visual improvement of the right eye. these early ﬁndings.2She underwent an outpatient temporal artery biopsy two days The ESR is a well-known marker for inﬂammatory con-later, which conﬁrmed the diagnosis of temporal arteritis. The ditions, including GCA. Most patients with GCA have anpatient’s oral prednisone dose was increased to 80 mg daily ESR greater than 50 mm/hr.2 Although GCA studies have notat that time. By six weeks, her CRP had normalized and the established a well-deﬁned normal ESR, past studies have sug-ESR had decreased to 56 mm/hr; minimal improvement in her gested a normal value of (age/2) for men and (age + 10)/2right eye’s vision was noted, whereas no visual changes had for women.2,6 A 2002 meta-analysis found that only 4% ofoccurred in the left eye. A gradual taper of prednisone was patients with biopsy-proven GCA had normal ESRs.6 As adone over three months. Over this period, her vision slowly nonspeciﬁc marker of inﬂammation, an ESR greater than 50improved but not completely back to her baseline. has a reported speciﬁcity of 48%.2 The CRP level has been found to be a more sensitive indicator of disease than the ESR both at diagnosis and during relapse.4 One small study foundTemporal arteritis that a CRP greater than 6 mg/dL occurred in 49 of 55 cases ofTemporal arteritis, also called giant-cell arteritis (GCA), is a GCA.7 There is conﬂicting literature on the accuracy of CRPgranulomatous arteritis of the aorta and its major branches or ESR to diagnose and follow GCA, with some authors favor-with a predilection to affect the extracranial branches of the ing CRP and others favoring ESR.2 Following both may becarotid artery.1 Although it can be seen in a variety of popu- helpful.lations, there is an epidemiologic predilection for people of The presence of normocytic, normochromic anemia isNorthern European decent and those living at higher lati- another helpful ﬁnding. Although pooled data have showntudes.2 Women are twice as likely to be affected as men. Cases only 44% sensitivity for positive biopsy, anemia can be helpfulare rare before 50 years of age; the incidence increases with when evaluating disease activity.8 Studies have shown a nega-age, peaking in the eighth decade.2 The incidence of temporal tive correlation between the presence of anemia and the like-arteritis is 15 to 25 per 100,000 in adults over 50 years of age lihood to progress to ischemic complications, such as perma-in the United States, and peaks at 1100 per 100,000 persons at nent vision loss.285 years of age.2 Temporal artery biopsy conﬁrms GCA in 50–80% of cases, In giant-cell arteritis, transmural inﬂammation of the arter- demonstrating a panmural mononuclear cell inﬁltration thaties induces luminal occlusion through intimal hyperplasia.3 can be granulomatous with histiocytes and giant cells.1 ToClinical symptoms reﬂect end-organ ischemia. Branches of the increase yield, the length of the biopsy specimen should beexternal and internal carotid arteries are particularly suscep- at least 3–5 cm and sampled at multiple levels.1 Biopsy doestible. Their involvement leads to the classic manifestations of not need to be performed urgently in the ED; it can be per-blindness, headache, scalp tenderness and jaw claudication.3 formed as an outpatient.9 In patients suspected of havingSystemic symptoms (fatigue, malaise, anorexia, fever) are GCA, treatment with steroids should be instituted immedi-present in about half of patients.4 A headache is probably the ately to preserve vision while a prompt temporal artery biopsymost frequent symptom, occurring in two-thirds of patients.2,4 is arranged.1 Although steroid therapy may affect biopsyThe pain is frequently severe and tends to be located over results, inﬂammatory changes usually persist for 2 to 4 weeksthe temporal or occipital areas; however, it may be less well- after initiation of treatment.9deﬁned. Scalp tenderness is usually conﬁned to the temporal Steroids prevent visual complications in GCA, and bringand, less commonly, occipital arteries, but may be diffuse. On about rapid improvement in clinical symptoms.1 The opti-physical examination, the frontal or parietal branches of the mal initial dosage remains controversial, but most investiga-superﬁcial temporal arteries may be thickened, nodular, ten- tors support that prednisone be initiated at a dose of 40–der or occasionally erythematous.4 Pulses may be decreased 60 mg/day.1 Symptomatic improvement usually occurs withinor absent. Nearly half of patients suffer jaw claudication. In the ﬁrst 1 to 2 weeks following the initiation of prednisone,rare cases, vascular narrowing may lead to infarction of the accompanied by a reduction in ESR over the ﬁrst month. Thescalp or tongue.4 duration of maintenance therapy with prednisone (following Unilateral or bilateral blindness (resulting from arteritis of a taper) may last for one year or more, depending upon thethe intraorbital posterior ciliary and central retinal arteries) is patient’s response.9 Although thromboembolic occlusion is
Syncope and monocular vision loss in a 76-year-old female 15not a likely mechanism in the development of GCA, ther- REFERENCESapeutic beneﬁt in its treatment has been reported with the  Langford CA. Vasculitis in the geriatric population. Clinuse of low-dose aspirin.3 Prevention of platelet aggregation Geriatr Med 2005;21:631–47.is potentially effective, even in patients with partial luminal  Donnelly JA, Torregiani S. Polymyalgia rheumatica andocclusion. giant cell arteritis. Clin Fam Pract 2005;7:225–47.  Weyand CM, Goronzy JJ. Mechanisms of disease: medium- and large-vessel vasculitis. N Engl J Med 2003;349:160–9.KEY TEACHING POINTS  Salvarani C, Cantini F, Boiardi L, et al. Medical progress: polymyalgia rheumatica and giant-cell arteritis. N Engl J1. Symptoms of temporal arteritis (also known as giant-cell Med 2002;347:261–71. arteritis) may be nonspeciﬁc, including headache, scalp  Younger DS. Headaches and vasculitis. Neurol Clin N Am tenderness, jaw claudication and gradual vision loss. 2004;22:207–28.2. If left untreated, temporal arteritis can result in unilateral  Smetana GW, Shmerling RH. Does this patient have tempo- or bilateral blindness. ral arteritis? JAMA 2002;287:92–101.3. The erythrocyte sedimentation rate (ESR) and C-reactive  Kyle V, Cawston TE, Hazleman BL. Erythrocyte sedimen- protein (CRP) are the most useful laboratory tests in tation rate and C reactive protein in the assessment of polymyalgia rheumatica: giant cell arteritis on presentation diagnosing and following the clinical course of temporal and during follow up. Ann Rheum Dis 1989;48:667–71. arteritis.  Evans JM, O’Fallon WM, Hunder GG. Increased incidence4. Temporal artery biopsy is the gold standard for the diagno- of aortic aneurysm and dissection in giant cell (tempo- sis of temporal arteritis. ral) arteritis: a population-based study. Ann Intern Med5. Prednisone is the mainstay of treatment for temporal 1995;122:505–7. arteritis, and should be started once the diagnosis of tem-  Egland AG, Jackson LW. Temporal arteritis. eMedicine poral arteritis is considered, before a temporal artery Website. Available at http://www.emedicine.com/EMERG/ biopsy is performed or the results are known. topic568.htm. Accessed June 24, 2008.
5Eye pain and blurred vision in an 89-year-old femaleHISTORY OF PRESENT ILLNESSAn 89-year-old female with an ophthalmologic history signif-icant for open angle glaucoma in both eyes, who had failedmedical management and had undergone trabeculectomy withmitomycin C treatment to the left eye six months earlier, pre-sented to the ED with several days of progressively worseningvision, redness, pain, photophobia and discharge from her lefteye. She denied trauma or new eye drops and did not wearcontact lenses.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient was an elderly female inno acute discomfort.VITAL SIGNS Temperature 98.6◦ F (37◦ C) Figure 5.1 Left eye of an 89-year-old female with progressively wors- Pulse 88 beats/minute ening vision, redness, pain and photophobia. Blood pressure 150/90 mmHg Respirations 18 breaths/minute Oxygen saturation 99% on room airEYES: Visual acuity: 20/40 OD; ﬁnger counting at 5 feet OS. PERRL, EOMI. Intraocular pressures measured 10 mmHgOD and 18 mmHg OS, respectively. Gross inspection of the left eye: redness and swellingto lids, conjunctival injection, mucoid discharge, layering ofmilky material to inferior portion of cornea (Figure 5.1). What is your diagnosis? 17
18 HEENT Treatment with empiric antibiotics must be prompt ANSWER because endophthalmitis can result in a poor visual outcomeThe diagnosis is endophthalmitis with hypopyon. Figure 5.1 if not treated aggressively.4 Emergent consultation with andemonstrates several of the ﬁndings of this condition: a red ophthalmologist is necessary once this diagnosis is enter-eye with circumlimbal ﬂush, a hypopyon (inﬂammatory cells tained. Endophthalmitis is an ophthalmologic emergency, asand exudates [pus] layered in the anterior chamber of the eye), the patient is in danger of losing his or her vision.2 Emergencyand purulent discharge on the lid margin and eyelashes. The treatment should begin with a dose of broad-spectrum intra-patient received gatiﬂoxacin 0.3% eye drops to the left eye, venous antibiotics. Intravitreal antimicrobial therapy remainsand her eye was subsequently dilated with tropicamide 1% the mainstay of treatment.3 The majority of patients requireand phenylephrine 2.5% drops. The patient was taken to the intravitreal injections, vitreous tap, subconjunctival steroids orOR emergently by the ophthalmologist, where a vitrectomy vitrectomy to prevent loss of the eye.4with intravitreal injection of antibiotics was performed. Thepatient was discharged that same day to continue gatiﬂoxacinand prednisolone eye drops every hour while awake, with a KEY TEACHING POINTSfollow-up appointment with the ophthalmologist the follow- 1. Endophthalmitis is an ophthalmologic emergency requir-ing day. ing a high index of suspicion and prompt consultation with an ophthalmologist.Endophthalmitis 2. Initial symptoms of endophthalmitis include pain, redness, ocular discharge and blurring of vision.Endophthalmitis is an infection involving the deep struc- 3. Common signs include decreased visual acuity, lid swelling,tures of the eye, namely the anterior, posterior and vitre- conjunctival and corneal edema, anterior chamber cellsous chambers.1 Noninfectious (sterile) endophthalmitis may and ﬁbrin, hypopyon, vitreous inﬂammation, retinitis, andresult from various causes, such as retained native lens mate- blunting of the red reﬂex.rial after an operation or from toxic agents.2 The two classi- 4. Intravitreal antimicrobial therapy remains the mainstay ofﬁcations of endophthalmitis are endogenous and exogenous. treatment for infectious endophthalmitis; the majority ofEndogenous endophthalmitis results from the hematogenous patients require intravitreal injections, vitreous tap, sub-spread of organisms from a distant source of infection (e.g., conjunctival steroids or vitrectomy to prevent loss of theendocarditis).2 Exogenous endophthalmitis results from direct eye.inoculation of the eye as a complication of ocular surgery, for-eign bodies, or blunt or penetrating trauma.1,2 Acute postoperative endophthalmitis refers to infectious REFERENCESendophthalmitis that occurs shortly after ocular surgery. Most  Burnette DD. Ophthalmology. In: Marx JA, Hockberger RS,patients present within 1 to 2 weeks of surgery, often within Walls RM, et al. (eds). Rosen’s Emergency Medicine: Con-a few days. Initial symptoms are often rapidly progressive, cepts and Clinical Practice, 6th ed. Mosby, 2006:1052.including pain, redness, ocular discharge and blurring.3 Com-  Egan DJ, Radin PJ, Peak DA. Endophthalmitis. eMedicinemon signs include decreased visual acuity, lid swelling, con- Website. Available at http://www.emedicine.com/emerg/junctival and corneal edema, anterior chamber cells and ﬁb- topic880.htm. Accessed June 27, 2008.rin, hypopyon, vitreous inﬂammation, retinitis, and blunting  Lemley CA, Han DP. Endophthalmitis: a review of currentof the red reﬂex.3 Common pathogens of endophthalmitis are evaluation and management. Retina 2007;27:662–80.Staphylococcus, Streptococcus and Bacillus1 . Endophthalmitis  Naradzay J, Barish RA. Approach to ophthalmologic emer-caused by H. inﬂuenza has been documented, occurring from gencies. Med Clin N Am 2006;90:305–28.6 days up to 18 months after invasive eye surgery.4
6Palpitations and chest heavinessin a 26-year-old femaleHISTORY OF PRESENT ILLNESS NECK: Supple, no jugular venous distension.A 26-year-old female with no signiﬁcant medical history pre- CARDIOVASCULAR: Tachycardic rate, regular rhythm, no rubs,sented to the ED complaining of two hours of palpitations, murmurs or gallops.mild chest pressure and general body weakness. She deniedshortness of breath, nausea, sweating or leg swelling. She LUNGS: Clear to auscultation bilaterally.denied drugs, alcohol or tobacco use, as well as pregnancy. ABDOMEN: Soft, nontender, nondistended.PHYSICAL EXAMINATION EXTREMITIES: No clubbing, cyanosis or edema; radial pulsesGENERAL APPEARANCE: The patient was well nourished and were rapid and weak.well hydrated, appeared tired but easily arousable. NEUROLOGIC: Nonfocal.VITAL SIGNS Temperature 97.2◦ F (36.2◦ C) The patient was placed on the cardiac monitor, a peripheral Pulse 142 beats/minute intravenous line was placed and a 12-lead ECG was obtained Blood pressure 123/70 mmHg (Figure 6.1). Respirations 20 breaths/minute Oxygen saturation 100% on room air What is your diagnosis?HEENT: Unremarkable. Figure 6.1 12-lead ECG from a 26-year-old female with palpitations and chest pressure. 21
22 Cardiovascular involved in re-entry. Left axis deviation is noted with left pos- ANSWER terior fascicular tachycardia; right axis deviation is presentThe diagnosis is idiopathic fascicular ventricular tachycardia with left anterior fascicular tachycardia. IFVT shows a typical(IFVT). The ECG in Figure 6.1 shows a tachycardia with- rSR morphology in lead V1.3 This type of idiopathic ventric-out obvious P waves, widened QRS complexes with a regu- ular tachycardia is also known as intrafascicular tachycardia,lar rhythm and rate of 142, and a right bundle branch block verapamil-sensitive VT, or Belhassen tachycardia.3pattern with a left anterior fascicular block. The patient was Fascicular tachycardia is typically seen in individuals with-initially given adenosine IV without any affect on the rate out structural heart disease, usually occurring in patients 15–or rhythm. The patient was then given IV diltiazem, which 40 years old. It occurs more frequently in men than women.1–3caused a slowing of the ventricular rate. A repeat ECG Patients tend to present with paroxysmal sustained tachycar-(Figure 6.2) was obtained, which demonstrated P waves inde- dia; initiation of tachycardia may occur with exercise. Ter-pendent of QRS complexes. This ﬁnding is consistent with mination usually requires administration of an intravenousAV dissociation and ventricular tachycardia arising in the antiarrhythmic medication.3 Sometimes the tachycardia canHis-Purkinje system. Shortly thereafter, her rhythm sponta- be incessant, resulting in tachycardia-induced cardiomyopa-neously converted to normal sinus rhythm (Figure 6.3). A bed- thy. Symptoms may range from none to palpitations, short-side echocardiogram performed in the ED after cardioversion ness of breath, fatigue or dizziness; syncope or sudden deathdemonstrated normal left ventricular function with an ejection is extremely rare in these patients.3fraction of 55%. The patient was admitted to the telemetry Intravenous verapamil is effective in terminating theunit for continued monitoring overnight, and was started on IFVT;1–3 in 1981, Belhassen et al. were among the ﬁrst to reportﬂecainide and metoprolol orally. She was discharged from the termination or suppression of IFVT by the calcium-channelhospital the following day in normal sinus rhythm with normal blocker, verapamil.4 However, the efﬁcacy of oral verapamilvital signs, with close follow up in the cardiology clinic. in preventing tachycardia relapse is variable.2 Calcium-chan- nel blockers should be used with extreme caution, especially if a wide-complex tachycardia is present or the diagnosis ofIdiopathic fascicular ventricular tachycardia IFVT is in question. In these cases, an adenosine trial shouldIdiopathic monomorphic ventricular tachycardia (VT) can be occur ﬁrst. Although fascicular tachycardias do not generallysubdivided into three distinct subgroups: fascicular, adenosine- respond to adenosine, termination of VT originating fromsensitive, and automatic (propranolol-sensitive) VT.1 Idiopa- the left anterior fascicle by intravenous adenosine has beenthic fascicular ventricular tachycardia (IFVT) is characterized documented.1 Radiofrequency catheter ablation proceduresby a relatively narrow QRS complex and a right bundle branch have demonstrated a 90% success rate for the treatment ofblock pattern.2 The QRS axis depends on which fascicle is fascicular tachycardia with minimal complications.3 Figure 6.2 12-lead ECG from a 26-year-old female with palpitations after treatment with IV diltiazem (arrows on lead II identify P waves).
Palpitations and chest heaviness in a 26-year-old female 23 Figure 6.3 12-lead ECG from a 26-year-old female with palpitations demonstrating normal sinus rhythm.KEY TEACHING POINTS including ventricular tachycardia. Despite being the treat- ment for IFVT, adenosine is a safer ﬁrst-line agent.1. Idiopathic fascicular ventricular tachycardia (IFVT) is an important cardiac dysrhythmia with speciﬁc electrocardio- REFERENCES graphic features (a relative narrow QRS complex and a right bundle branch block pattern) and therapeutic options  Kassotis J, Slesinger T, Festic E, et al. Adenosine-sensitive (verapamil, diltiazem or adenosine). wide-complex tachycardia: an uncommon variant of idio-2. IFVT usually occurs in young patients from 15–40 years of pathic fascicular ventricular tachycardia – a case report. Angiology 2003;54:369–72. age without structural heart disease.  Johnson F, Venugopal K, Khadar SA, et al. Idiopathic fasci-3. Symptoms of IFVT range from none to palpitations, short- cular ventricular tachycardia. Indian Pacing Electrophysiol J ness of breath, fatigue or dizziness. Syncope or sudden 2004;4:98–103. death is extremely rare in these patients.  Chiu C, Sequeira IB. Diagnosis and treatment of idiopathic4. Intravenous verapamil is effective in terminating IFVT, ventricular tachycardia. AACN Clinical Issues 2004;15:449–61. whereas catheter ablation procedures demonstrate a 90%  Belhassen B, Rotmensch H, Laniado S. Response of recur- success rate for the long-term suppression of these dys- rent sustained ventricular tachycardia to verapamil. Br Heart rhythmias. J 1981;46:679–82.5. Caution should be taken in using calcium-channel blockers as ﬁrst-line treatment for any wide-complex tachycardia,
7Chest pain in a 26-year-old maleHISTORY OF PRESENT ILLNESS HEENT: PERRL, EOMI, dry mucous membranes.A 26-year-old male with no signiﬁcant medical history pre- NECK: Supple, no jugular venous distension.sented to the ED complaining of several hours of subster-nal chest pain after using cocaine daily for the preceding six CARDIOVASCULAR: Tachycardic rate, regular rhythm withoutdays. His last cocaine use was 24 hours prior to presentation. rubs, murmurs or gallops.He described the chest pain as central, pressure-like, constant LUNGS: Clear to auscultation bilaterally.and nonradiating. He also reported associated palpitations,shortness of breath and diaphoresis, as well as several days of ABDOMEN: Soft, nontender, nondistended.insomnia and anorexia. He had been drinking tequila for the EXTREMITIES: No clubbing, cyanosis or edema, brisk radialpast 24 hours in an effort to “calm himself down.” and dorsalis pedis pulses.PHYSICAL EXAMINATION SKIN: Warm and moist, no rashes.GENERAL APPEARANCE: The patient appeared well developed NEUROLOGIC: Nonfocal.and well nourished, anxious and diaphoretic, and in no acutediscomfort. The patient was placed on the cardiac monitor, a peripheralVITAL SIGNS intravenous line was placed and blood was drawn and sent for Temperature 99.1◦ F (37.3◦ C) laboratory testing. A 12-lead ECG was obtained (Figure 7.1). Pulse 132 beats/minute Blood pressure 150/92 mmHg What is your diagnosis? Respirations 24 breaths/minute Oxygen saturation 98% on room air Figure 7.1 12-lead ECG from a 26-year-old male with several hours of chest pain. 25
26 Cardiovascular Nitroglycerin has been shown to alleviate cocaine-induced ANSWER vasoconstriction in patients with CAD.6 Furthermore, theThe diagnosis is cocaine-associated chest pain. The ECG early use of lorazepam in combination with nitroglycerin(Figure 7.1) demonstrates sinus tachycardia, rate 142, with seems to be more efﬁcacious than nitroglycerin alone in reliev-nonspeciﬁc ST-T wave changes. The patient received a total ing chest pain associated with cocaine use.7 Patients who con-of 3 liters normal saline IV infusion, three 1-mg doses of tinue to have chest pain despite the administration of oxygen,lorazepam IV, aspirin 162 mg orally, and was observed for benzodiazepines, aspirin and nitroglycerin may be treatedeight hours in the ED. His chest pain resolved with intra- with low-dose IV phentolamine (1 mg).4 Phentolamine hasvenous ﬂuids and lorazepam. Laboratory tests revealed an ini- been shown to reverse cocaine-induced coronary artery vaso-tial troponin I less than 0.02 ng/mL (normal 0.00–0.09 ng/mL), constriction in humans.CK 120 U/L (normal 38–174 U/L), creatinine of 1.36 mg/dL A prospective study has attempted to validate the use(normal 0.8–1.5 mg/dL) and hematocrit of 52% (normal 39– of 9- to 12-hour observation periods in low- to moderate-51%), with the remainder of laboratory tests within normal risk patients who experience cocaine-associated chest pain.8limits. A repeat troponin I obtained four hours following Patients with normal troponin I levels, no evidence of newthe ﬁrst was also normal (< 0.02 ng/mL). On discharge, the ischemic changes on ECG and no cardiovascular complica-patient was symptom-free with a pulse of 90 beats/minute and tions (AMI, dysrhythmias or recurrent symptoms) were dis-a blood pressure of 126/80 mmHg. The patient was instructed charged from the observation unit. During the 30-day follow-to avoid cocaine and was scheduled for an outpatient ECG up period, none of the 302 patients in the cohort died from atreadmill, which subsequently did not demonstrate any evi- cardiovascular event, and only 4 patients with detailed follow-dence of exercise-induced ischemia. up had a MI (1.6%); all four nonfatal MIs occurred in patients who continued to use cocaine. These results suggest that an observation period of 9–12 hours for low- to moderate-riskCocaine-associated chest pain patients presenting with cocaine-associated chest pain appearsIn two separate studies of patients presenting to the ED to be safe, and that continued use of cocaine may result inwith cocaine-associated chest pain, the incidence of acute a small percentage of nonfatal MIs in low- to moderate-riskmyocardial infarction (AMI) in these patients was found individuals.to be 6%.1,2 Several mechanisms have been proposed forthe manner in which cocaine causes cardiac ischemia and KEY TEACHING POINTSinfarction in individuals who use cocaine. These mechanismsinclude coronary vasoconstriction, increased platelet aggre- 1. The rate of AMI in patients presenting to an EDgation, thrombus formation leading to MI, myocardial toxic- with cocaine-associated chest pain is approximately 6%,ity and increased cardiac demand for oxygen resulting from although the overall prevalence is likely to be lower asadrenergic stimulation.3 In addition, chronic cocaine users not all individuals seek medical attention or admit to usingmay be prone to premature atherosclerosis of their coronary cocaine.arteries. 2. Benzodiazepines should be given, particularly to an agi- The initial stabilization and nonpharmacological treatment tated patient or one with hyperdynamic vital signs.of patients with cocaine-associated chest pain is similar to that 3. The early use of lorazepam in combination with nitroglyc-of patients with typical angina or MI resulting from atheroscle- erin seems to be more efﬁcacious than nitroglycerin alonerotic coronary artery disease (CAD): bed rest, oxygen, car- in relieving chest pain associated with cocaine use.diac monitor and IV. Patients whose chest pain may be 4. Beta-blockers are contraindicated in the setting of cocaine-caused by ischemia should receive aspirin if there are no con- associated chest pain or myocardial ischemia.traindications (e.g., known allergy or suspected subarachnoid 5. An observation period of 9–12 hours for low- to moderate-hemorrhage).4 Benzodiazepines (diazepam or lorazepam) risk patients presenting with cocaine-associated chest painshould be administered, particularly in the agitated patient appears to be safe; continued use of cocaine may result in aand in those with hyperdynamic vital signs (common with small percentage of nonfatal MIs in low- to moderate-riskrecent cocaine use).3 Benzodiazepines have been demon- individuals.strated to reduce the heart rate and systemic arterial pres-sure in cocaine-intoxicated patients. Beta-blockers are contra- REFERENCESindicated in the setting of cocaine-associated myocardial  Hollander JE, Hoffman RS, Gennis P, et al. Prospective mul-ischemia.3–5 Cocaine decreases left coronary artery diameter ticenter evaluation of cocaine-associated chest pain. Acadand coronary sinus blood ﬂow while increasing coronary Emerg Med 1994;1:330–9.vascular resistance, effects that are exacerbated by beta-  Weber JE, Chudnofsky CR, Boczar M, et al. Cocaine-adrenergic blockade. These effects presumably occur through associated chest pain: how common is myocardial infarction?unopposed alpha-adrenergic stimulation. Acad Emerg Med 2000;7:873–7.
Chest pain in a 26-year-old male 27 Levis JT, Garmel GM. Cocaine-associated chest pain. Emerg  Brogan WC, Lange RA, Kim AS, et al. Alleviation of Med Clin N Am 2005;23:1083–103. cocaine-induced coronary vasoconstriction by nitroglycerin. Hahn IH, Hoffman RS. Diagnosis and treatment of acute J Am Coll Cardiol 1991;18:581–6. myocardial infarction: cocaine use and acute myocardial  Honderick T, Williams D, Seaberg D, et al. A prospective, infarction. Emerg Med Clin N Am 2001;19:1–18. randomized, controlled trial of benzodiazepines and nitro- McCord J, Jneid H, Hollander JE, et al. Management of glycerin or nitroglycerin alone in the treatment of cocaine- cocaine-associated chest pain and myocardial infarction. A associated acute coronary syndromes. Am J Emerg Med scientiﬁc statement from the American Heart Association 2003;21:39–42. Acute Cardiac Care Committee of the Council on Clinical  Weber JE, Shofer FS, Larkin L, et al. Validation of a brief Cardiology. Circulation 2008;117:1897–907. observation period for patients with cocaine-associated chest pain. N Engl J Med 2003;348:510–7.
8Palpitations in a 36-year-old maleHISTORY OF PRESENT ILLNESS HEENT: Unremarkable.A 36-year-old male with no signiﬁcant medical history pre- NECK: Supple, no jugular venous distension.sented to the ED complaining of 30 minutes of palpitations,described as a rapid, irregular heart beat. The patient reported CARDIOVASCULAR: Tachycardic rate with an irregularly irreg-mild shortness of breath and fatigue but denied chest pain, ular rhythm; no rubs, murmurs or gallops.nausea or sweating. He described several similar episodes LUNGS: Clear to auscultation bilaterally.in the past, which had always resolved spontaneously within ABDOMEN: Soft, nontender, nondistended.two hours. Earlier that day, the patient had exercised stren-uously and did not drink much water afterward. He denied EXTREMITIES: No clubbing, cyanosis or edema.tobacco, intravenous drugs, cocaine or methamphetamine use, NEUROLOGIC: Nonfocal.and drank alcohol only occasionally. The patient was placed on the cardiac monitor and a 12-leadPHYSICAL EXAMINATION ECG was obtained (Figure 8.1). A peripheral intravenous lineGENERAL APPEARANCE: The patient appeared well nourished, was placed, blood was drawn and sent for laboratory test-well developed and in no acute distress. ing, and intravenous ﬂuids (normal saline 2-liter bolus) wereVITAL SIGNS administered. Laboratory tests, including a complete blood Temperature 97◦ F (36.1◦ C) count, electrolyte panel, creatinine, glucose and troponin I, Pulse 125 beats/minute were within normal limits. A portable chest radiograph was Blood pressure 147/80 mmHg normal. Respirations 18 breaths/minute Oxygen saturation 100% on room air What is your diagnosis? Figure 8.1 12-lead ECG from a 36-year-old male with palpitations. 29
30 Cardiovascular aspirin (but not warfarin).2 Patients with paroxysmal atrial ﬁb- ANSWER rillation (i.e., self-terminating) and persistent atrial ﬁbrillationThe diagnosis is rapid atrial ﬁbrillation. The ECG (Fig- (i.e., lasting more than seven days or requiring cardioversion)ure 8.1) demonstrates atrial ﬁbrillation with a rapid ventric- appear to have a risk of stroke that is similar to that of patientsular response of approximately 131 beats/minute. Two 10-mg with permanent atrial ﬁbrillation.3 Atrial ﬁbrillation is associ-IV doses of diltiazem were given for rate control. After three ated with an increase in the relative risk of death ranging fromhours, the patient stated his symptoms had resolved, and a 1.3 to 2.6, independent of other risk factors.1,4repeat ECG was obtained (Figure 8.2). In most cases, atrial ﬁbrillation is associated with cardio- The repeat ECG demonstrated normal sinus rhythm, rate vascular disease (i.e., hypertension, coronary artery disease,of 81 beats/minute, without acute ST-T wave changes. The cardiomyopathy, and valvular disease). In some cases, atrialpatient was discharged from the ED, started on atenolol with ﬁbrillation results from another supraventricular tachycardiaclose follow up in the cardiology clinic. (e.g., Wolff-Parkinson-White syndrome). Other predisposing conditions include excessive alcohol intake, hyperthyroidism, and pulmonary disorders, including pulmonary embolism.2Atrial ﬁbrillation “Lone” atrial ﬁbrillation (i.e., occurring in the absence ofElectrocardiographically, atrial ﬁbrillation is characterized by a cardiac or other explanation) is common, particularly inthe presence of rapid, irregular ﬁbrillatory waves that vary in patients with paroxysmal atrial ﬁbrillation – up to 45% of suchsize, shape and timing.1 This set of ﬁndings is usually associ- patients have no underlying cardiac disease.2ated with an irregular ventricular response, although regular- Patients with atrial ﬁbrillation may have palpitations, dysp-ization may occur in patients with complete heart block, an nea, fatigue, lightheadedness or syncope. These symptoms areaccelerated junctional or idiopathic rhythm, or a ventricular- usually related to the elevated heart rate, and in most patientspaced rhythm. Atrial ﬁbrillation is the most common dys- can be mitigated with the use of pharmacologic therapy.1,2rhythmia that requires treatment, with an estimated preva- The patient’s history and physical examination should focuslence in the United States of 2.3 million patients in 2001.2 on the potential causes of atrial ﬁbrillation. The “minimumThis prevalence increases with age – atrial ﬁbrillation occurs evaluation” recommended at diagnosis should include a 12-in 3.8% of people 60 years of age and older and in 9.0% of lead ECG, chest radiograph, transthoracic echocardiography,those over 80 years.2 and serologic tests of thyroid function.2,5 The most devastating consequence of atrial ﬁbrillation is Patients presenting in rapid atrial ﬁbrillation with sig-stroke, due to thromboembolism typically emanating from the niﬁcant hemodynamic instability or with signs and symp-left atrial appendage. The rate of stroke varies but may range toms of ongoing cardiac ischemia should be emergently car-from 5.0–9.6% per year among patients at high risk taking dioverted using synchronized, electrical cardioversion (after Figure 8.2 12-lead ECG of a 36-year-old male following two doses of diltiazem and resolution of palpitations.
Palpitations in a 36-year-old male 31careful assessment of the airway, breathing and circula- KEY TEACHING POINTStion). In patients who are hemodynamically stable and with- 1. Electrocardiographically, atrial ﬁbrillation is characterizedout ischemia, rate control is the ﬁrst priority. A number by the presence of rapid, irregular ﬁbrillatory waves thatof pharmacologic agents are available to control the heart vary in size, shape and timing.rate and rhythm. First-line therapy for rate control includes 2. The most devastating consequence of atrial ﬁbrillation isintravenous β-adrenergic blockers (e.g., metoprolol IV) or stroke due to thromboembolism; the rate of stroke maycalcium-channel blockers (e.g., diltiazem IV). Digoxin is use- range from 5.0–9.6% per year among patients at high riskful in combination with other agents, or when β-adrenergic not taking warfarin.blocking agents and calcium-channel blockers are not well 3. Patients presenting in rapid atrial ﬁbrillation with signif-tolerated.6 Current guidelines recommend a target ventricu- icant hemodynamic instability or with signs and symp-lar rate during atrial ﬁbrillation of 60–80 beats/minute at rest toms of acute cardiac ischemia should be emergently car-and 90–115 beats per minute during exercise.2,5 dioverted using synchronized, electrical cardioversion. A number of agents may maintain sinus rhythm (e.g., β- 4. Rate control with pharmacologic agents (e.g., beta- oradrenergic blockers, amiodarone, procainamide, ﬂecainide, calcium-channel blockers) is the primary goal in hemody-sotalol).2 The use of β-adrenergic blocking agents may be namically stable patients presenting in rapid atrial ﬁbrilla-effective in adrenergically-mediated and paroxysmal atrial ﬁb- tion.rillation. With the exception of β-adrenergic blocking agents, 5. Spontaneous conversion to sinus rhythm within 24 hoursmost antiarrhythmic drugs carry a risk of serious adverse after the onset of atrial ﬁbrillation is common, occurring ineffects. Antiarrhythmic therapy should be chosen on the basis up to two-thirds of patients.of the patient’s underlying cardiac condition.2 Spontaneous conversion to sinus rhythm within 24 hours REFERENCESafter the onset of atrial ﬁbrillation is common, occurring inup to two-thirds of patients.1 Once the duration of atrial  Falk RH. Medical progress: atrial ﬁbrillation. N Engl J Medﬁbrillation exceeds 24 hours, the likelihood of conversion 2001;344:1067–78.decreases. Synchronized, direct-current cardioversion or early  Page RL. Clinical practice: newly diagnosed atrial ﬁbrilla- tion. N Engl J Med 2004;351:2408–16.drug therapy to restore sinus rhythm should be considered  Hart RG, Pearce LA, Rothbart RM, et al. Stroke with inter-in patients in whom the dysrhythmia has lasted less than mittent atrial ﬁbrillation: incidence and predictors during48 hours or who take long-term warfarin therapy. In many aspirin therapy. J Am Coll Cardiol 2000;35:183–7.patients, the precise time of onset of atrial ﬁbrillation cannot  Benjamin EJ, Wolf PA, D’Agostino RB, et al. Impact ofbe determined accurately. In these circumstances, it is recom- atrial ﬁbrillation on the risk of death: the Framingham Heartmended to administer anticoagulation therapy to the patient Study. Circulation 1998;98:946–52.before attempting cardioversion. There are two alternative  Fuster V, Ryden LE, Asinger RW, et al. ACC/AHA/ESCapproaches: outpatient systemic anticoagulation with warfarin guidelines for the management of patients with atrial ﬁbril-to achieve an international normalized ratio of 2.0–3.0 for lation: executive summary. J Am Coll Cardiol 2001;38:1231–at least three weeks, followed by cardioversion or cardiover- 66.sion guided by transesophageal echocardiography. Regardless  Farshi R, Kistner D, Sarma JS, et al. Ventricular rate con- trol in chronic atrial ﬁbrillation during daily activity and pro-of which of these approaches is taken, anticoagulation ther- grammed exercise: a cross-over open-label study of ﬁve drugapy is mandatory for a minimum of three to four weeks after regimens. J Am Coll Cardiol 1999;33:304–10.cardioversion.1
9Chest pressure for two days in a 37-year-old maleHISTORY OF PRESENT ILLNESS CARDIOVASCULAR: Distant heart sounds, audible S1 and S2,A 37-year-old male with a medical history signiﬁcant for unable to assess for rubs, murmurs or gallops.Becker’s muscular dystrophy, cardiomyopathy and congestive LUNGS: Rales at the lung bases bilaterally, no rhonchi orheart failure presented to the ED with two days of chest pres- wheezes.sure. He reported the pressure as constant, rated at a level of3 (on a scale of 0 to 10), and described the pressure as slightly ABDOMEN: Soft, nontender, nondistended.worsening on deep inspiration. He described increased short- EXTREMITIES: Trace lower extremity edema bilaterally to mid-ness of breath with exertion and a cough productive of clear anterior shin.sputum but denied fevers, chills, nausea, lightheadedness or NEUROLOGIC: Nonfocal.sweating. The patient was placed on the cardiac monitor, a peripheralPHYSICAL EXAMINATION intravenous line was placed and blood was drawn and sent forGENERAL APPEARANCE: The patient was a pale, obese male laboratory testing. A 12-lead ECG (Figure 9.1) and a portablewho appeared in no acute discomfort. chest radiograph were obtained (Figure 9.2, panel A). Labo-VITAL SIGNS ratory tests were signiﬁcant for a leukocyte count of 18 K/μL Temperature 97.5◦ F (36.4◦ C) (normal 3.5–12.5 K/μL) with 90% neutrophils (normal 50– Pulse 118 beats/minute 70%), hematocrit of 31% (normal 39–51%), creatinine of Blood pressure 102/72 mmHg 1.5 mg/dL (normal < 1.3 mg/dL) and a positive D-dimer. The Respirations 18 breaths/minute troponin I was within normal limits. A bedside echocardio- Oxygen saturation 96% on room air gram was obtained (Figure 9.3).HEENT: Unremarkable. What is your diagnosis?NECK: Supple, mild jugular venous distension noted. 33
Figure 9.1 12-lead ECG from 37-year-old male with chest pressure for two days. A BFigure 9.2 Portable chest radiograph from a 37-year-old male with chest pressure for two days (panel A);comparison with a portable chest radiograph obtained from the same patient ﬁve days earlier (panel B). Figure 9.3 Echocardiogram from a 37-year-old male with chest pres- sure for two days (arrow, right ventricle).
Chest pressure for two days in a 37-year-old male 35 tamponade by increasing the heart rate to maintain cardiac ANSWER output. This compensatory mechanism is maintained until lateThe diagnosis is pericardial effusion with cardiac tamponade. in the course; decompensation may occur quickly.The ECG demonstrates low voltage and poor R wave progres- In cardiac tamponade, the ECG classically shows decreas-sion (Figure 9.1), whereas the chest radiograph shows marked ing voltage or electrical alternans, although the latter is rare.1cardiomegaly compared with a portable chest radiograph ﬁve Electrical alternans on the ECG is pathognomonic of cardiacdays previously during a chest pain evaluation (Figure 9.2, tamponade. It is characterized by alternating levels of ECGpanels A and B). The bedside echocardiogram demonstrates voltage of the P waves, QRS complexes and T waves, thea moderate circumferential pericardial effusion with signs of result of the heart swinging in a large effusion. The chesttamponade (evidence of right atrial collapse, Figure 9.3). The radiograph may demonstrate an enlarged cardiac silhouettepatient was taken to the OR and underwent a pericardial after as little as 200 mL of ﬂuid accumulation.2 This enlargedwindow procedure using video-assisted thoracoscopic surgery cardiac silhouette occurs in patients with slow ﬂuid accu-(VATS) performed by the cardiothoracic surgeon to relieve mulation, compared to a normal cardiac silhouette seen inthe tamponade and drain the pericardial effusion. Seven hun- patients with rapid ﬂuid accumulation and tamponade. Thus,dred milliliters of straw-colored ﬂuid was removed during the chronicity of the effusion may be suggested by the pres-VATS; bacterial and fungal cultures of the pericardial ﬂuid ence or absence of an enlarged cardiac silhouette.2returned negative. The etiology of the pericardial ﬂuid and Echocardiography is the diagnostic procedure of choice toresulting tamponade was determined to be viral. identify pericardial effusions and cardiac tamponade.3 In the normal pericardium, there is approximately 30–50 mL of ﬂuid between the visceral and parietal pericardium.4 This amountCardiac tamponade of ﬂuid is usually not visible on ultrasound. The pericardiumCardiac tamponade is the result of compression of the should appear echogenic. If an effusion is present, an ane-myocardium by the contents of the pericardium. This com- choic (dark) space will be evident between the pericardiumpression is generally caused by ﬂuid but in rare cases may be and the beating heart. With a large or rapidly developing peri-caused by gas, pus, blood, or a combination of materials.1 Car- cardial effusion, this anechoic space surrounding the heartdiac tamponade is a continuum reﬂecting the amount of ﬂuid may be associated with diastolic collapse of the right atrium(or other material), its rate of accumulation, and the condition or right ventricle.4 Right atrial collapse is virtually 100% sen-of the heart. The three stages necessary for cardiac tamponade sitive for cardiac tamponade but is less speciﬁc.3 Duration ofto develop include ﬂuid ﬁlling the recesses of the parietal peri- right atrial collapse exceeding one-third of the cardiac cyclecardium, ﬂuid accumulating faster than the rate of the pari- increases speciﬁcity without sacriﬁcing sensitivity. Left atrialetal pericardium’s ability to stretch, and ﬂuid accumulating collapse is seen in about 25% of patients and is speciﬁc forfaster than the body’s ability to increase blood volume to cardiac tamponade.3 Left ventricular collapse is less commonsupport right ventricle ﬁlling pressures.1 The ﬁnal result of due to the muscularity of the left ventricle’s wall.these processes is increased pericardial pressure, which causes Initial treatment of cardiac tamponade includes intra-decreased cardiac compliance and decreased blood ﬂow into venous ﬂuids to augment volume to the right ventricle, whichthe heart, which leads to decreased cardiac output. The most increases the ﬁlling pressure in an effort to overcome the pres-important factor in the development of tamponade is the rate sure of pericardial constriction.1 Pericardiocentesis, prefer-of ﬂuid accumulation.1 The main pathophysiologic derange- ably ultrasound-guided, is the treatment of choice. Enoughment of cardiac tamponade is reduced cardiac output. ﬂuid should be withdrawn to result in hemodynamic stability. In the United States, malignant disease is the most com- If tamponade recurs, pericardiocentesis may be repeated or amon cause of pericardial effusion with tamponade.2 Other drainage catheter can be left in the pericardial space.1 A peri-causes of pericardial effusions that may result in tampon- cardiotomy may ultimately be necessary. Cardiac tamponadeade include infection, connective tissue disease, heart failure, often has a high mortality rate, depending on the severity andvalvular heart disease, myocardial infarction, uremia, cardiac nature of the underlying disease, the time course of onset, andsurgery, trauma and idiopathic.3 Although malignancy is the the rapidity of diagnosis and successful intervention.1most common etiology of pericardial effusion in developedcountries (including the United States), tuberculosis shouldbe considered in endemic areas. Acute pericardial tamponade KEY TEACHING POINTSoccurs in approximately 2% of penetrating chest trauma; thiscondition is rarely seen in blunt trauma.2 1. Cardiac tamponade results from increased pericardial pres- Cardiac tamponade symptoms are usually nonspeciﬁc. The sure due to a rapidly accumulating pericardial effusion,patient may complain of chest pain, cough or dyspnea.1 which causes decreased cardiac compliance and decreasedThe classic triad of cardiac tamponade described by Beck is blood ﬂow into the heart, in turn leading to decreased car-hypotension, distended neck veins, and mufﬂed heart sounds. diac output.These signs may be absent if tamponade develops quickly or 2. In the United States, malignancy is the most commonif the patient is hypovolemic.1 Initially, the heart responds to cause of pericardial effusion with tamponade; other causes
36 Cardiovascular include infection, connective tissue disease, heart failure, REFERENCES valvular heart disease, myocardial infarction, uremia, car- diac surgery, trauma and idiopathic.  Jouriles NJ. Pericardial and myocardial disease. In: Marx JA,3. The classic triad of cardiac tamponade (hypotension, dis- Hockberger RS, Walls RM, et al. (eds). Rosen’s Emergency tended neck veins, and mufﬂed heart sounds) is seen in less Medicine: Concepts and Clinical Practice, 6th ed. Mosby, 2006;1285–6. than 40% of patients with cardiac tamponade.  Valley VT, Fly CA. Pericarditis and cardiac tamponade.4. In cardiac tamponade, the ECG may show evidence of eMedicine Website. Available at http://www.emedicine.com/ low voltage or electrical alternans, whereas the chest radio- emerg/topic412.htm. Accessed June 26, 2008. graph may demonstrate an enlarged cardiac silhouette.  Hold BD. Pericardial disease and pericardial tamponade.5. Echocardiography is the study of choice for diagnosing car- Crit Care Med 2007;25:S355–64. diac tamponade; the treatment of cardiac tamponade is vol-  Tang A, Euerle B. Emergency department ultrasound and ume augmentation and pericardiocentesis. echocardiography. Emerg Med Clin N Am 2005;23:1179–94.
10Low back pain and leg weakness in a 40-year-old maleHISTORY OF PRESENT ILLNESS CARDIOVASCULAR: Regular rate and rhythm without rubs,A 40-year-old male with a history of hypertension and med- murmurs or gallops.ication noncompliance presented to the ED complaining of LUNGS: Clear to auscultation bilaterally.the sudden onset of low back pain associated with weaknessand numbness of his left leg. The pain occurred suddenly as ABDOMEN: Soft, nontender, nondistended, no pulsatilethe patient was bending over to pick up his son. He described masses.his back pain as a “tearing” with radiation down his left leg, BACK: No thoracic or lumbar spine tenderness or erythema;and rated the pain at a level of 10 (on a scale of 0 to 10). The no costovertebral angle tenderness.patient denied abdominal or chest pain, shortness of breath,fevers, or bowel or bladder incontinence. He reported some EXTREMITIES: Left leg was pale and cool; left femoral, dorsalisnausea without vomiting. He denied any history of previous pedis and posterior tibialis pulses were absent.back trauma or back problems. He had a history of hyperten- NEUROLOGIC: Notable for left lower extremity paralysis (leftsion for which he was prescribed medication but stopped it leg strength 0/5 proximal and distal) with decreased sensationsome time ago. He denied tobacco or intravenous drug use, over the entire left leg.and drank alcohol occasionally. A peripheral intravenous line was placed, blood was drawnPHYSICAL EXAMINATION and sent for laboratory testing. Laboratory tests were signif-GENERAL APPEARANCE: The patient was a well-developed icant for a leukocyte count of 18.1 K/μL (normal 3.5–12.5male in signiﬁcant discomfort. K/μL), creatinine of 1.4 mg/dL (normal < 1.3 mg/dL), potas-VITAL SIGNS sium of 2.8 mEq/L (normal 3.5–5.3 mEq/L), bicarbonate of Temperature 97.7◦ F (36.5◦ C) 19 mEq/L (normal 22–30 mEq/L) and lactic acid of 4.2 mmol/L Pulse 59 beats/minute (normal 0.7–2.1 mmol/L). A CT angiogram (CTA) of the Blood pressure 268/119 mmHg chest, abdomen and pelvis was obtained (Figures 10.1 and Respirations 22 breaths/minute 10.2). Oxygen saturation 100% on room air What is your diagnosis?HEENT: Unremarkable.NECK: Supple, no jugular venous distension. 37
A B C DFigure 10.1 CTA of chest and abdomen from a 40-year-old male with sudden onset of low back pain and leftleg paralysis (panels A–D represent superior to inferior transverse images). Figure 10.2 Sagittal reconstruction image of CTA of chest, abdomen and pelvis from a 40-year-old male with sudden onset low back pain and left leg paralysis.
Low back pain and leg weakness in a 40-year-old male 39 ANSWERThe diagnosis is type B aortic dissection. The CTA demon-strates a type B aortic dissection, beginning distal to the take-off of the left subclavian artery, extending throughout thethoracic aorta and into the left common iliac, left external iliacand left femoral artery (Figures 10.1 and 10.2). An intimal ﬂapis also seen in the celiac axis, superior mesenteric artery andleft renal artery (Figure 10.1, panels C and D). Decreased per-fusion of the left kidney is apparent compared to the rightkidney. An esmolol and nitroprusside drip were started for bloodpressure control, and the patient was given DilaudidTM andZofranTM for pain and nausea control. The vascular surgeryservice was consulted emergently. The patient was taken tothe OR where endovascular stents of the distal aorta and leftiliac artery were successfully placed, resulting in return of pal-pable distal pulses in the left lower extremity (Figure 10.3). Figure 10.4 Stanford classiﬁcation for aortic dissections.Aortic dissectionAortic dissection is a longitudinal cleavage of the aortic the ascending aorta (Figure 10.4). Type A dissections involvemedia created by a dissecting column of blood.1,2 Acute the ascending aorta; type B dissections do not. Dissections thataortic dissection has been estimated to affect 14–20 mil- involve the ascending aorta are much more lethal than thoselion individuals globally per year, with an incidence of limited to the distal aorta, and call for a different therapeu-2.9 per 100,000 population per year.3 Dissections predomi- tic approach. In the International Registry of Acute Aorticnantly affect males (male/female ratio 5:1). Two-thirds involve Dissection (IRAD), 62% of dissections are type A and 38%the ascending aorta (proximal), with a peak incidence for are type B.1 Patients with distal dissections tend to be older,proximal dissections being 50–60 years of age and 60–70 years heavy smokers with chronic lung disease, and more often haveof age for distal dissections.3 Hypertension, the most common generalized atherosclerosis and hypertension compared withrisk factor associated with aortic dissection, is seen in most patients who have proximal aortic dissections.1patients. Aortic dissection is uncommon before age 40 except The classic presenting symptom of aortic dissection isin association with congenital heart disease, Ehlers-Danlos or abrupt onset of chest pain. With distal dissections, the painMarfan syndrome, giant cell arteritis and pregnancy. More is located in the back and is characterized as “tearing” inthan 2000 cases of aortic dissection occur each year in the half of cases. Two-thirds of these cases additionally presentUnited States; it is the most common acute illness of the with “sharp” pain, and approximately one-ﬁfth present withaorta.4 Common misdiagnoses include myocardial infarction, “migratory” pain. In almost half of cases, the pain primarilyatypical chest pain, congestive heart failure and gastrointesti- involves or includes the abdominal area.3 Syncope is muchnal bleeding.4 more commonly associated with dissections involving the Anatomic classiﬁcation is important for diagnosis and ther- ascending aorta or retrograde arch. Paralysis is reported toapy. The Stanford classiﬁcation is based on the involvement of occur in 2–8% of patients with distal dissection, and hyper- tension is much more common than hypotension (more than 70% versus more than 5%, respectively).3 Approximately 14% of patients who have dissections involving the distal aorta present with femoral pulse deﬁcits.3 Routine chest radiograph will be abnormal in 80–90% of patients but the abnormalities are nonspeciﬁc and rarely diagnostic.1 Mediastinal widening occurs in greater than 75% of cases, and may occur in the ascending aorta, aortic arch or the descending portion of the thoracic aorta; it may be difﬁ- cult to differentiate from aortic tortuosity that is associated with chronic hypertension. The “calcium sign” (deﬁned as a A B separation of the intimal calcium deposit from the outermostFigure 10.3 Intraoperative aortic angiogram from a 40-year-old male portion of the aorta by more than 5 mm) is an uncommonwith type B aortic dissection (panel A) demonstrating endovascular radiographic manifestation of aortic dissection. Up to 12% ofplacement of distal aortic stent (panel B). patients with aortic dissection have a normal chest radiograph;
40 Cardiovasculartherefore, a plain chest radiograph is inadequate to rule out 80 patients treated medically yielded a two-year survival rateaortic dissection.1 of 94.9% using the endovascular approach versus 67.5% in the Imaging modalities to conﬁrm aortic dissection include medically-treated group.8aortography, CT scanning, MRI and echocardiography.1–5 CTscanning is useful in hemodynamically-stable patients but has KEY TEACHING POINTSpotential limitations in patients with contrast allergy. MRI isas accurate as CT but is limited to hemodynamically-stable 1. Acute aortic dissection is a true emergency requiringpatients. Transesophageal echocardiography (TEE) is prefer- prompt diagnosis and vascular surgery consultation.able to transthoracic echocardiography (TTE) and is as accu- 2. Hypertension is the most common risk factor for aortic dis-rate as CT or MRI for detection of aortic dissection. Advan- section.tages of TEE include its portability and that it does not require 3. Stanford type A dissections involve the ascending aorta,contrast. whereas Stanford type B dissections do not. Opioids should be administered for pain control and to 4. Symptoms and signs of aortic dissection can include tear-decrease sympathetic tone in patients with acute aortic dis- ing chest pain radiating to the back, back pain, limb pain,section. The two goals of medical management are to reduce weakness or numbness, syncope, pulse deﬁcits, and hyper-blood pressure and to decrease the rate of arterial pulse tension that is difﬁcult to control or refractory to medicalincrease (dP/dt) to diminish shearing forces. Sodium nitro- management.prusside should be titrated to maintain the systolic blood 5. CTA is most useful in making the diagnosis of aortic dissec-pressure at 100–120 mmHg or at the lowest level to main- tion in stable patients. Other diagnostic modalities includetain vital organ perfusion. Because nitroprusside increases the MRI, transesophageal echocardiography and conventionalheart rate and may also increase dP/dt, a beta-blocker must aortography.be started before or in conjunction with sodium nitroprus- 6. Immediate treatment of patients with aortic dissectionside. Esmolol is an ultrashort-acting beta-blocker that is eas- involves opioid analgesia and strict blood pressure controlily titrated. Esmolol is typically administered as a continu- with esmolol and sodium nitroprusside (or LabetalolTM asous infusion of 50–300 μg/kg/min, with a 500 μg/kg loading a single agent).dose given over 1 minute before the infusion is begun or the 7. Deﬁnitive treatment of type A dissection is surgical. Typerate is increased.6 Labetalol has both alpha-blocking and beta- B dissection may be medically managed in uncompli-blocking activity and can be used as monotherapy. A sug- cated cases, whereas complicated cases (progression of thegested dose is an initial 20 mg IV bolus every 5 to 10 minutes, dissection, rapid expansion, end-organ ischemia, ongoingincrementally increased to 80 mg until a target heart rate has pain, uncontrolled hypertension or rupture) require anbeen reached or a total of 300 mg is given.1,2 open surgical approach or endovascular repair. Type A acute aortic dissections require prompt surgicaltreatment. Deﬁnitive treatment of type B acute aortic dis- REFERENCESsections is less clear. At most institutions, medical therapywith aggressive antihypertensive agents and beta-blockers is  Ankel F. Aortic Dissection. In: Marx JA, Hockberger RS, Walls RM, et al. (eds). Rosen’s Emergency Medicine: Con-used in the ICU setting.7 Operative intervention for acute cepts and Clinical Practice, 6th ed. Philadelphia: Mosby,type B dissections is reserved for life-threatening compli- 2006;1324–9.cations, such as progression of the dissection, rapid expan-  Osinuga O, Kesari S, Hmidi A, et al. Aortic dissection.sion, end-organ ischemia caused by side-branch compromise, eMedicine Website. Available at http://www.emedicine.com/ongoing pain, uncontrolled hypertension or rupture.7 Open MED/topic2784.htm. Accessed June 25, 2008.surgical interventions involve a combination of graft replace-  Karmey-Jones R, Simeone A, Meissner M, et al. Descendingment, closure of the open entry site or fenestration to cre- thoracic aortic dissections. Surg Clin N Am 2007;87:1047–86.ate a re-entry tear.7 Endovascular stent grafting in patients  Rogers RL, McCormack R. Aortic disasters. Emerg Medwith type B dissections has demonstrated promising short- and Clin N Am 2004;22:887–908.mid-term results. Proposed advantages of this less-invasive  Nienaber CA. The diagnosis of thoracic aortic dissection byapproach include shorter operative times, decreased need for noninvasive imaging procedures. N Engl J Med 1993;328:1–9.  Frakes MA. Esmolol: a unique drug with ED applications.general anesthesia, lack of aortic cross-clamping, avoidance J Emerg Nurs 2001;27:47–51.of cardiopulmonary bypass, avoidance of major thoracic or  Lee JT, White RA. Current status of thoracic aortic endo-thoracoabdominal incisions, less pain, quicker recovery, and graft repair. Surg Clin N Am 2004;84:1295–318.shorter hospital and ICU stays.7 Endovascular stenting may  Nienaber CA, Zannetti S, Barbieri B, et al. Investigation ofalso play a role in patients with uncomplicated type B dis- stent grafts in patients with type B Aortic Dissection: designsections. A retrospective analysis of 80 patients with type of the INSTEAD trial – a prospective, multicenter, Euro-B aortic dissection treated endovascularly compared with pean randomized trial. Am Heart J 2005;149:592–9.
11Acute chest pain in a 42-year-old maleHISTORY OF PRESENT ILLNESS LUNGS: Clear to auscultation bilaterally.A 42-year-old male with a medical history signiﬁcant for ABDOMEN: Soft, nontender, nondistended.hypertension and hyperlipidemia presented to the ED com-plaining of substernal chest pain that started four hours prior EXTREMITIES: No clubbing, cyanosis or edema.to presentation. The pain was located in the left upper chest NEUROLOGIC: Nonfocal.and was described as dull and constant. He rated his painat a level of 4 (on a scale of 0 to 10), with radiation to his A 12-lead ECG was obtained (Figure 11.1), and the patientback. The pain was aggravated by movement and worsened was placed on the cardiac monitor. A peripheral intravenouson deep inspiration. He denied any nausea, vomiting, sweat- line was placed, and blood was drawn and sent for labora-ing or shortness of breath, as well as recent cough or fevers. tory testing. The patient received aspirin 162 mg orally andHe also denied recent long trips or leg swelling. The patient morphine sulfate IV for his pain. A portable chest radiographhad undergone an exercise treadmill test six months earlier, was obtained (Figure 11.2). Laboratory results were signiﬁ-which revealed no evidence of exercise-induced ischemia. cant for a positive D-dimer; the remainder of the laboratory tests (complete blood count, electrolytes, creatinine, glucosePHYSICAL EXAMINATION and troponin I) were normal. A CT angiogram of the chest didGENERAL APPEARANCE: The patient appeared well developed, not demonstrate evidence of pulmonary embolism. A secondwell hydrated, and in no acute distress. troponin I obtained eight hours after the onset of symptomsVITAL SIGNS was normal (<0.02 ng/mL). Temperature 97.6◦ F (36.4◦ C) The patient was discharged from the ED with the diagno- Pulse 56 beats/minute sis of chest pain, not otherwise speciﬁed. The patient’s pain Blood pressure 142/74 mmHg had not completely resolved and progressively worsened after Respirations 22 breaths/minute discharged. The patient returned to the ED later that same Oxygen saturation 97% on room air evening, a repeat ECG was obtained (Figure 11.3), and a repeat troponin I obtained 13 hours after the onset of the painHEENT: Unremarkable. was normal.NECK: Supple, no jugular venous distension.CARDIOVASCULAR: Regular rate and rhythm without rubs, What is your diagnosis?murmurs or gallops. 41
Figure 11.1 12-lead ECG from a 41-year-old male with left-sided chest pain for four hours. Figure 11.2 Chest radiograph from a 41-year-old male with left-sided chest pain for four hours.Figure 11.3 12-lead ECG from a 41-year-old male 13 hours after the onset of left-sided chest pain.
Acute chest pain in a 42-year-old male 43 through four classic stages.6 Stage I is characterized by ANSWER ST-segment elevation, prominent T waves and PR-segmentThe diagnosis is acute pericarditis. The initial ECG obtained depression. Stage II is characterized by a normalization ofdemonstrates minimal ST-segment elevation in leads I, II, V4 - the initial abnormalities, namely resolution of the ST-segmentV6 , with PR-segment elevation in lead aVR, ﬁndings consis- elevation. Stage III involves T wave inversion, usually in thetent with early pericarditis. The chest radiograph was evalu- same distribution where ST-segment elevation was encoun-ated as low lung volumes without inﬁltrate or effusion. The tered. Finally, Stage IV is a normalization of all changes withrepeat ECG obtained 13 hours after the onset of symptoms a return to the baseline ECG. Persistent ST-segment eleva-demonstrates diffuse ST-segment elevation, concave-upward tion and pathologic Q waves are not encountered in patientsin appearance, PR depression in leads I, II, V3-V6, with PR- with pericarditis – these ECG ﬁndings should suggest anothersegment elevation in lead aVR, indicative of acute pericardi- etiology.6tis. The patient received morphine sulfate IV in the ED and Although the white cell count, erythrocyte sedimentationwas started on indomethacin 25 mg orally every eight hours at rate (ESR) and serum C-reactive protein (CRP) concentra-discharge. On a follow-up visit with his primary care physician tions usually are elevated in patients with acute pericarditis,four days later, the patient reported marked improvement in these tests provide little insight into the cause of the disease.3his symptoms. Troponin levels are elevated in 35–50% of patients with peri- carditis, a ﬁnding thought to be caused by epicardial inﬂam- mation rather than myocyte necrosis.3,7 The magnitude of theAcute pericarditis elevation in the serum troponin concentration appears to cor-Acute pericarditis, a diffuse inﬂammation of the pericardial relate with the magnitude of the ST-segment elevation, andsac and superﬁcial myocardium, has a number of underlying the concentration usually returns to normal within one to twocauses. These include infection (primarily viral), immunologic weeks after diagnosis. An elevated troponin does not pre-disorders, uremia, trauma, malignancy, cardiac ischemia and dict an adverse outcome, although a prolonged elevation (last-acute myocardial infarction.1 In clinical practice using a tra- ing longer than two weeks) suggests myocarditis, which has aditional diagnostic approach, idiopathic and viral acute peri- worse prognosis.3,7carditis is found in 80–90% of cases in immunocompetent The diagnostic test of choice for large effusions, cardiacpatients from developed countries.2 The incidence of peri- tamponade and constrictive pericarditis is two-dimensionalcarditis in postmortem studies ranges from 1–6%, whereas it Doppler echocardiography.8 This imaging modality canis diagnosed antemortem in only 0.1% of hospitalized patients demonstrate moderate or large effusions. In cardiac tampon-and in 5% of patients seen in EDs with chest pain without ade, Doppler examination may show the characteristic swing-myocardial infarction.3 The possible sequelae of pericarditis ing motion of the heart that gives rise to electrical alternansinclude cardiac tamponade, recurrent pericarditis and pericar- on the ECG. Doppler studies are helpful in differentiatingdial constriction.3 pericarditis from restrictive cardiomyopathy.8 Transthoracic More than half of patients with pericarditis will present echocardiography is generally not required in patients withcomplaining of chest pain that may radiate to the back, neck unequivocal evidence of pericarditis and no poor prognosticor shoulders.4 If pain radiates to one or both trapezius muscle indicators.3ridges, it may be due to pericarditis because the phrenic nerve Most patients with idiopathic pericarditis can be man-(which innervates these muscles) traverses the pericardium.3 aged conservatively, with a nonsteroidal anti-inﬂammatoryIn contrast to acute coronary syndromes, pericardial pain typ- drug (NSAID) such as indomethacin, ibuprofen or aspirin.ically worsens with inspiration and is improved while sitting up These agents are believed to be equally effective.8 Colchicineand leaning forward. Approximately 25–40% of patients with (administered at a dose of 0.6 mg twice daily) appears topericarditis will complain of dyspnea, and 17% of fever.4 be effective alone or in combination with ibuprofen in treat- The most common physical ﬁnding in patients with peri- ing acute pericarditis, although it has not been tested in ran-carditis is a pericardial friction rub, which occurs in approxi- domized trials; it is preferred in patients who have recurrentmately 50–85% of cases.3–5 A pericardial friction rub is best pericarditis.3 Patients who do not respond to an NSAID mayheard at the lower sternal border or apex when the patient is need a short course of prednisone (5–10 mg per day for one tositting forward on his or her hands and knees. Other ﬁndings two weeks).8 Rarely, patients do not respond to this therapy oron physical exam may include fever (may reach 104◦ F/40◦ C), show evidence of recurrent pericarditis; these patients requirecardiac dysrhythmias (e.g., premature atrial and ventricular a prolonged corticosteroid course (i.e., several months).contractions), tachypnea and dyspnea.5 Individuals with asso- Most patients with acute pericarditis have a brief andciated cardiac tamponade may show jugular venous disten- benign course, and can be managed as an outpatient withsion, tachycardia, hypotension or pulsus paradoxus. NSAIDs. Indicators of a poor prognosis in patients with peri- The 12-lead ECG in patients with acute pericarditis clas- carditis include temperature above 100.4◦ F (38◦ C), a sub-sically shows widespread upward concave ST-segment ele- acute onset, an immunosuppressed state, pericarditis associ-vation and PR-segment depression.3 In addition, lead aVR ated with trauma, a history of oral anticoagulation therapy,on the ECG can demonstrate ST-segment depression and myopericarditis, a large pericardial effusion or cardiacPR-segment elevation.1 The ECG abnormalities evolve tamponade.3 Patients with one or more of these criteria are at
44 Cardiovascularincreased risk for serious complications and should be admit- REFERENCESted to the hospital.  Williamson K, Mattu A, Plautz CU, et al. Electrocar- diographic applications of lead aVR. Am J Emerg MedKEY TEACHING POINTS 2006;24:864–74.  Imazio M, Cecchi E, Demichelis B, et al. Indicators of poor1. Pain from pericarditis typically worsens on inspiration and prognosis of acute pericarditis. Circulation 2007;115:2739–44. improves while sitting up and leaning forward.  Lange RA, Hillis LD. Acute pericarditis. N Engl J Med2. The most common physical ﬁnding in patients with peri- 2004;351:2195–202. carditis is a pericardial friction rub, which occurs in approx-  Ringstrom E, Freedman J. Approach to undifferentiated imately 50–85% of cases. chest pain in the emergency department. Mt Sinai J Med 2006;73:499–505.3. The 12-lead ECG in acute pericarditis classically shows  Valley VT, Fly CA. Pericarditis and cardiac tamponade. widespread upward concave ST-segment elevation, PR- eMedicine Website. Available at http://www.emedicine.com/ segment depression and PR-segment elevation in lead emerg/topic412.htm. Accessed July 10, 2008. aVR.  Brady WJ. ST segment and T wave abnormalities not caused4. Plasma troponin levels are elevated in 35–50% of patients by acute coronary syndromes. Emerg Med Clin N Am with pericarditis, a ﬁnding thought to be caused by epicar- 2006;24:91–111. dial inﬂammation rather than myocyte necrosis.  Bonnefoy E, Gordon P, Kirkorian G, et al. Serum cardiac5. The treatment of choice for idiopathic pericarditis is troponin I and ST-segment elevation in patients with acute NSAIDs. pericarditis. Eur Heart J 2000;21:832–6.  Goyle KK, Walling AD. Diagnosing pericarditis. Am Fam Physician 2006;66:1695–702.
12Rapid heart rate in a 47-year-old maleHISTORY OF PRESENT ILLNESS HEENT: Unremarkable.A 47-year-old male with a medical history signiﬁcant for dia- NECK: Supple, no jugular venous distension.betes, hypertension and chronic obstructive pulmonary dis-ease (COPD) presented to the ED complaining of two hours CARDIOVASCULAR: Tachycardic rate, regular rhythm, unableof palpitations and rapid heart rate associated with mild, sub- to assess for rubs, murmurs or gallops.sternal chest pain and shortness of breath. The patient denied LUNGS: Clear to auscultation bilaterally.lightheadedness or dizziness and had not experienced simi-lar episodes in the past. He reported that his symptoms had ABDOMEN: Soft, nontender, nondistended.started suddenly while at work. EXTREMITIES: No clubbing, cyanosis or edema; brisk capillary reﬁll.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient was a moderately obese NEUROLOGIC: Nonfocal.male, slightly diaphoretic but in no acute distress. The patient was placed on the cardiac monitor, and a 12-leadVITAL SIGNS ECG was obtained (Figure 12.1). A peripheral intravenous Temperature 98.0◦ F (36.6◦ C) line was placed, and blood was drawn and sent for laboratory Pulse 198 beats/minute testing. Blood pressure 150/90 mmHg Respirations 22 breaths/minute Oxygen saturation 100% on room air What is your diagnosis? Figure 12.1 12-lead ECG from a 47-year-old male with rapid heart rate. 45
46 Cardiovascular associated with hypertrophic cardiomyopathy or Ebstein’s ANSWER anomaly, atrial tachycardias in patients with congenital orThe diagnosis is supraventricular tachycardia (SVT). The acquired heart disease). Re-entry dysrhythmias are usuallypatient was given 6 mg adenosine IV rapidly while the 12-lead induced by premature atrial or ventricular ectopic beats. Pre-ECG was continuously recording (Figure 12.2). The patient cipitating factors such as hyperthyroidism, excessive intakeconverted to normal sinus rhythm, and a repeat ECG was of caffeine, alcohol or recreational drugs increase the risk ofobtained (Figure 12.3). Laboratory tests revealed a normal recurrence.1complete blood count, electrolytes, BUN, creatinine, glucose, Common symptoms of SVT include palpitations, anxiety,and troponin I. A second troponin I drawn eight hours after lightheadedness, chest pain, pounding in the neck and chest,the onset of symptoms was also within normal limits. The and dyspnea; syncope is uncommon. SVTs have a suddenpatient remained in normal sinus rhythm and was discharged onset and termination, in contrast to sinus tachycardias, whichfrom the ED without complications after several hours of accelerate and decelerate gradually. Physical examinationobservation. during episodes may reveal the “frog sign” – prominent jugu- lar venous A waves due to atrial contraction against the closed tricuspid valve.2 The usual presentation of SVT on ECG isSupraventricular tachycardia a narrow complex tachycardia (QRS interval less than 120The term supraventricular tachycardia (SVT) refers to parox- msec) with a rate of 140–280 beats/minute.3 In less than 10%ysmal tachydysrhythmias that require atrial or atrioventricular of cases, wide complex tachycardia is the manifestation ofnodal tissue (or both) for their initiation and maintenance.1 SVT.1 After restoration of sinus rhythm, the 12-lead ECGThe incidence of SVT is about 35 cases per 100,000 persons should be examined for the presence of delta waves, whichper year; the prevalence is about 2.25 per 1000.1 SVT is often indicate an accessory pathway (bypass tract). If delta wavesrecurrent, occasionally persistent, and a frequent cause of are present, referral to a cardiologist should occur.visits to EDs and primary care physician ofﬁces. SVTs are When a patient presents in SVT and is hemodynam-not usually associated with structural heart disease, although ically stable, attempting a therapeutic/diagnostic maneuverthere are exceptions (e.g., the presence of accessory pathways with vagal stimulation is reasonable.4 The maneuvers include Figure 12.2 12-lead ECG showing conversion of SVT to normal sinus rhythm after administration of 6 mg adenosine IV rapid bolus (arrow indicates adenosine administration).
Rapid heart rate in a 47-year-old male 47 Figure 12.3 12-lead ECG from a 47-year-old male presenting with SVT, obtained after conversion to normal sinus rhythm.carotid massage (in patients without carotid bruits or known trials with different antidysrhythmic agents should occur onlycarotid artery disease), Valsalva maneuver, and application of after careful consideration of their possible negative hypoten-ice bag to the face (stimulates the diving reﬂex). These maneu- sive, bradycardic and proarrhythmic effects. At any point,vers increase vagal tone, thus slowing conduction through the electrical cardioversion is an alternative; this technique is gen-atrioventricular (AV) node.1,4,5 A continuous 12-lead ECG erally considered in hemodynamically stable patients if AV-recording of the episode should be obtained during vagal nodal blocking agents fail.maneuvers because the way in which the dysrhythmias resolve In ambulatory patients with frequent episodes of SVT (twomay provide clues to their mechanism. In rare cases, episodes or more per month), ECG recordings or event recorders mayof SVT are so poorly tolerated (e.g., result in hemodynamic be useful to document dysrhythmias in the outpatient set-instability) that they require immediate electrical cardio- ting. In patients presenting with SVT, an outpatient echocar-version. diogram should be considered to rule out structural heart If the dysrhythmia is not terminated by vagal maneuvers, disease, even though this is uncommon. Because electrolyteadenosine (6 or 12 mg IV) will usually cause AV-nodal block, abnormalities and hyperthyroidism may contribute to SVT,either terminating the dysrhythmia or allowing visualization it is reasonable to check potassium and serum thyrotropinof the underlying mechanism.5 Data from randomized trials levels; however, these tests generally have a low yield. SVTshows that SVT is terminated in 60–80% of patients treated presents infrequently as a wide complex tachycardia, in whichwith 6 mg adenosine, and in 90–95% of those treated with there is an associated bundle-branch block or conduction over12 mg.6 In patients with atrial tachycardia, adenosine causes a an accessory pathway. Wide QRS complex, regular tachycar-transient AV-nodal block or interrupts the tachycardia. ECG dias should routinely be treated as ventricular tachycardia,monitoring is required during the administration of adeno- unless the diagnosis of SVT with aberrant conduction or SVTsine, and resuscitation equipment should be available in the with preexcitation is certain.1 Adenosine and other AV-nodalevent that the rare complications of bronchospasm or ventric- blocking agents are generally ineffective and potentially dele-ular ﬁbrillation occur.7 Adenosine is contraindicated in heart terious in patients with ventricular tachycardia.transplant recipients and should be used cautiously in patientswith severe obstructive lung disease.1 KEY TEACHING POINTS If SVT is refractory to adenosine or rapidly recurs, thetachycardia can usually be terminated by the administration 1. SVT frequently occurs in young, healthy individuals and isof an intravenous calcium-channel blocker (e.g., diltiazem, usually not associated with structural heart disease.verapamil) or a beta-blocker (e.g., metoprolol).1 As a next 2. Common symptoms of SVT include palpitations, anxiety,step, procainamide, ibutilide, propafenone or ﬂecainide can be lightheadedness, chest pain, pounding in the neck andgiven intravenously if the blood pressure is stable.8 Sequential chest, and dyspnea; syncope is uncommon.
48 Cardiovascular3. Hemodynamically unstable patients in SVT require imme-  Stahmer SA, Cowan R. Tachydysrhythmias. Emerg Med Clin diate electrical cardioversion. N Am 2006;24:11–40.4. Treatment for hemodynamically stable patients in SVT  Haro LH, Hess EP, Decker WW. Arrhythmias in the ofﬁce. should begin with vagal maneuvers, followed by intra- Med Clin N Am 2006;90:417–38. venous adenosine, which has both diagnostic and therapeu-  Hood RE, Shorofsky SR. Management of arrhythmias in the emergency department. Cardiol Clin 2006;24:125–33. tic value.  DiMarco JP, Miles W, Akhtar M, et al. Adenosine for parox-5. SVT infrequently presents as a wide complex tachycardia. ysmal supraventricular tachycardia: dose ranging and com- Wide QRS complex, regular tachycardias should routinely parison with verapamil: assessment in placebo-controlled, be treated as ventricular tachycardia unless the diagnosis of multicenter trials. Ann Intern Med 1990;113:996. SVT with aberrancy or SVT with preexcitation is certain.  Xanthos T, Ekmektzoglou KA, Vlachos IS, et al. A prog- nostic index for the successful use of adenosine in patients with paroxysmal supraventricular tachycardia in emergencyREFERENCES settings: a retrospective study. Am J Emerg Med 2008;26: Delacretaz E. Clinical practice: supraventricular tachycardia. 304–9. N Engl J Med 2006;354:1039–51.  Glater KA, Dorostkar PC, Yang Y, et al. Electrophysio- Gursoy S, Steurer G, Brugada J, et al. The hemodynamic logic effects of ibutilide in patients with accessory pathways. mechanism of pounding in the neck in atrioventricular nodal Circulation 2001;104:1933–9. reentrant tachycardia. N Engl J Med 1992;327:772–4.
13Chest pain and syncope in a 48-year-old maleHISTORY OF PRESENT ILLNESS Blood pressure 80/40 mmHgA 48-year-old male with a medical history signiﬁcant for Respirations 22 breaths/minutetobacco use was brought to the ED by paramedics after a syn- Oxygen saturation 99% on room aircopal episode. The patient reported substernal chest pressure HEENT: Unremarkable.followed by the onset of lightheadedness, at which time heexperienced a transient loss of consciousness. Upon arousal NECK: Supple, no jugular venous distension.by his coworkers, he was still experiencing chest pressure and CARDIOVASCULAR: Bradycardic rate, regular rhythm, withoutlightheadedness. The patient was found to have a heart rate of rubs, murmurs of gallops. Weak radial and dorsalis pedis50 beats/minute with a blood pressure of 80/40 mmHg and was pulses.transported to the ED code III. A peripheral intravenous linewas established en route, and aspirin 162 mg orally, atropine LUNGS: Clear to auscultation bilaterally.1 mg and 500 mL normal saline IV were administered by the ABDOMEN: Soft, nontender, nondistended.paramedics without signiﬁcant improvement in his blood pres-sure or heart rate. EXTREMITIES: No clubbing, cyanosis or edema. NEUROLOGIC: NonfocalPHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient appeared well developed The patient was placed on the cardiac monitor, supplementaland well hydrated, spoke in full sentences, and was in moder- oxygen was administered (2 liters by nasal cannula) and a 12-ate distress. lead ECG was obtained (Figure 13.1).VITAL SIGNS Temperature 98.6◦ F (37◦ C) What is your diagnosis? Pulse 50 beats/minute 49
50 Cardiovascular Figure 13.1 12-lead ECG from a 48-year-old male with chest pain and hypotension following a syncopal episode.
Chest pain and syncope in a 48-year-old male 51 ST-segment elevation, in descending order, are leads III, aVF ANSWER and II. A total of 80–90% of patients who have ST-segmentThe diagnosis is inferior wall myocardial infarction (MI) elevation in these inferior leads have an occlusion of the RCA;with complete (third-degree) heart block. The 12-lead ECG however, an occlusion of the left circumﬂex coronary artery(Figure 13.1) demonstrates signiﬁcant ST-segment elevation (LCx) can produce a similar ECG pattern. In addition to ST-in leads II, III and aVF, with reciprocal ST-segment depres- segment elevation in the inferior leads (II, III and aVF), recip-sion in leads I and aVL, consistent with an inferior wall rocal ST-segment depression in lead aVL is seen in almost allmyocardial infarction, as well as a junctional escape rhythm patients who have an acute inferior STEMI.1(ventricular rate 50 beats/minute). Transcutaneous pacing Acute inferior wall STEMI is often complicated by high-was initiated with improvement of the heart rate to 60 degree atrioventricular (AV) block, the incidence reported tobeats/minute and blood pressure to 110/70 mmHg. An inter- be 6–13%.2 Patients with complete heart block (CHB) areventional cardiologist was immediately notiﬁed, the patient signiﬁcantly more likely to die during hospitalization thanreceived eptiﬁbatide and heparin IV and was urgently trans- patients without CHB (likely related to infarct size rather thanported to the cardiac catheterization laboratory. Coronary the presence of heart block).3,4 The heart block may be a grad-angiogram revealed a 100% occlusion of the proximal right ual delay of conduction or the abrupt onset of third-degreecoronary artery (RCA) and moderate to severe disease of the heart block.4 Most patients will develop heart block withinostial and proximal left anterior descending (LAD) artery. 24 hours of admission. The duration of CHB varies dramat-Successful percutaneous coronary intervention (PCI) with ically from a few minutes to more than 10 days; permanentaspiration thrombectomy and stent placement of the prox- pacemaker implantation is seldom required. Additionally, theimal RCA occlusion occurred, along with temporary pace- duration of hospitalization is signiﬁcantly longer for patientsmaker insertion. A repeat ECG obtained two hours following with CHB than those without CHB.3admission demonstrated a normal sinus rhythm with resolu- Treatment of patients with inferior wall STEMI and CHBtion of acute ischemic changes (Figure 13.2). The patient was involves immediate stabilization of the airway, breathing anddischarged on hospital day #5 in good condition, with close circulation (ABCs). Intravenous atropine (0.5–1.0 mg) mayfollow up in the cardiology clinic. be administered in hemodynamically unstable patients to improve the heart rate and blood pressure. If unsuccessful, temporary transcutaneous pacing should be initiated. Treat-Inferior wall myocardial infarction and complete ment of STEMI includes oral aspirin, heparin, a glycopro-heart block tein IIb/IIIa inhibitor (such as eptiﬁbatide, abciximab orIn inferior wall ST-segment elevation myocardial infarction tiroﬁban) and emergent cardiac catheterization. If a car-(STEMI), the leads showing the greatest magnitude of diac catheterization laboratory is not immediately available, Figure 13.2 12-lead ECG from a 48-year-old male with chest pain and hypotension post-PCI.
52 Cardiovascularﬁbrinolytic agents (thrombolytics) are recommended. Beta- 3. Treatment of patients with inferior wall MI and CHBblockers (e.g., metoprolol) and nitrates should not be ad- involves stabilization of the ABCs, attempts to override theministered to patients who are already bradycardic and hypo- block (IV atropine and transcutaneous pacing), and treat-tensive. ment of the underlying cause (STEMI). The exact cause of heart block in inferior wall MI is unclear 4. Medications that lower the heart rate or blood pres-but is likely due to ischemia without necrosis of the AV node.3 sure (e.g., metoprolol, nitroglycerin) should be used withCHB in inferior MI usually involves the supra-Hisian AV extreme caution (or not at all) in patients with inferior walljunction due to hypoperfusion of the AV-nodal artery (vir- MI and CHB.tually all inferior MIs have occlusion proximal to the AV- 5. The exact cause of heart block in inferior wall MI is unclearnodal artery).1,3 An alternative hypothesis involves increased but is likely due to ischemia without necrosis of the AVvagal tone, called the Bezold-Jarisch reﬂex.3 This mechanism node.does not explain the correlation of increased infarct size withheart block or the cases of sudden CHB without sinus slow- REFERENCESing. Others have suggested that high levels of potassium andadenosine near the conducting tissue after cardiac cell infarc-  Altar S, Barbagelata A, Birnbaum Y. Electrocardiographiction might cause transient blocks.1,3 diagnosis of ST-elevation myocardial infarction. Cardiol Clin 2006;24:343–65.  Ramamurthy S, Anandaraja S, Matthew N. PercutaneousKEY TEACHING POINTS coronary intervention for persistent complete heart block complicating inferior myocardial infarction. J Invasive Car-1. In acute inferior wall MI, the leads showing the greatest diol 2007;19:E372–4. magnitude of ST-segment elevation, in descending order,  Chiu C-A, Youssef AA, Wu C-J, et al. Impact of PercuSurge are leads III, aVF and II. Patients with ST-segment eleva- GuardWire device on prevention and reduction of recovery tion in these inferior leads have an occlusion of the RCA time from complete heart block in patients with acute infer- (80–90% of the time) or the LCx artery (10–20%). ior myocardial infarction undergoing primary percutaneous2. Acute inferior wall myocardial infarction (MI) is compli- coronary intervention. Int Heart J 2007;48:35–44. cated by high-degree atrioventricular (AV) block in 6–13%  Rotondo N, Pollack ML, Chan TC. Electrocardiographic of cases. manifestations: acute inferior wall myocardial infarction. J Emerg Med 2004;26:433–40.
14Syncope and hypotension in a 54-year-old maleHISTORY OF PRESENT ILLNESS HEENT: Unremarkable.A 54-year-old male with a medical history signiﬁcant for dia- NECK: Supple, jugular venous distension present.betes, hypertension and atrial ﬁbrillation on CoumadinTM pre-sented to the ED following a syncopal episode while having CARDIOVASCULAR: Distant heart sounds, regular rate andhis blood drawn. He reported feeling lightheaded during the rhythm, unable to assess for rubs, murmurs or gallops; periph-procedure and lost consciousness for one minute while seated. eral pulses palpable and alternating between weak and strong.He denied chest pain, shortness of breath or palpitations prior LUNGS: Clear to auscultation bilaterally.to the event, and awakened within one minute. He continuedto feel lightheaded so was brought to the ED in a wheelchair ABDOMEN: Soft, nontender, nondistended.and placed on the cardiac monitor. RECTAL: Normal tone, soft brown stool, hemoccult negative.PHYSICAL EXAMINATION EXTREMITIES: No clubbing, cyanosis or edema.GENERAL APPEARANCE: The patient appeared well hydrated, NEUROLOGIC: Nonfocal.awake and alert, and in no acute distress.VITAL SIGNS A peripheral intravenous line was placed and blood was Temperature 97.9◦ F (36.6◦ C) drawn and sent for laboratory testing, which was signiﬁcant for Pulse 92 beats/minute a creatinine of 2.1 mg/dL (normal range <1.3 mg/dL), lactic Blood pressure 100/60 mmHg acid of 2.7 mmol/L (normal 0.7–2.1 mmol/L), and an Interna- Respirations 22 breaths/minute tional Normalized Ratio (INR) of 6.0 (therapeutic range 2.0– Oxygen saturation 97% on room air 3.0). A 12-lead ECG (Figure 14.1) and portable chest radio- graph (Figure 14.2) were obtained. What is your diagnosis? 53
54 Cardiovascular Figure 14.1 12-lead ECG from a 54-year-old male with syncope and hypotension. Figure 14.2 Portable chest radiograph from a 54-year-old male with syncope and hypotension.
Syncope and hypotension in a 54-year-old male 55 ANSWERThe diagnosis is cardiac tamponade secondary to pericardialeffusion (hemopericardium). The hemopericardium resultedfrom a markedly elevated INR (6.0). The ECG demonstrateslow voltage throughout, whereas the chest radiograph showscardiomegaly. A bedside cardiac ultrasound was performed bythe emergency physician, which demonstrated a large pericar-dial effusion (Figure 14.3). The patient was given a total of1 liter normal saline IV, as well as vitamin K 10 mg subcu-taneously and 4 units of fresh frozen plasma to reverse theanticoagulation. A portable echocardiogram was performed,which conﬁrmed a pericardial effusion with signs of tampon-ade including right ventricular collapse (Figure 14.4). Fol-lowing reversal of the anticoagulation, a pericardiocentesis Figure 14.4 Echocardiogram from a 54-year-old male with hemoperi-performed under ﬂuoroscopy by the cardiologist removed cardium and cardiac tamponade (area between cursors = pericardial1100 mL of blood from the pericardium, with immediate effusion).improvement in the patient’s hemodynamics and symptoms. Symptoms of cardiac tamponade include dyspnea, tachyp-Cardiac tamponade nea and fatigue. Signs include tachycardia, jugular venous dis-Cardiac tamponade is a true emergency that occurs when ﬂuid tension, a quiet precordium, hypotension, and pulsus para-accumulation within the pericardium causes pericardial pres- doxus (inspiratory drop in systolic blood pressure of 10%sure to exceed cardiac chamber diastolic pressure. This con- or 10 mmHg).1,3 Although a pericardial rub typically disap-dition prevents cardiac ﬁlling.1 Three factors determine the pears when an effusion develops, a rub caused by pericardial-clinical presentation: the volume of ﬂuid, the rate at which pleural friction may still be heard (typically on inspiration).1the ﬂuid accumulates, and pericardial compliance.1 If the ﬂuid The elevated pericardial pressure resulting in elevated rightaccumulates rapidly or the pericardium is pathologically stiff, atrial and venous pressures causes a characteristic jugularrelatively small amounts of ﬂuid can result in marked eleva- venous waveform lacking the Y descent. The changes resulttions in intrapericardial pressure. Rapidly evolving hemoperi- from decreased right atrial emptying due to impaired ventric-cardium (200–300 mL) is more likely to cause death from ular expansion and ﬁlling.1 The Kussmaul sign, a paradoxicalcardiac tamponade than slowly evolving pericardial ﬂuid accu- increase in jugular venous pulse with inspiration, can also bemulation (500–2000 mL), the latter allowing for accommoda- seen but is not speciﬁc for tamponade (it may also be seen intion of greater volumes due to gradual distension of the peri- constrictive pericarditis, restrictive cardiomyopathy and rightcardial sac.2 The normal volume of pericardial ﬂuid (30–50 ventricular infarction).3mL) reﬂects a balance between production and reabsorption.2 Chest radiographs and ECGs are often unreliable for the prompt diagnosis of cardiac tamponade because ﬁndings are not speciﬁc and may not be present.4 Chest radiograph may demonstrate an enlarged cardiac silhouette (observed in more than 90% of cardiac tamponade cases) or a silhouette in the shape of a water bottle, which suggests cardiomegaly.4 ECGs in cardiac tamponade may show low-amplitude QRS complexes (signifying low voltage) and may depict electri- cal alternans (caused by “swinging” of the oscillating heart in the buoyant pericardial sac); this latter effect is seen in 10–20% of tamponade cases, most of which are neoplastic in origin.4 Cardiac ultrasound is the primary diagnostic modality for the initial detection of pericardial effusion. This can be done at the bedside by emergency physicians.5,6 Pericardial ﬂuid ﬁrst accumulates posterior to the heart when the patientFigure 14.3 Bedside cardiac ultrasound from a 54-year-old male with is examined in the supine position. Small amounts of ﬂuidsyncope and hypotension, demonstrating large pericardial effusion can be present even in healthy individuals.5 As the effusion(vertical dashed line). LV = left ventricle, RV = right ventricle, increases, it extends laterally; with large effusions, the echo-LA = left atrium. free (dark) space expands to surround the entire heart. When
56 Cardiovascularthe ability of the pericardium to stretch is exceeded by rapid KEY TEACHING POINTSor massive accumulation of ﬂuid, any additional ﬂuid causes 1. Cardiac tamponade is an emergency that occurs whenpressure within the pericardial sac to signiﬁcantly increase. ﬂuid accumulation within the pericardium causes pericar-When the increasing intrapericardial pressure exceeds the dial pressure to exceed cardiac chamber diastolic pressure,intracardiac pressure, the positive transmural pressure gradi- which prevents cardiac ﬁlling.ent compresses the adjacent cardiac chamber or chambers.5 2. Symptoms of tamponade include dyspnea, tachypnea, andRight atrial inversion (during ventricular systole, while the fatigue; signs include tachycardia, jugular venous disten-atrium is relaxed) is usually an early sign of compression, fol- sion, a quiet precordium, hypotension, and pulsus para-lowed by diastolic compression of the right ventricular outﬂow doxus.tract. Right ventricular diastolic collapse generally requires a 3. In patients with cardiac tamponade, the chest radiographgreater pressure difference between the intrapericardial space may demonstrate cardiomegaly, whereas the ECG mayand the intracardiac chambers than does right atrial collapse. show low voltage or electrical alternans.Right ventricular collapse is therefore a more speciﬁc but less 4. Cardiac ultrasound is the study of choice for diagnosingsensitive indicator of hemodynamically signiﬁcant pericardial pericardial effusion and cardiac tamponade.compression.5 5. Treatment of cardiac tamponade includes intravenous ﬂuid There is no effective medical therapy for cardiac tampon- augmentation and pericardiocentesis to remove the effusion.ade, although intravenous ﬂuids may be of temporary beneﬁtif the patient is hypovolemic.1 Inotropic agents are not bene-ﬁcial due to the intense endogenous adrenergic stimulation REFERENCESalready present. The heart rate and cardiac contractility are  Shiber JR. Purulent pericarditis: acute infections and chronicgenerally already at a maximum when tamponade is present.1 complications. Hosp Physician 2008;44:9–18.If the patient is unstable, immediate relief of tamponade  Swaminathan A, Kandaswamy K, Powari M, et al. Dyingby percutaneous subxiphoid needle aspiration is required. In from cardiac tamponade. World J Emerg Surg 2007;2:22.hemodynamically stable patients, echocardiography-guided  Force T. The cancer patient and cardiovascular disease. In:pericardiocentesis or pericardiocentesis performed under Libby P, Bonow RO, Mann DL, et al. (eds). Braunwald’sﬂuoroscopy is the treatment of choice.1,3 A catheter is usually Heart Disease: A Textbook of Cardiovascular Medicine, 8thleft in the pericardial space to drain any recurrent effusion; ed. Philadelphia: Saunders, 2008:2105.surgical drainage employing either a subxiphoid window or an  Ariyarajah V, Spodick DH. Cardiac tamponade revisited:open thoracotomy is also an option. a postmortem look at a cautionary case. Tex Heart Inst J 2007;34:347–51. Hong et al. described a case of a 70-year-old male on war-  Wann S, Passen E. Echocardiography in pericardial disease.farin for mitral valve replacement presenting to the ED with J Am Soc Echocardiogr 2007;21:7–13.cardiac tamponade.7 The patient’s INR was 7.5, and urgent  Mandavia DP, Hoffner RJ, Mahaney K, et al. Bedsidepericardiocentesis and pericardiotomy resulted in the drain- echocardiography by emergency physicians. Ann Emerg Medage of 1300 mL of pericardial blood. Similar to this case, 2001;38:377–82.our case demonstrates that overanticoagulation with warfarin  Hong YC, Chen YG, Hsiao CT, et al. Cardiac tamponademay contribute to the development of hemopericardium and secondary to haemopericardium in a patient on warfarin.resulting tamponade. Emerg Med J 2007;24:679–80.
15Palpitations and shortness of breath in a 69-year-old maleHISTORY OF PRESENT ILLNESS Blood pressure 110/70 mmHgA 69-year-old male with a medical history signiﬁcant for a Respirations 22 breaths/minuteprevious myocardial infarction, two-vessel coronary artery Oxygen saturation 98% on room airbypass graft, diabetes, congestive heart failure and ischemic HEENT: Unremarkable.cardiomyopathy (ejection fraction 40%) presented to the EDby ambulance complaining of palpitations and shortness of NECK: Supple, no jugular venous distension.breath. The patient experienced a brief syncopal episode when CARDIOVASCULAR: Tachycardic, regular heart sounds, unablegetting up from bed immediately before his wife called emer- to appreciate rubs, murmurs or gallops. Palpable and rapidgency services. In the ED, the patient appeared awake, alert radial and dorsalis pedis pulses.and in no acute distress. His medications included aspirin, LUNGS: Clear to auscultation bilaterally.felodipine, furosemide, insulin and Flomax R . In the ED, thepatient denied chest pain or shortness of breath but reported ABDOMEN: Soft, nontender, nondistended.palpitations and feeling lightheaded. RECTAL: Brown stool, hemoccult negative. EXTREMITIES: No clubbing, cyanosis or edema.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient was an elderly-appearing NEUROLOGIC: Nonfocal.male lying supine on the gurney, awake, alert and in no acute A 12-lead ECG was obtained (Figure 15.1) and the patient wasdiscomfort. placed on the cardiac monitor. A peripheral intravenous line wasVITAL SIGNS placed, and blood was drawn and sent for laboratory testing. Temperature 98.1◦ F (36.7◦ C) Pulse 180 beats/minute What is your diagnosis? Figure 15.1 12-lead ECG from a 69-year-old male with palpitations and shortness of breath. 57
58 Cardiovascular tachycardia (VT) or, less commonly, an SVT with aberrant ANSWER conduction. Other rare causes of wide complex tachycardiaThe ECG demonstrated a wide complex tachycardia (QRS (WCT) include medications (e.g., tricyclic antidepressants,>150 msec, rate 174), consistent with ventricular tachycar- digitalis, lithium, cocaine, diphenhydramine), hyperkalemia,dia. The patient was given amiodarone 150 mg intravenously post-cardiac arrest and WCTs with pre-excitation syndromesover 10 minutes, followed by the initiation of an amiodarone (i.e., Wolff-Parkinson-White syndrome).2IV drip at 1 mg/min. The patient converted to sinus rhythm In several large series concerned with the differential diag-shortly after initiation of the amiodarone drip, with a repeat nosis of wide QRS tachycardias, the overwhelming majority ofECG demonstrating ﬁrst-degree AV block and ST-segment cases are VT (up to 80%); the next largest group is SVT withdepression in leads II, aVF, V5 and V6 (Figure 15.2). An initial aberrancy, with other diagnoses contributing a small fractiontroponin I obtained on presentation was 0.05 ng/mL (normal of cases.3 From a practical standpoint, it is clear that the major0.00–0.09 ng/mL). Because of the ST-segment depression note differential diagnosis of WCT is between VT and SVT withon the repeat ECG, a heparin infusion was initiated. A repeat aberrancy. A frequently used diagnostic algorithm by Bru-troponin I obtained eight hours after presentation peaked at gada to identify VT on ECG incorporates many previously5.2 ng/mL. The patient underwent placement of an internal published morphologic criteria in a step-wise algorithm. It hascardioverter-deﬁbrillator (ICD) the following day. been demonstrated to have good sensitivity and speciﬁcity in the absence of pre-existing intraventricular conduction abnor- malities (Table 15.1).4,5Wide complex tachycardia With regard to distinguishing VT from SVT with aber-Tachycardias (rate greater than 100 beats/minute) can be rancy, most clinical situations of WCT will be VT in etiologydivided into two categories based on the width of the QRS (more than 70% of the time). A corollary to this is if therecomplexes: narrow complex (QRS duration ≤120 msec) or is doubt as to the etiology of the WCT, the safest approachwide complex (QRS duration >120 msec) tachycardias.1,2 If is to treat the rhythm as VT.3 Most patients who presentthe dysrhythmia has a narrow QRS complex, it is by deﬁni- with VT have underlying heart disease. Individuals with pre-tion a supraventricular tachycardia (SVT). These dysrhyth- vious myocardial infarction (MI) or known coronary arterymias are often well tolerated by patients in good health. These disease (CAD) are approximately four times more likely topatients can be treated using vagal maneuvers, intravenous present with ventricular rather than supraventricular etiolo-adenosine or calcium-channel blockers, and discharged from gies of their WCT.6the ED to complete their evaluation as an outpatient if the Patients in VT without a pulse require immediate deﬁb-SVT converts to sinus rhythm with a controlled rate.1 If the rillation. If the patient has a pulse and is hemodynamicallytachycardia has a wide QRS complex, it is either ventricular unstable, synchronized cardioversion should be performed as Figure 15.2 12-lead ECG from a 69-year-old male with palpitations and shortness of breath following treatment with IV amiodarone.
Palpitations and shortness of breath in a 69-year-old male 59 TABLE 15.1 Diagnosis of wide QRS complex tachycardia Step 1: Is there absence of an RS complex in all precordial leads V1 to V6 ? If yes, then the rhythm is VT. Step 2: Is the interval from the onset of the R wave to the nadir of the S wave greater than 100 msec (0.10 sec) in any precordial leads? If yes, then the rhythm is VT. Step 3: Is there AV dissociation? If yes, then the rhythm is VT. Step 4: Are morphology criteria for VT present (Table 15.2)? If yes, then the rhythm is VT. From Stahmer SA, Cowan R, Emerg Med Clin North Amer 2006;24:11–40.quickly as possible (consider sedation). The patient should KEY TEACHING POINTSbe supported using advanced cardiac life support (ACLS) 1. In greater than 70% of cases of wide complex QRS tachy-guidelines. In a stable patient with sustained, monomorphic cardia, the diagnosis will be ventricular tachycardia (VT);VT, pharmacologic therapy may augment cardioversion. In therefore, when in doubt, treat as VT.the acute phase of treatment, the intravenous drug of choice is 2. Amiodarone is the drug of choice for patients presentingamiodarone, particularly in patients with an impaired cardiac with stable VT, particularly in those with impaired ejectionejection fraction.1,7 Amiodarone should be administered as a fractions.150 mg IV bolus over 10 minutes, followed by an infusion at 3. Pulseless VT mandates deﬁbrillation; unstable patients1 mg/min for six hours, decreasing to 0.5 mg/min subsequently. presenting with VT with a pulse require immediate elec-Other medications that can be used include procainamide, trical cardioversion.which may be especially useful when atrial ﬁbrillation with 4. All patients presenting with VT should be admitted for fur-pre-excitation is suspected. Once stabilized, all patients who ther evaluation and treatment.have VT should be admitted to the hospital for further evalu- 5. Deﬁnitive therapy of VT or VF in selected patients (e.g.,ation and treatment. elderly, post-myocardial infarction, post-resuscitation from In elderly patients with VT, deﬁnitive therapy often man- near fatal ventricular dysrhythmias) involves placement ofdates placement of an implantable cardioverter-deﬁbrillator an implantable cardioverter-deﬁbrillator (ICD).(ICD). With a two-year mortality rate of 30% after MI, ICDsare common in elderly patients. The MADIT and AVID trialsdemonstrated that ICDs are superior to pharmacologic ther- REFERENCESapy alone.7–9  Hood RE, Shorofsky SR. Management of arrhythmias in the emergency department. Cardiol Clin 2006;24:125–33. TABLE 15.2 Morphology criteria for ventricular tachycardia  Hollowell H, Mattu A, Perron AD, et al. Wide-complex Right bundle type requires waveform from V1 and V6 tachycardia: beyond the traditional differential diagnosis of ventricular tachycardia vs supraventricular tachycardia with V1 V6 aberrant conduction. Am J Emerg Med 2005;23:876–89. Monophasic R wave Reversal of rsR’ R/S < 1  Miller JM, Das MK, Yadav AV, et al. Value of the 12-lead ECG in wide QRS tachycardia. Cardiol Clin 2006;24:439–51.  Brugada P, Brugada J, Mont L, et al. A new approach to the differential diagnosis of a regular tachycardia with a wide QRS complex. Circulation 1991;83:1649–59.  Stahmer SA, Cowan R. Tachydysrhythmias. Emerg Med Clin Left bundle type requires any of the below morphologies N Am 2006;24:11–40.  Garmel GM. Wide complex tachycardias: understanding this V1 or V2 V6 (qR or QS) complex condition. Part I – epidemiology and electrophysi- ology. West J Emerg Med 2008;9:28–39.  Gupta R, Kaufman S. Cardiovascular emergencies in the elderly. Emerg Med Clin N Am 2006;24:339–70.  Moss AJ, Hall WJ, Cannom DS, et al. Improved survival R wave > 30 msec, with an implanted deﬁbrillator in patients with coronary dis- Notched downstroke of S wave, ease at high risk for ventricular arrhythmia. N Engl J Med Greater than 100 msec (0.1 sec) nadir S wave 1996;335:2933–40.  AVID Investigators. A comparison of antiarrhythmic-drug therapy with implantable deﬁbrillators in patients resusci- From Stahmer SA, Cowan R, Emerg Med Clin North Amer 2006;24: 11–40. tated from near fatal ventricular arrhythmias. N Engl J Med 1997;337:1576–83.
16Chest pain following emotional stress in a 70-year-old femaleHISTORY OF PRESENT ILLNESS HEENT: UnremarkableA 70-year-old female with a medical history signiﬁcant for NECK: Supple, no jugular venous distension.hypertension, hypercholesterolemia and paroxysmal atrial ﬁb-rillation presented to the ED complaining of chest pain for CARDIOVASCULAR: Regular rate and rhythm without rubs,several hours after being emotionally distressed over her hus- murmurs or gallops.band’s recent illness and hospitalization. She described her LUNGS: Clear to auscultation bilaterally.pain as pressure-like, located centrally without radiation, andrated it at a level of 8 (on a scale of 0 to 10). The pressure was ABDOMEN: Soft, nontender, nondistended.associated with diaphoresis but was not associated with short- RECTAL: Normal tone, brown stool, hemoccult negative.ness of breath or nausea. Her medications included Cozaar R ,diltiazem, hydrochlorothiazide, warfarin and simvastatin. She EXTREMITIES: No clubbing, cyanosis or edema.did not drink or smoke, and lived with her husband. NEUROLOGIC: Nonfocal.PHYSICAL EXAMINATION The patient was placed on the cardiac monitor, a 12-lead ECGGENERAL APPEARANCE: The patient appeared well nourished, was obtained (Figure 16.1) and compared to an ECG fromwell hydrated, was tearful and in moderate discomfort. six months earlier (Figure 16.2). A peripheral intravenous lineVITAL SIGNS was placed, blood was drawn and sent for laboratory testing, Temperature 98◦ F (36.6◦ C) and the patient was given aspirin, intravenous heparin and Pulse 80 beats/minute eptiﬁbatide (Integrilin R ). The initial troponin I returned ele- Blood pressure 160/90 mmHg vated at 4.2 ng/mL (normal 0.00–0.09 ng/mL). The patient was Respirations 20 breaths/minute taken emergently for coronary angiography, which demon- Oxygen saturation 100% on room air strated normal coronary arteries as well as mild inferior and anterior wall hypokinesis and apical left ventricular ballooning. What is your diagnosis? 61
62 Cardiovascular Figure 16.1 12-lead ECG from a 70-year-old female with chest pressure for several hours. Figure 16.2 12-lead ECG from a 70-year-old female six months prior to ED presentation.
Chest pain following emotional stress in a 70-year-old female 63 On coronary angiography, patients do not show evidence ANSWER of obstructive coronary artery disease. In addition, repeatThe diagnosis is Takotsubo cardiomyopathy (“broken heart echocardiography demonstrates complete resolution of leftsyndrome”) due to emotional stress and adrenergically medi- ventricular (LV) dysfunction, usually within two to fourated myocardial injury. The ECG (Figure 16.1) demonstrates weeks, with a normal ejection fraction and no residual wallST-segment elevation in the anterolateral leads (V1 –V6 ), motion abnormalities.2 Takotsubo cardiomyopathy is stronglywhich were new compared to a prior ECG from this patient suggested by the following four key clinical criteria:(Figure 16.2). The patient was discharged on hospital day r a setting of acute emotional stress;#2 and instructed to continue her previous medications, and r symptoms and ﬁndings suggestive of acute coronary syn-begin aspirin and clopidogrel for one month. An echocardio-gram performed one week after discharge demonstrated glob- drome (ACS) with normal coronary arteries on angio-ally decreased left ventricular function, as well as wall motion graphy; r echocardiographic demonstration of LV dysfunction withabnormalities of the inferior, apical and lateral walls. preserved function at the base and akinesia of all other segments; andTakotsubo cardiomyopathy r restoration of normal LV function within several weeks ofTakotsubo cardiomyopathy is a transient cardiomyopathy symptom onset.2characterized by marked apical hypokinesis and ballooning inthe absence of signiﬁcant coronary artery disease.1 Takotsubo, The precise mechanism that causes this type of LV dysfunc-from tako (octopus) and tsubo (jar), is a Japanese term for a tion is unknown. The most commonly discussed mechanismround-bottomed, narrow-necked jar used to trap octopus in for this condition is stress-induced catecholamine release.5Japan.1 Similar to this octopus jar, the heart’s appearance on Studies have shown plasma catecholamine levels in patientsa left ventriculogram in Takotsubo cardiomyopathy appears with Takotsubo cardiomyopathy to be 2–3 times greater thanwide at the apex during end systole, with narrowing where those in patients with classic myocardial infarction, and 7–there is basilar hyperkinesis.1 Typically, patients with Takot- 34 times greater than published normal values.2,6 Elesbersubo cardiomyopathy present with symptoms consistent with et al. demonstrated that impaired myocardial perfusion dueacute myocardial infarction, including chest pain, ST-segment to abnormal microvascular blood ﬂow is frequently presentchanges and positive cardiac enzymes following a exposure in patients with apical ballooning syndrome (ABS), and cor-to emotional stress.2 Receiving news of a sudden death, par- relates with the extent of myocardial injury, indicating thatticipating in an argument, attending a funeral, observing an microvascular dysfunction plays a pivotal role in the patho-armed robbery and even a surprise party have been docu- genesis of myocardial stunning in this syndrome.7 Fortunately,mented as precipitating events occurring shortly before the the prognosis is favorable for patients with Takotsubo car-onset of cardiac symptoms.2 diomyopathy who survive the initial heart failure episode A striking preponderance of female patients with this syn- using general symptomatic and supportive measures; LV sys-drome (often postmenopausal) compared with male patients tolic function typically returns to normal within a few weeks.2(6:1) has been identiﬁed.3 The clinical background associatedwith transient apical ballooning is remarkably similar in most KEY TEACHING POINTScases. The patient is typically a female in her seventh decade,evaluated for the sudden onset of cardiac symptoms such as 1. Takotsubo cardiomyopathy is a transient cardiomyopathydyspnea or chest pain.4 In most instances, these symptoms characterized by marked apical hypokinesis and ballooningoccur close in time to an identiﬁed “trigger.” This precipi- in the absence of signiﬁcant coronary artery disease. How-tating event is commonly, but not exclusively, an emotional ever, it is a diagnosis of exclusion.one but may also be an acute medical illness, such as a severe 2. Patients with Takotsubo cardiomyopathy present withasthmatic attack.4 The majority of patients exhibit chest pain symptoms of acute myocardial infarction (AMI), includ-and ECG changes that suggest myocardial ischemia; however, ing chest pain, ST-segment changes and positive cardiacmost do not develop Q waves.4 ECG presentations can be enzymes following exposure to acute emotional stress.quite variable: ST-segment elevations similar to those in ST- 3. On coronary angiography, patients with Takotsubo car-segment elevation myocardial infarction (STEMI) are com- diomyopathy do not show evidence of obstructive coronarymon but not the rule.3 Often, deep T-wave inversions follow artery disease.where the ST-segment elevations occurred in the acute setting 4. Elevation of plasma catecholamine levels and abnormalrather then the classic pattern of Q wave development. The microvascular blood ﬂow most likely play important rolesmost common leads demonstrating ST-segment elevation are in the development of Takotsubo cardiomyopathy.leads V1 –V3 and, occasionally, leads I and aVL.3 Myocardial 5. The prognosis is favorable for patients with Takotsubo car-enzyme release is less than expected given the ECG ﬁndings diomyopathy, with LV systolic function typically returningand wall motion abnormalities demonstrated. to normal within a few weeks.
64 Cardiovascular  Merchant EE, Johnson SW, Nguyen P, et al. Takotsubo car-REFERENCES diomyopathy: a case series and review of the literature. West Kolkebeck TE. Takotsubo cardiomyopathy: an unusual syn- J Emerg Med 2008;9:104–11. drome mimicking an ST-elevation myocardial infarction. Am  Wittstein IS, Theimann DR, Lima JAC, et al. Neurohor- J Emerg Med 2007;25:92–5. monal features of myocardial stunning due to sudden emo- Mitchell SA, Crone RA. Takotsubo cardiomyopathy: a case tional stress. N Engl J Med 2005;352:539–48. report. J Am Soc Echocardiogr 2006;19:1190.e9–10.  Elesber A, Lerman A, Bybee KA, et al. Myocardial perfu- Geninatti M, Thames M. All stressed out and no pump to go. sion in apical ballooning syndrome correlate of myocardial Am J Emerg Med 2007;25:202–7. injury. Am Heart J 2006;152:469.e9–13. Aurigemma GP, Tighe DA. Echocardiography and rever- sible left ventricular dysfunction. Am J Med 2006;119:18–21.
17General body weakness and slow heart rate in a 72-year-old maleHISTORY OF PRESENT ILLNESS Blood pressure 150/90 mmHgA 72-year-old male with a medical history signiﬁcant for coro- Respirations 20 breaths/minutenary artery disease, hypertension, hyperlipidemia and dia- Oxygen saturation 98% on room airbetes presented to the ED complaining of two months of HEENT: Unremarkable.gradually worsening fatigue and general body weakness. Thepatient saw his primary care provider (PCP) one week earlier NECK: No jugular venous distension.and had his metoprolol dose reduced from 50 mg orally daily CARDIOVASCULAR: Bradycardic, regular rate without rubs,to 25 mg orally daily secondary to fatigue and poor medica- murmurs or gallops.tion tolerance. One week prior to presentation, he discontin-ued his metoprolol without resolution of his symptoms. On LUNGS: Clear to auscultation bilaterally.the day of presentation to the ED, he noted a slow heart rate ABDOMEN: Soft, nontender, nondistended.when checking his radial pulse. He denied chest pain or short-ness of breath, abdominal pain, nausea and vomiting but felt EXTREMITIES: No clubbing, cyanosis or edema.lightheaded when standing. NEUROLOGIC: Nonfocal.PHYSICAL EXAMINATION The patient was placed on the cardiac monitor, a 12-lead ECGGENERAL APPEARANCE: The patient appeared well nourished, was obtained (Figure 17.1), a peripheral intravenous line waswell hydrated and in no acute distress. placed, and blood was drawn and sent for laboratory testing.VITAL SIGNS Temperature 97.8◦ F (36.5◦ C) What is your diagnosis? Pulse 37 beats/minute 65
66 Cardiovascular Figure 17.1 12-lead ECG from a 72-year-old male with fatigue and general body weakness.
General body weakness and slow heart rate in a 72-year-old male 67 to combinations of 4:1 or 3:2 patterns.2 Mobitz Type II carries ANSWER a worse prognosis than Mobitz Type I, and may require per-The diagnosis is 2:1 atrioventricular block (one conducted manent pacemaker placement if the patient is symptomatic.atrial complex for every nonconducted beat). Based upon this When the ratio of AV conduction is 2:1, it is impossible toECG alone, it is impossible to determine whether the patient determine whether the patient has Mobitz Type I or Type IIhas Mobitz Type I or Type II conduction. Laboratory tests conduction. In this case, some authors recommend describingwere normal (complete blood count, electrolytes, BUN, cre- the 2:1 conduction pattern without categorizing it as Type I oratinine, glucose, troponin I). The patient was admitted to Type II.2 Nonetheless, the physician should initially “assumetelemetry for monitoring. He continued to maintain a heart the worst” in situations of 2:1 conduction; that is, the block israte in the 30s with a normal blood pressure and without symp- Mobitz II unless proven otherwise.1toms. A cardiology consult was obtained, and the patient was Third-degree AV block (complete heart block) occursdiagnosed with a high-grade second-degree atrioventricular when no atrial impulses reach the ventricles.4 The atria and(AV) block. The patient underwent a permanent pacemaker ventricles thus function independently (i.e., there is AV disso-placement with resolution of the block and was discharged ciation), and the atrial rate is faster than the ventricular ratefeeling much improved on hospital day #4. because the latter is an escape rhythm. The atrial impulses (P waves) “march” out on the ECG, as do the ventricular depo- larizations (QRS complexes), yet they are unrelated. Ven-Atrioventricular (AV) blocks tricular escape rhythms are usually associated with a worseIn ﬁrst-degree AV block, the PR interval is prolonged, with a prognosis and are more commonly caused by acquired (non-duration greater than 0.20 sec, and is constant without pro- congenital) conditions. It is possible that no escape rhythm isgressive change.1 The P wave has normal morphology and generated, resulting in asystole.4precedes every QRS complex. The QRS complex usually hasa normal morphology and axis. Every atrial complex is con-ducted to the ventricles. First-degree AV block can be a nor- KEY TEACHING POINTSmal ﬁnding, especially in healthy young adults or athletes.2 It 1. First-degree AV block can be a normal ﬁnding, especiallymay occur pathologically because of conduction disease in the in healthy young adults or athletes.AV node or the His-Purkinje system, acute myocardial infarc- 2. For second-degree AV blocks, Mobitz Type II carries ation (particularly inferior MI), myocarditis, electrolyte distur- worse prognosis than Mobitz Type I, and may requirebances and the use of AV nodal-blocking agents.2 permanent pacemaker placement if the patient is symp- Second-degree AV block refers to a disorder of the car- tomatic.diac conduction system in which some atrial impulses are not 3. When the ratio of AV conduction is 2:1, it is impossible toconducted to the ventricles.3 Electrocardiographically, some P determine whether the patient has Mobitz Type I or Typewaves are not followed by a QRS complex. Second-degree AV II conduction; assume that the block is Mobitz II unlessblock is composed of two types: Mobitz I (Wenckebach) block proven otherwise.and Mobitz II. Mobitz I second-degree AV block is character- 4. Third-degree AV block (complete heart block) occursized by a progressive prolongation of the PR interval, which when no impulses from the atria reach the ventricles,results in a progressive shortening of the R–R interval. Ulti- resulting in AV dissociation. This requires permanentmately, the atrial impulse fails to conduct, a QRS complex is pacemaker placement.not generated and there is no ventricular contraction. The PRinterval is the shortest in the ﬁrst beat in the cycle, whereas theR–R intervals between conducted beats are constant.3 Mobitz REFERENCESI block is caused by conduction delay in the AV node (72% of  Brady WJ, Harrington RA. Atrioventricular block. In: Chanpatients) or the His-Purkinje system (the remaining 28%).3 TC, Brady WJ, Harrigan RA, et al. (eds). ECG in Emergency Mobitz II second-degree AV block is characterized by Medicine and Acute Care. Philadelphia: Elsevier, 2005;85–9.an unexpected nonconducted atrial impulse.3 Thus, the PR  Patel PM, Wu W-C. The electrocardiogram in the primaryand R–R intervals between conducted beats are constant. In care ofﬁce. Prim Care Clin Ofﬁce Pract 2005;32:901–30.Mobitz II block, the conduction delay occurs infranodally. The  Levine MD. Heart block, second degree. eMedicine Web-QRS complex is likely to be wide, except in patients where site. Available at http://www.emedicine.com/emerg/topic234.the delay is localized to the bundle of His. The usual pattern htm. Accessed June 30, 2008.of dropped beats in Mobitz II block ranges from two con-  Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricu-ducted atrial complexes for every nonconducted beat (3:1), up lar conduction blocks. Emerg Med Clin N Am 2006;24:1–9.
18Headache, neck pain and chest pain in a 73-year-old maleHISTORY OF PRESENT ILLNESSA 73-year-old male with a medical history signiﬁcant forhypertension, coronary artery disease and prior myocardialinfarction presented to the ED complaining of a headache,neck pain and chest pain for one hour. The patient was lean-ing over his bathroom sink when he experienced the suddenonset of a severe, bitemporal headache that quickly radiateddown his posterior neck and into his back, left chest and ster-num. The patient described the pain as a heaviness and ratedit at a level of 8 (on a scale from 0 to 10). He reported asso-ciated sweating and shortness of breath, but denied nausea orvomiting, dizziness, focal weakness, numbness, visual changesor slurred speech. He had taken three sublingual nitroglyc-erin tablets prior to arrival without improvement in his symp-toms, as well as 81 mg of aspirin. His medications includedaspirin, clonidine, lisinopril, lovastatin and bisoprolol/hydro-chlorothiazide. He denied tobacco, alcohol or recreationaldrug use. He was a practicing Jehovah’s Witness. Figure 18.1 Portable chest radiograph of a 73-year-old male with headache, neck pain and chest pain.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient appeared awake and alert, EXTREMITIES: 2+ pitting edema of bilateral lower extremities.and in mild discomfort. Strong and equal peripheral pulses in upper and lower extrem- ities.VITAL SIGNS Temperature 97.4◦ F (36.3◦ C) NEUROLOGIC: Nonfocal. Pulse 75 beats/minute Blood pressure 189/73 mmHg A peripheral intravenous line was placed, and blood was Respirations 20 breaths/minute drawn and sent for laboratory testing. An ECG was obtained Oxygen saturation 98% on room air that demonstrated a normal sinus rhythm with a ventricular rate of 82, multiple premature ventricular contractions, as wellHEENT: PERRL, EOMI. as ST-segment depression in leads I, II and V4 through V6 ,CARDIOVASCULAR: Regular rate and rhythm with II/VI dias- all new compared to a previous ECG obtained one year ear-tolic murmur at the left upper sternal border, no rubs or gal- lier. Laboratory tests (complete blood count, chemistry panellops. and troponin I) were all within normal limits. The patient was given sublingual nitroglycerin for his chest pain, and aLUNGS: Bilateral rales at the bases without wheezes or portable chest radiograph was obtained (Figure 18.1).rhonchi.ABDOMEN: Soft, nontender, nondistended. What is your diagnosis? 69
70 Cardiovascular dissection usually originates from a tear in the aortic intima. ANSWER It can then propagate proximally or distally, leading to manyThe diagnosis is aortic dissection, Stanford type A. The chest clinical features of dissection. Aortic dissections are classiﬁedradiograph demonstrated a widened mediastinum. A chest CT by the portion of the aorta involved. In the Stanford system,with intravenous contrast was obtained, which demonstrated a type A dissections involve the ascending aorta, either alone ortype A aortic dissection arising just above the level of the aor- with the descending aorta; type B dissections are conﬁned totic valve and involving the ascending, transverse and descend- the descending aorta (Figure 18.3).1 Dissections are also clas-ing thoracic aorta, extending into the abdominal aorta, ter- siﬁed as acute (if present less than two weeks) or chronic (ifminating just above the iliac bifurcation (Figure 18.2). The present longer than two weeks). The majority of thoracic aor-vascular surgeon was urgently consulted. An esmolol and tic dissections presenting to the ED are acute, presenting withnitroprusside IV drip were begun for blood pressure control, chest or back pain.and the patient was taken urgently to the OR for deﬁnitive More than 2000 cases of thoracic aortic dissection (TAD)surgical treatment of the dissection. occur annually in the United States.2 It is the most common acute illness of the aorta. Most cases occur in patients 50– 70 years old, with males predominating. Ascending aortic dis-Aortic dissection section left untreated carries a 75% mortality rate within theAn aortic dissection refers to the separation of the layers of ﬁrst two weeks alone; if the diagnosis remains unrecognized,the aortic wall (the intima, media and adventitia) with entry the mortality reaches 90% at one year.2,3 Estimated mortalityof blood into the aortic media, creating a false lumen.1 The rates are 1–2% per hour for the ﬁrst 24–48 hours.2 A B C D Figure 18.2 CT of the chest, abdomen and pelvis demonstrating Stanford type A aortic dissection in a 73-year- old male, with dissection from the aortic arch (panel A), extending into the ascending and descending aorta (panels B and C, arrows) and into the abdominal aorta (panel D).
Headache, neck pain and chest pain in a 73-year-old male 71 onset, pulse deﬁcits and neurologic deﬁcits increase the like- lihood of TAD, whereas a normal chest radiograph and the absence of acute-onset pain appear to decrease its likelihood. However, because the presentation of TAD is highly vari- able, the diagnosis cannot be ruled out based on medical his- tory, physical examination or plain radiography ﬁndings; fur- ther diagnostic testing is required to conﬁrm or rule out the diagnosis.5 The strategy employed to conﬁrm the diagnosis of TAD depends on the resources available, the patient’s clinical con- dition and one’s pretest suspicion. Unstable patients with a high pretest probability must not leave the ED (except to go to the operating room). In such patients, transesophageal echocardiography (TEE) can be performed at the bedside by a cardiologist. TEE is quick, portable, does not require expo- sure to contrast, and can be performed in the ED.1 It is highly accurate in experienced hands, with a sensitivity as high as Figure 18.3 Stanford classiﬁcation for aortic dissections. 98% and a speciﬁcity reported between 63–96%.1 The main disadvantage is its lack of universal availability. Chest CT is fast, universally available, noninvasive, less Risk factors for thoracic aortic dissection include hyper- operator dependent and highly accurate, with a sensitivity oftension, advanced age, male gender, pregnancy, bicuspid aor- 94% and a speciﬁcity of 87–100%.1 Multidetector row CTtic valve, coarctation of the aorta, connective tissue diseases scanners have a sensitivity of 99% for detecting TAD.3 Addi-such as Marfan’s syndrome and cocaine use.2 Ninety-ﬁve per- tionally, CT provides information about other potential diag-cent of patients with TAD report pain; most often, the pain is noses. Disadvantages of CT include the need for contrast dyeabrupt in onset, located in the anterior chest, posterior chest and the need to leave the ED. Aortography was the goldor back.1–3 The pain may be described as ripping or tearing; standard for diagnosis of TAD but has been supplanted byhowever, these terms are only used by 50% of patients.3 TAD CT scanning and TEE. Aortography has a sensitivity of 87%is associated with syncope in as many as 13% of patients; this and a reported speciﬁcity of 75–94%.1 Disadvantages to aor-may be the sole presenting symptom in 3% of patients. tography are that it is invasive, time-consuming and exposes On physical examination, approximately 50% of patients patients to a high volume of contrast dye. Finally, MRI is anwith TAD are hypertensive (SBP ≥150 mmHg), whereas 16% extremely accurate diagnostic modality for the diagnosis ofare hypotensive or in shock.3 The diastolic murmur of aor- TAD – its use will likely increase in the future.tic insufﬁciency is present in less than one-third of patients, The initial management of patients with TAD is aggres-whereas focal neurologic deﬁcits suggestive of cerebrovascu- sive heart rate and blood pressure control. In hypertensivelar accident are found in 5–17% of patients.3,4 Measurement patients, therapy begins with a short-acting, rapid-onset beta-of the blood pressure in both arms and the thigh demonstrates blocker, such as esmolol or metoprolol, with the goal of low-a systolic pressure differential of more than 20 mmHg in ering the heart rate to a target of 60 beats/minute.1 Following20–40% of patients.1 Myocardial infarction is a relatively rare the initiation of beta-blocker therapy, a potent IV vasodilatorcomplication of proximal aortic dissection, estimated to occur such as nitroprusside is added and titrated to a goal SBP ofin approximately 1–7% of all cases. ECGs obtained in such 100–120 mmHg. Monotherapy with IV labetalol is an excel-cases may show ST-segment elevation or depression consis- lent alternative. Pain should be controlled with narcotics.tent with infarction or ischemia.2,4 Hypotensive patients must be aggressively resuscitated with The chest radiograph is abnormal in 85–90% of patients.1 normal saline; however, inotropic agents should be avoidedMediastinal widening (more than 8 cm) is the most common as they increase shear stress. Despite the presence of cardiacﬁnding, occurring in 63% of type A dissections and 56% of ischemia in patients with TAD, anticoagulation and ﬁbrino-type B dissections.1 Other common CXR ﬁndings include sep- lytic therapy must be withheld as the consequences of sucharation of calcium (more than 5 mm) from the edge of the therapy can be devastating.1aortic wall, a blurred aortic knob, a left pleuroapical cap, a Further management of TAD is determined by the type ofleft pleural effusion, deviation of the paraspinous line, shift dissection and complications. Proximal dissections are a sur-and elevation of the right mainstem bronchus, and deviation gical emergency. Seventy-two percent of patients with typeof the trachea or esophagus to the right. A dissection are treated operatively, with an operative mor- Bushnell and Brown published an extensive review of the tality at experienced centers varying from 7–36%.1 Type Bliterature examining the usefulness and accuracy of medi- dissections are usually managed nonoperatively. Indicationscal history, physical examination and chest radiograph for for surgery include propagation of the dissection, increas-detecting acute TAD.5 They concluded that pain of abrupt ing size of the hematoma, compromise of major branches
72 Cardiovascularof the aorta, impending rupture or bleeding into the pleur- 4. The initial management patients with TAD is aggressiveal cavity. Endovascular therapy with stent placement in some heart rate and blood pressure control, whereas furthercenters is becoming increasingly popular for both type A management of TAD is determined by the type of dis-and B dissections in the appropriate setting. Given the high section and complications (surgery for type A dissections,morbidity and mortality and need for close monitoring, all medical management for type B dissections).patients with aortic dissections must be managed in the 5. Endovascular stent placement has become an option forICU. the treatment of aortic dissections in the appropriate setting.KEY TEACHING POINTS REFERENCES1. Ascending aortic dissection left untreated has a 75% mor- tality rate within the ﬁrst two weeks alone; if the diagnosis  Gupta R, Kaufman S. Cardiovascular emergencies in the remains unrecognized, the mortality reaches 90% at one elderly. Emerg Med Clin N Am 2006;24:339–70. year.  Rogers RL, McCormack R. Aortic disasters. Emerg Med Clin N Am 2004;22:887–908.2. Risk factors for TAD include hypertension, advanced age,  Kelly BS. Evaluation of the elderly patient with acute chest male gender, pregnancy, bicuspid aortic valve, coarctation pain. Clin Geriatr Med 2007;23:327–49. of the aorta, connective tissue diseases and cocaine use.  Haro LH, Krajicek M, Lobl JK. Challenges, controversies,3. Because the presentation of TAD is highly variable, the and advances in aortic catastrophes. Emerg Med Clin N Am diagnosis cannot be ruled out based on medical history, 2005;23:1159–77. physical examination or plain radiography; further diag-  Bushnell J, Brown J. Rational clinical examination abstract: nostic testing is required with chest CT or TEE to conﬁrm clinical assessment for acute thoracic aortic dissection. Ann or rule out the diagnosis. Emerg Med 2005;46:90–2.
19Near syncope, tachycardia and chest pain in a 74-year-old femaleHISTORY OF PRESENT ILLNESS PHYSICAL EXAMINATIONA 74-year-old female with a history of hyperlipidemia, hyper- GENERAL APPEARANCE: The patient was awake and alert, andtension, and dyspnea of unclear etiology complained to her in no acute distress.husband of mild chest pressure and lightheadedness while VITAL SIGNSbrushing her teeth. Her husband checked her blood pres- Temperature 98.6◦ F (37◦ C)sure and found it to be 74/50 mmHg with a heart rate of Pulse 53 beats/minute110 beats/minute per automatic blood pressure cuff, so he Blood pressure 100/60 mmHgcalled emergency services. The patient had undergone a stress Respirations 22 breaths/minutethallium test six months prior to presentation, which showed Oxygen saturation 99% on room airevidence of moderate to severe stress-induced myocardialischemia in the septum and inferior wall. A coronary artery HEENT: Unremarkablecatheterization shortly afterward demonstrated a 45% ejec- NECK: Supple, no jugular venous distension.tion fraction with an area of focal basal inferior hypokinesisbut no obstructive coronary disease. Her prior ECG showed CARDIOVASCULAR: Bradycardic rate, regular rhythm withouta ﬁrst-degree heart block with right bundle branch block and rubs, murmurs or gallops.left posterior fascicular blocks. Approximately one week prior LUNGS: Clear to auscultation bilaterally.to presentation, the patient complained of being lightheaded,which prompted reduction of her metoprolol in half to 12.5 mg ABDOMEN: Soft, nontender, nondistended.once daily. EXTREMITIES: No clubbing, cyanosis or edema; weak periph- Upon arrival to the patient’s residence, the paramedics eral pulses.found the patient awake and in a wide complex tachycardiaat 200 beats/minute with a monomorphic, uniform and reg- NEUROLOGIC: Nonfocal.ular QRS morphology (Figure 19.1, panel A). The patientwas given intravenous lidocaine, which resulted in the rhythm The patient was placed on the cardiac monitor, a peripheralnoted in Figure 19.1, panel B. The patient’s blood pressure intravenous line was placed, and blood was drawn and sentimproved slightly to a systolic pressure of 100 mmHg. She was for laboratory testing. A 12-lead ECG revealed continuationtransported code III to the ED, where she continued to com- of the rhythm noted in Figure 19.1, panel B, without obviousplain of mild lightheadedness but denied chest pain or short- ST-T wave changes. Laboratory tests (including a completeness of breath. blood count, electrolytes, creatinine, glucose and troponin I) were within normal limits. What is your diagnosis? 73
74 Cardiovascular A B Figure 19.1 Rhythm strip of a 74-year-old female before (panel A) and after (panel B) administration of pre-hospital IV lidocaine.
Near syncope, tachycardia and chest pain in a 74-year-old female 75 Lidocaine blocks sodium channels, predominantly in the ANSWER open (or possibly inactivated) state. It has rapid onset andThe diagnosis is complete atrioventricular (AV) block (third- offset, and does not affect normal sinus node automatic-degree heart block) following conversion from ventricular ity in usual doses. In Purkinje ﬁbers in vitro, lidocainetachycardia with lidocaine. Upon presentation to the ED, she depresses normal as well as abnormal forms of automatic-remained in third-degree heart block with what appeared to ity, as well as early and late after-depolarizations.3 It canbe a junctional escape rhythm at 53 beats/minute. A tem- convert areas of unidirectional block into bidirectional blockporary jugular venous pacing wire was placed in the ED. during ischemia and prevent development of VF by prevent-Despite adjustments to the pacemaker’s sensitivity, the pacer ing fragmentation of organized large wave fronts into hetero-spikes were falling on the T waves, at which time the pace- geneous wavelets. In vivo, lidocaine has minimal effect onmaker was temporarily turned off while the pacemaker wire automaticity or conduction except in unusual circumstances.was repositioned. Approximately three minutes later, the Patients with pre-existing sinus node dysfunction, abnormalpatient lost consciousness and became pulseless. The resultant His-Purkinje conduction, or junctional or ventricular escaperhythm shown in Figure 19.2 (panel D) is polymorphic ven- rhythms can develop depressed automaticity or conductiontricular tachycardia consistent with torsades de pointes. The following IV lidocaine.3 Occasional sinus node depression andpatient was immediately deﬁbrillated at 200 Joules (bipha- His-Purkinje block have been reported with its use.sic), which restored her rhythm to second-degree heart block. In this patient, a previous ECG demonstrated an incom-The patient regained consciousness and her pacemaker was plete trifascicular block (bifascicular block with ﬁrst-degreeimmediately turned back on with the rate set at 90 to over- AV block), placing her at increased risk to progress to third-ride her intrinsic rhythm. The patient was admitted to the ICU degree (complete) AV block. In addition, as the patient hadand ultimately underwent permanent internal cardioverter- known disease of the His-Purkinje system, the use of lidocainedeﬁbrillator (ICD) placement. to suppress ventricular tachycardia resulted in additional sup- pression of conduction through this diseased system, result- ing in complete heart block. Finally, it is possible that theTrifascicular block, complete heart block and lidocaine patient was experiencing AV nodal blockade during the weekIntraventricular conduction abnormalities (IVCA) comprise prior to presentation when she described feeling lightheadeda group of abnormalities seen on the ECG that may confuse to her doctor, at which time the dose of her beta-blocker wasclinicians and can conceal potentially lethal disease entities, reduced.such as acute myocardial infarction (AMI).1 There are multi-ple types of IVCAs, each with its unique clinical signiﬁcance.It is useful to categorize conduction abnormalities (blocks) KEY TEACHING POINTSby the number of fascicles involved. Electrical conduction 1. Patients who have multifascicular block have advancedfrom the bundle of His is relayed to the right bundle and conduction system disease that may progress to completethe anterior and posterior divisions of the left bundle.2 Uni- heart block and sudden cardiac death.fascicular blocks, such as right bundle branch block (RBBB), 2. All patients with third-degree heart block require admis-left anterior fascicular block (LAFB) and left posterior fas- sion to either a telemetry ﬂoor (if hemodynamically stablecicular block (LPFB), are the result of a conduction distur- and transcutaneous pacing achieves capture) or an inten-bance in one fascicle. Bifascicular blocks, such as left bundle sive care unit. The decision on telemetry versus intensivebranch block (LBBB), the combination of RBBB and LAFB, care should be made in conjunction with the cardiologist,or RBBB and LPFB, occur when two of the three fascicles based on hospital resources.are involved. Trifascicular block denotes a block in all three 3. Patients with complete AV block and concomitant acutefascicles.1 MI, active myocardial ischemia, congestive heart failure, Trifascicular block can present as a bifascicular block plus wide complex escape rhythm or symptoms of hypoperfu-a third-degree AV block. If the block in one of the fascicles sion may require early placement of a permanent pace-is incomplete, the ECG generally demonstrates a bifascicu- maker, particularly if difﬁculty obtaining capture from anlar block and a ﬁrst- or second-degree AV block. If conduc- external or transvenous pacemaker is encountered.4tion in the dysfunctional fascicle also fails, complete heart 4. Patients with pre-existing sinus node dysfunction, abnor-block ensues. Patients who have multifascicular block have mal His-Purkinje conduction, or junctional or ventricu-advanced conduction system disease that may progress to lar escape rhythms can develop depressed automaticity orcomplete heart block and sudden cardiac death. The cumu- conduction following IV lidocaine administration.lative three-year rate of sudden death in patients who havebifascicular block has been estimated to be 35% in patientswho have LBBB, 11% in patients who have RBBB andLAFB, and 7% in patients who have RBBB and LPFB.1
Figure 19.2 Continuous rhythm strip from a 74-year-old female after turning off temporary pacing wire (panelA, third-degree AV block converting to wide complex QRS tachycardia; panel B, conversion to monomorphicventricular tachycardia (VT); panel C, monomorphic VT degenerating to torsades de pointes; panel D, torsadesde pointes).
Near syncope, tachycardia and chest pain in a 74-year-old female 77  Miller JM, Zipes DP. Therapy for cardiac arrhythmias. In:REFERENCES Libby P, Bonow RO, Mann DL, et al. (eds). Braunwald’s Rogers RL, Mitarai M, Mattu A. Intraventricular conduction Heart Disease: A Textbook of Cardiovascular Medicine, 8th abnormalities. Emerg Med Clin N Am 2006;24:41–51. ed. Philadelphia: Saunders, 2008;788–9. Perron AD, Sweeney T. Arrhythmic complications of acute  Levine MD, Brown DFM. Heart block, third degree. coronary syndromes. Emerg Med Clin N Am 2005;23:1065– eMedicine Website. Available at http://www.emedicine.com/ 82. emerg/topic235.htm. Accessed June 19, 2008.
20Chest pain for 12 hours in a 75-year-old femaleHISTORY OF PRESENT ILLNESS HEENT: Unremarkable.A 75-year-old female with a medical history signiﬁcant for NECK: Supple, no jugular venous distension.hypertension presented to the ED complaining of substernalchest pressure radiating to the left chest that started 12 hours CARDIOVASCULAR: Tachycardic rate, regular rhythm withoutearlier. The pressure was constant, rated at a level of 7 (on rubs, murmurs or gallops.a scale of 0 to 10), and had not abated. The patient denied LUNGS: Clear to auscultation bilaterally.associated nausea, vomiting, shortness of breath or diaphore-sis, and had not experienced similar symptoms in the past. The ABDOMEN: Soft, nontender, nondistended.patient did not smoke or drink and denied a family history of RECTAL: Brown stool, hemoccult negative.coronary artery disease. Her only medications were lisinopriland atenolol. EXTREMITIES: No clubbing, cyanosis or edema. NEUROLOGIC: Nonfocal.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient appeared well nourished, The patient was placed on the cardiac monitor, a stat 12-leadwell hydrated and in no acute distress. ECG was obtained (Figure 20.1) and a peripheral intravenousVITAL SIGNS line was placed, with blood drawn and sent for laboratory Temperature 98.5◦ F (36.9◦ C) testing. Pulse 128 beats/minute Blood pressure 139/70 mmHg What is your diagnosis? Respirations 18 breaths/minute Oxygen saturation 98% on room air 79
80 Cardiovascular Figure 20.1 12-lead ECG from a 75-year-old female with chest pain for 12 hours.
Chest pain for 12 hours in a 75-year-old female 81 distal to the origin of the ﬁrst diagonal branch in a vessel ANSWER that wraps around to supply the inferoapical region of theThe diagnosis is acute anterior myocardial infarction (MI). left ventricle.1 New right bundle-branch block with a Q waveThe patient’s ECG showed sinus tachycardia, rate 128, with preceding the R wave in lead V1 is a speciﬁc but insensitiveST-segment elevation in leads V1 to V4 , with reciprocal ST- marker of proximal occlusion of the LAD artery in associa-segment depression in leads II, III and V6 . The patient tion with anteroseptal MI.received aspirin orally, sublingual nitroglycerin, intravenous Coronary artery disease is the leading cause of death inmetoprolol, intravenous heparin and Integrilin (glycoprotein the United States. In 2006, approximately 1.2 million Amer-IIb/IIIa inhibitor). The patient was taken for emergent per- icans sustained a MI.2 Of these, one-quarter to one-third hadcutaneous transluminal coronary angioplasty (PTCA), which an ST-segment elevation MI (STEMI). Of all patients hav-revealed a 99% stenosis of her left anterior descending (LAD) ing an MI, 25–35% will die before receiving medical atten-coronary artery. The LAD was stented and the patient was tion, most often from ventricular ﬁbrillation. For those whoadmitted to the ICU, where she continued to improve with reach a medical facility, the prognosis is considerably betterresolution of her ST-segment elevations (Figure 20.2, ECG and has improved over the years: in-hospital mortality ratesobtained two weeks post-angioplasty). fell from 11.2% in 1990 to 9.4% in 1999.2 Most of this decline is due to decreasing mortality rates among patients with STEMI as a consequence of improvements in initial therapy, includ-Anterior myocardial infarction ing ﬁbrinolysis and primary percutaneous coronary interven-In MI of the anterior wall, ST-segment elevation in leads V1 , tion (PCI). In an analysis by the National Registry of Myocar-V2 and V3 indicates occlusion of the left anterior descending dial Infarction (NRMI), the rate of in-hospital mortality wascoronary artery.1 ST-segment elevation in these three leads 5.7% among those receiving reperfusion therapy, compared toand in lead aVL in association with ST-segment depression of 14.8% among those who were eligible for but did not receivemore than 1 mm in lead aVF indicates proximal occlusion of such therapy.2the LAD artery. In this case, the ST-segment vector is directed In comparison with conservative medical management,upward, toward leads V1 , aVL and aVR, and away from the ﬁbrinolytic therapy leads to improved left ventricular sys-inferior leads. ST-segment elevation in leads V1 , V2 and V3 tolic function and survival in patients with MI associatedwithout signiﬁcant inferior ST-segment depression suggests with either ST-segment elevation or left bundle-branch blockocclusion of the LAD artery after the origin of the ﬁrst diago- (LBBB).2 However, ﬁbrinolytic therapy has several limita-nal branch. tions, including patients with contraindications to ﬁbrinolysis ST-segment elevation in leads V1 , V2 and V3 with eleva- (27% in one report), failure of thrombolytic therapy to opention in the inferior leads suggests occlusion of the LAD artery occluded vessels (15% of patients given thrombolytics) and Figure 20.2 12-lead ECG from a 75-year-old female two weeks following PTCA for an acute anterior MI, demonstrating resolution of signiﬁcant ST-segment elevation in anterior leads.
82 Cardiovascularreocclusion of the infarct-related artery within three months venous infusion of heparin. The researchers found that theafter MI in patients receiving thrombolytic therapy (25% of ﬁnal left ventricular infarct size was signiﬁcantly smaller inpatients).2 patients assigned to the invasive group (median = 8%) ver- Primary PCI consists of urgent balloon angioplasty (with or sus those assigned to the conservative group (median =without stenting) with platelet glycoprotein IIb/IIIa inhibitors 13%).5 The average difference in ﬁnal left ventricular infarctbut not ﬁbrinolytic therapy to open the infarct-related artery size between the invasive and conservative groups was 5%.during an acute STEMI. After identifying the site of recent The outcomes of death, recurrent MI or stroke at 30 daysthrombotic occlusion on coronary angiography, a metal wire occurred in 8 patients in the invasive group (4.4%) and 12is advanced past the thrombus over which a balloon catheter patients in the conservative group (6.6%), a 33% lower risk(with or without a stent) is positioned at the site of the occlu- of these outcomes for patients in the invasive group. Thesion and inﬂated, thereby mechanically restoring antegrade researchers concluded that this ﬁnding increased the evidenceﬂow. Primary PCI restores angiographically normal ﬂow in supporting the invasive strategy and deserves considerationthe previously occluded artery in more than 90% of patients, when current treatment guidelines for this category of patientswhereas ﬁbrinolytic therapy is reported to do so in only 50– is reassessed.60% of such patients.2 In a meta-analysis of 23 randomized, controlled compar-isons of PCI (involving 3872 patients) and ﬁbrinolytic ther- KEY TEACHING POINTSapy (3867 patients), the rate of death four to six weeks after 1. An ECG demonstrating ST-segment elevation in leads V1 ,treatment was signiﬁcantly lower among those who underwent V2 and V3 is consistent with an anterior wall myocardialprimary PCI (7% versus 9%).3 Rates of nonfatal reinfarction infarction (MI) and indicates occlusion of the left anteriorand stroke were also signiﬁcantly reduced. Most of these trials descending (LAD) artery.were performed in high-volume interventional centers by 2. In comparison with conservative management, ﬁbrinolyticexperienced operators with minimal delay after the patient’s therapy leads to improved left ventricular systolic func-arrival. If primary PCI is performed at low-volume centers by tion and survival in patients with ST-segment eleva-less-experienced operators with longer delays between arrival tion myocardial infarction (STEMI) or left bundle-branchand treatment, such superior outcomes may not be seen. block (LBBB). One of the indications for thrombolysis is ongoing symp- 3. Primary percutaneous coronary intervention (PCI) re-toms for less than 12 hours. One nonsystematic review found stores angiographically normal ﬂow in previously occludedthat the earlier thrombolytic treatment was given after the artery in more than 90% of patients, whereas ﬁbrinolyticonset of symptoms, the greater the absolute beneﬁt of treat- therapy does so only in 50–60% of such patients.ment.4 For each hour of delay in thrombolytic treatment, theabsolute risk reduction (ARR) of death decreased by 0.16%(ARR for death if given within 6 hours of symptoms = 3%; REFERENCESARR for death if given 7–12 hours after onset of symp-  Zimetbaum PJ, Josephson ME. Current concepts: use of thetoms = 2%).4 Too few people in the review received treatment electrocardiogram in acute myocardial infarction. N Engl Jmore than 12 hours after the onset of symptoms to determine Med 2003;348:933–40.whether the beneﬁts of thrombolytic treatment given after  Keeley EC, Hillis LD. Primary PCI for myocardial infarction12 hours would outweigh the risks. with ST-segment elevation. N Engl J Med 2007;356:47–54. Schomig and colleagues conducted a study to assess  Keeley EC, Boura JA, Grines CL. Primary angioplasty ver-whether an invasive strategy based on PCI with stent- sus intravenous thrombolytic therapy for acute myocardialing is associated with reduction of infarct size in patients infarction: a quantitative review of 23 randomised trials.with acute STEMI presenting greater than 12 hours after Lancet 2003;361:13–20.  Fibrinolytic Therapy Trialists’ (FTT) Collaborative Group.the symptom onset, compared to conventional conserva- Indications for ﬁbrinolytic therapy in suspected acutetive treatment strategy.5 Conducted from May 2001 to myocardial infarction: collaborative overview of early mor-December 2004, the study included 365 patients aged 18– tality and major morbidity results of all randomized trials of80 years without persistent heart attack symptoms admit- more than 1000 patients. Lancet 1994;343:311–22.ted with the diagnosis of acute STEMI between 12–48 ¨  Schomig A, Mehilli J, Antoniucci D, et al. Mechanical reper-hours from symptom onset. Patients were randomized to fusion in patients with acute myocardial infarction present-receive either an invasive strategy (n = 182), based pre- ing more than 12 hours from symptom onset. A randomizeddominantly on coronary stenting plus intravenous abciximab controlled trial. JAMA 2005;293:2865–72.(a glycoprotein IIb/IIIa inhibitor), or conventional conserva-tive treatment strategy (n = 183), which included an intra-
21Shortness of breath and cough in an 80-year-old femaleHISTORY OF PRESENT ILLNESS CARDIOVASCULAR: Distant heart sounds, regular rate andAn 80-year-old female with a medical history signiﬁcant for rhythm without rubs, murmurs or gallops, palpable radial andchronic obstructive pulmonary disease, hypertension, hyper- dorsalis pedis pulses bilaterally.lipidemia and chronic upper back pain presented to the ED LUNGS: Diminished breath sounds throughout, diffuse wheez-complaining of two weeks of increasing shortness of breath, ing, scattered rhonchi, prolonged expiratory phase.cough, wheezing and dyspnea on exertion. Her symptomshad acutely worsened over the past two days, and were not ABDOMEN: Soft, nontender, nondistended.relieved with her ipratropium inhaler. She was seen by her RECTAL: Normal tone, brown stool, hemoccult negative.primary care provider nine days previously and started clar-ithromycin for bronchitis. The patient denied fever or chills, EXTREMITIES: No clubbing, cyanosis or edema.chest pain, leg swelling, focal weakness, numbness or tingling. NEUROLOGIC: Nonfocal.She reported chronic back pain, which had not worsened. A peripheral intravenous line was placed, blood was drawnPHYSICAL EXAMINATION and sent for laboratory testing, and a 12-lead ECG andGENERAL APPEARANCE: The patient was breathing rapidly, portable chest radiograph were obtained (Figures 21.1 andappeared dyspneic and spoke only four- or ﬁve-word sen- 21.2, respectively). The patient received multiple bronchodila-tences. tor treatments (nebulized albuterol and ipratropium bromide)VITAL SIGNS and prednisone 60 mg orally with minimal improvement of Temperature 98.3◦ F (36.8◦ C) her symptoms. Laboratory tests revealed a leukocyte count of Pulse 95 beats/minute 12.7 K/μL (normal 3.5–12.5 K/μL) with 87% neutrophils Blood pressure 106/71 mmHg (normal 50–70%), hematocrit of 32% (normal 34–46%), brain Respirations 32 breaths/minute natriuretic peptide (BNP) of 384 pg/mL (normal <100 pg/ Oxygen saturation 87% on room air mL), D-dimer positive, troponin I less than 0.02 ng/mL (nor- 93% on 2 liters oxygen by mal 0.00–0.09 ng/mL); the remainder of the patient’s labora- nasal canula tory tests (electrolytes, creatinine and glucose) were within normal limits.HEENT: PERRL, EOMI, oropharynx dry.NECK: Supple, no jugular venous distension. What is your diagnosis? 83
84 Cardiovascular Figure 21.1 12-lead ECG from an 80-year-old female with cough and shortness of breath. Figure 21.2 Portable chest radiograph from an 80-year-old female with cough and shortness of breath.
Shortness of breath and cough in an 80-year-old female 85 during pregnancy. In younger patients, inherited conditions ANSWER such as Marfan syndrome, Ehlers-Danlos syndrome, bicuspidThe diagnosis is Stanford type A aortic dissection. The ECG aortic valve, coarctation of the aorta and Turner syndromedemonstrates a regular sinus rhythm, rate 93, with diffuse predispose to AAD.2 Depending on the study population,T-wave ﬂattening. The portable chest radiograph shows a the incidence of AAD ranges from 5–30 cases per 1 millionleft base inﬁltrate or effusion, as well as an interstitial radio- population per year.3pacity in the right lower lung zone, cardiomegaly, and medi- Aortic dissections are classiﬁed by the portion of the aortaastinal widening. A CT angiogram of the chest was obtained to involved. In the Stanford system, type A dissection involvesrule out pulmonary embolism (positive D-dimer), which sub- the ascending aorta, either alone or with the descending aorta.sequently demonstrated an aortic dissection extending from Type B dissection is conﬁned to the descending aorta.4 In thethe aortic root into the ascending arch (Stanford type A), DeBakey classiﬁcation, type I dissection involves the entireas well as a small pericardial effusion and bilateral pleural aorta, type II dissection involves only the ascending aorta, andeffusions (Figure 21.3). Dilatation of the ascending aorta was type III dissection involves only the descending aorta, spar-noted to be 5 cm maximally; the dissection ﬂap did not deﬁni- ing the ascending aorta and the arch.2 Classiﬁcation by site istively extend into the supra-arch vessels. The aortic arch cal- important because it carries both therapeutic and prognosticiber was noted to be 3 cm. The patient was admitted to the signiﬁcance. Dissections are also classiﬁed temporally as acutecardiothoracic surgery service for emergent repair of her aor- (present less than two weeks) and chronic (present longer thantic dissection. Intraoperative diagnosis was subacute Stanford two weeks).4 The majority of aortic dissections are acute.type A aortic dissection with early cardiac tamponade. The classic description of pain in AAD is the instanta- neous onset of chest pain that is maximal at its onset and described as knife-like, ripping or tearing.3 This presenta-Aortic dissection tion is often the exception rather than the rule. Sharp, knife-Acute aortic dissection (AAD) is a cardiovascular emer- like or tearing pain is reported only in approximately 50%gency that requires prompt diagnosis and treatment. AAD of patients.3 Patients with dissections of the descending aortausually occurs in the presence of hypertension. The condi- more commonly report back pain rather than chest pain;tion arises as an intimal tear of the aorta; blood later dis- patients with descending AADs are also more likely to reportsects into the aortic media to form a false and true lumen.1 radiation of pain to the hips and legs. More than one-thirdSystemic hypertension is thought to be the most important of patients present with symptoms attributable to secondarypredisposing factor.2 Other acquired predisposing conditions organ involvement (e.g., neurologic symptoms, syncope,include direct trauma, iatrogenic retrograde dissection from abdominal pain, gastrointestinal bleeding, dysphagia andcatheter-related aortic intimal injury and previous valvular, hoarseness).3coronary bypass or aortic surgery. Cocaine use also predis- In patients presenting with symptoms concerning forposes to aortic dissection by the sudden increase in aortic wall AAD, an ECG should be obtained to assess for cardiacstress created by catecholamine surge.2 An unexplained rela- ischemia. Although normal in only 30% of aortic dissections,tionship may exist between aortic dissection and pregnancy, there are no ECG ﬁndings pathognomonic for AAD.4 Thewith about half of all dissections in young women occurring chest radiograph is abnormal in 85–90% of patients, with A B Figure 21.3 Chest CT from an 80-year-old female demonstrating Stanford type A aortic dissection (arrow, panel A) and dilated aortic arch (arrow, panel B).
86 Cardiovascularmediastinal widening larger than 8 cm being the most com- cope (33.9% vs. 11.7%), congestive heart failure (19.7% vs.mon ﬁnding (occurs in 63% of type A dissections and 56% of 3.9%), and stroke (11.3% vs. 4.7%) were more frequent pre-type B dissections).4 At most centers, helical CT has become senting signs in group 1. Diabetes (10.2% vs. 4.0%), aorticthe emergency imaging modality of choice, with diagnos- aneurysm (29.5% vs. 13.1%), and prior cardiovascular surgerytic accuracy in the detection of AAD approaching 100%.1,3 (48.1% vs. 19.7%) were also more common in group 1. In-Although the sensitivity and speciﬁcity of MRI ranges from hospital mortality was greater in group 1 (33.3% vs. 23.2%),95–100%, technical limitations (long study times, restricted especially due to type B dissection (43.8% vs. 10.4%), and thepatient access, restricted monitoring) limit its use in the emer- prevalence of aortic rupture was greater among patients withgent setting. Transesophageal echocardiography is an accept- type B dissection in group 1 (18.8% vs. 5.9%).able modality for diagnosing AAD (its reported sensitivityapproaches 98%), particularly in unstable patients.1,3 KEY TEACHING POINTS The initial management of all patients with aortic dissec-tion is medical, with aggressive heart rate and blood pressure 1. Acute aortic dissection is a vascular emergency that arisescontrol. In hypertensive patients, therapy begins with a beta- as an intimal tear of the aorta. Blood later dissects into theblocker (esmolol or metoprolol) with the goal of lowering the aortic media to form a false and true lumen.heart rate to 60 beats/minute. This is followed by the addi- 2. In the Stanford classiﬁcation system, type A dissectiontion of a potent IV vasodilator such as nitroprusside, which involves the ascending aorta, either alone or with the des-is titrated to achieve a systolic pressure of 100–120 mmHg.4 cending aorta; type B dissection is conﬁned to the descend-Proximal dissections (Stanford type A) are a surgical emer- ing aorta.gency, whereas type B dissections are usually managed non- 3. Sharp, knife-like or tearing pain is reported only in approx-operatively. imately 50% of patients with AAD; other ﬁndings include von Kodolitsch et al. evaluated 250 patients in a prospec- abnormal chest radiography and pulse or blood pressuretive, observational study with acute chest pain, back pain or differentials between upper extremities.both and clinical suspicion of AAD in an attempt to identify 4. Helical CT (in stable patients) and transesophageal echo-independent predictors of AAD.5 Aortic pain with immedi- cardiography (in unstable patients) are the imaging modal-ate onset, a tearing or ripping character or both; mediasti- ities of choice for diagnosing aortic dissection.nal widening, aortic widening or both on chest radiography; 5. Type A dissections are surgical emergencies, whereas typeand pulse differentials, blood pressure differentials or both B dissections are generally managed nonoperatively (med-(p < 0.001 for all) were identiﬁed as independent predictors ical management with strict blood pressure control).of AAD. Probability of aortic dissection was low with absenceof all three variables (7%), intermediate with isolated ﬁndings REFERENCESof aortic pain or mediastinal widening (31% and 39%, respec-tively), and high with isolated pulse or blood pressure differ-  Jeudy J, Waite S, White CS. Nontraumatic thoracic emergen-entials or any combination of the three variables (≥83%). In cies. Radiol Clin N Am 2006;44:273–93.this study, 4% of all aortic dissections were assigned to the  Kamalakannan D, Rosman HS, Eagle KA. Acute aortic dis-low-probability group, 19% to the intermediate-probability section. Crit Care Clin 2007;44:779–800.group, and 77% to the high probability group.  Winters ME, Kluetz P, Zilberstein J. Back pain emergencies. Med Clin N Am 2006;90:505–23. Park et al. evaluated the clinical characteristics and out-  Gupta R, Kaufman S. Cardiovascular emergencies in thecomes of patients with painless AAD in a retrospective case elderly. Emerg Med Clin N Am 2006;24:339–70.record study.6 Of 977 patients in the International Registry  von Kodolitsch Y, Schwartz AG, Nienaber CA. Clinicalof Acute Aortic Dissection (IRAAD) database from 1997 to prediction rule of acute aortic dissection. Arch Intern Med2001, 63 (6.4%) had painless AAD (group 1) and 914 (93.6%) 2000;160:2977–82.had painful AAD (group 2). Patients in group 1 were older  Park SW, Hutchinson S, Mehta RH, et al. Association ofthan those in group 2 (mean age 66 vs. 61 years). Type A dis- painless acute aortic dissection with increased mortality.section was more frequent in group 1 (74.6% vs. 60.9%). Syn- Mayo Clin Proc 2004;79:1252–7.
22Weakness, fatigue and shortness of breath in an 88-year-old maleHISTORY OF PRESENT ILLNESS HEENT: Unremarkable.An 88-year-old male with a medical history signiﬁcant for NECK: No jugular venous distension.diabetes, hyperlipidemia, chronic kidney disease and hypo-thyroidism was brought to the ED by ambulance complaining CARDIOVASCULAR: Regular, bradycardic rate without rubs,for two weeks of worsening shortness of breath, fatigue and murmurs or gallops.general body weakness. He denied chest pain, cough, fevers, LUNGS: Bilateral rales at the bases without wheezes orabdominal pain, lightheadedness or dizziness. The patient rhonchi.reported a 10 lb (4.5 kg) weight gain over the last severalmonths, and had noted some swelling of both legs during this ABDOMEN: Soft, nontender, nondistended.period. The patient’s medications included metformin, tera- EXTREMITIES: 2+ pitting edema bilaterally.zosin, lisinopril/hydrochlorothiazide, glipizide, levothyroxineand lovastatin. The patient denied tobacco or alcohol use. NEUROLOGIC: Nonfocal.PHYSICAL EXAMINATION A rhythm strip obtained from the paramedics was reviewedGENERAL APPEARANCE: The patient was sitting upright in no (Figure 22.1), and a 12-lead ECG was obtained (Figure 22.2).acute distress; he was noted to be slightly breathless while Laboratory test results included a troponin I of 0.08 ng/mLspeaking, unable to complete full sentences. (normal 0.0–0.09 ng/mL), a brain natriuretic peptide (BNP) level of 560 pg/mL (normal <100 pg/mL), a creatinine ofVITAL SIGNS 1.5 mg/dL (normal <1.3 mg/dL), and a potassium of 5.6 mEq/ Temperature 98.5◦ F (36.9◦ C) L (normal 3.5–5.3 mEq/L). A chest radiograph was obtained Pulse 38 beats/minute (Figure 22.3). Blood pressure 182/90 mmHg Respirations 20 breaths/minute Oxygen saturation 94% on room air What is your diagnosis? Figure 22.1 Rhythm strip from an 88-year-old male with weakness, fatigue and shortness of breath. 87
88 Cardiovascular Figure 22.2 12-lead ECG from an 88-year-old male with weakness, fatigue and shortness of breath. Figure 22.3 Chest radiograph of an 88-year-old male with weakness, fatigue and shortness of breath.
Weakness, fatigue and shortness of breath in an 88-year-old male 89 treating cardiologist. These patients, as with all patients in ANSWER third-degree heart block, require placement of a permanentThe diagnosis is third-degree heart block with congestive pacemaker.5heart failure exacerbation. The rhythm strip and ECG show Hemodynamically unstable patients may be treated withcomplete atrioventricular (AV) dissociation, whereas the atropine. However, if the rhythm is a wide complex escapechest radiograph demonstrates small bilateral pleural effu- rhythm, atropine is likely to be unsuccessful.4 In addition,sions with minimal pulmonary vascular congestion. Pacer caution should be taken when administering atropine to apads were applied to the chest, and a cardiology consult was patient with a suspected acute MI, as the resulting vago-obtained in the ED. The patient was admitted to the medicine lysis may lead to unopposed sympathetic stimulation. This canservice for urgent placement of a permanent transvenous cause increased ventricular irritability and potentially dan-pacemaker. gerous ventricular dysrhythmias. Similarly, isoproterenol may accelerate a ventricular escape rhythm but has a low probabil- ity for efﬁcacy. Hemodynamically unstable patients for whomThird-degree atrioventricular block timely cardiologic consultation is unavailable should undergoIn third-degree heart block, also known as complete heart temporary transvenous pacemaker insertion in the ED if tran-block, no atrial impulses reach the ventricle through the atrio- scutaneous pacing or pharmacologic therapy are unsuccessful.ventricular (AV) conduction system.1,2 Therefore, the atriaand ventricles are controlled by different pacemaker sites KEY TEACHING POINTSand function independently. The atrial pacemaker can beeither sinus or ectopic. The ventricular escape rhythm can 1. In third-degree (complete) heart block, atrial impulsesalso have varying pacemaker sites, resulting in differing rates. do not reach the ventricles through the AV conductionRarely, the ventricular escape rhythm is absent and the patient system.presents in asystole. More often, the site of escape is just below 2. Emergency management for patients in third-degree heartthe level of the AV block. block includes special attention to the ABCs. The atrial rate is usually greater than the ventricular rate 3. Patients in whom capture cannot be obtained with ain patients with third-degree AV block. There is no meaning- transcutaneous pacemaker require urgent placement offul relationship between the P waves and the QRS complexes. a transvenous pacemaker, even if the patient is asymp-The P waves appear in a regular rhythm and “march” through tomatic.the rhythm strip at a speciﬁc rate.1,2 The QRS complexes 4. Hemodynamically unstable patients should be givenshould appear in a regular fashion, and generally also “march” atropine, dopamine, or possibly isoproterenol to increasethrough the rhythm strip. The duration of the QRS complex the heart rate while a transcutaneous pacemaker is beingand the ventricular rate depend on the site of the block. When initiated for pacing.the ventricular escape rhythm is located near the His bun- 5. If a transcutaneous pacemaker does not capture anddle, the rate is greater than 40 beats/minute and the QRS improve the hemodynamic status of unstable patients, acomplexes tend to be narrow.1,3 When the site of escape is dis- transvenous pacemaker should be emergently inserted intal to the His bundle, the rate tends to be less than 40 beats/ the ED.minute and the QRS complexes tend to be wide. Emergency management for patients in third-degree heart REFERENCESblock should include special attention to the ABCs (airway,breathing and circulation), including supplemental oxygen,  Ufberg JW, Clark JS. Bradydysrhythmias and atrioventricu-initiation of an intravenous line, frequent monitoring of blood lar conduction blocks. Emerg Med Clin N Am 2006;24:1–9.pressure and continuous cardiac monitoring. AV-nodal block-  Brady, WJ, Harrigan, RA. Atrioventricular block. In: Chaning agents should be withheld, and transcutaneous pacing pads TC, Brady WJ, Harrigan RA, et al. (eds). ECG in Emergency Medicine and Acute Care. Philadelphia: Elsevier, 2005;86–8.should be applied and tested when needed.4 Patients in whom  Mangrum JM, DiMarco JP. The evaluation and managementcapture cannot be obtained with a transcutaneous pacemaker of bradycardia. N Engl J Med 2000;342:703–9.need urgent placement of a transvenous pacemaker, even if  Levine, MD. Heart block, third degree. eMedicine Website.the patient is asymptomatic. Hemodynamically stable patients Available at http://www.emedicine.com/emerg/topic235.htm.in whom transcutaneous pacing can be successfully performed Accessed June 30, 2008.can go to a telemetry bed or ICU at the discretion of the  Kusumoto, FM, Goldschlager, N. Medical progress: cardiac pacing. N Engl J Med 1996;334:89–98.
23Sudden onset of back pain in a 91-year-old maleHISTORY OF PRESENT ILLNESSA 91-year-old male with a medical history signiﬁcant forborderline hypertension presented to the ED complaining ofthe sudden onset of severe back pain beginning one hourprior to arrival. He described the pain as sharp and radiatingthroughout his entire back, from his upper thoracic area to hislumbar region. The patient denied chest pain, dyspnea, focalweakness or numbness. He did not take any medications. Thepatient was active, participating in many sports and had been aSenior Olympic gold medalist in swimming. He did not smokeor drink alcohol.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient was an athletic, well-hydrated male who appeared to be in moderate discomfort.VITAL SIGNS Temperature 98.0◦ F (36.6◦ C) Figure 23.1 Chest radiograph of a 91-year-old male with sudden onset Pulse 60 beats/minute of sharp back pain. Blood pressure 220/110 mmHg Respirations 22 breaths/minute Oxygen saturation 98% on room air The patient was placed on the cardiac monitor, a peripheral intravenous line was placed, and blood was drawn and sentHEENT: Unremarkable. for laboratory testing. Laboratory tests (including a completeNECK: Supple, no jugular venous distension. blood count, electrolytes, creatinine, glucose and troponin I) were all within normal limits. A 12-lead ECG demonstrated aCARDIOVASCULAR: Regular rate and rhythm without rubs, normal sinus rhythm, rate 55 beats/minute, without any acutemurmurs or gallops. ST-T wave changes. A portable chest radiograph was obtainedLUNGS: Bibasilar rales, no wheezes or rhonchi. (Figure 23.1).ABDOMEN: Soft, nontender, nondistended, without pulsatilemasses. What is your diagnosis?EXTREMITIES: No clubbing, cyanosis or edema; strong radial,femoral and dorsalis pedis pulses bilaterally.NEUROLOGIC: Nonfocal. 91
92 Cardiovascular Stanford type A (involving the ascending aorta or ascending ANSWER and descending aorta) or Stanford type B (involving only theThe diagnosis is a descending thoracic aortic intramural hema- descending aorta), analogous to aortic dissection.2 IMH of thetoma (Stanford type B). The chest radiograph demonstrates aorta is considered a variant of acute aortic dissection, witha widened mediastinum. A CT angiogram of the chest and hemorrhage within the wall of the aorta but lacking an intimalabdomen was obtained, which demonstrated a hematoma of tear or visible ﬂap.2,3 This lack of an intimal tear suggests thatthe arch and descending portion of the thoracic aorta, extend- the bleeding within the aortic wall likely comes from tearing ofing into the abdominal aorta (Figure 23.2). No obvious dis- the small penetrating blood vessels (the vaso vasorum) of thesection or intimal ﬂap was identiﬁed. A nitroglycerin drip for aortic wall. Because there are no tears in the aortic lining, thisblood pressure control was started, which brought his blood localized hematoma has no Doppler ﬂow seen on echocardio-pressure down to 130/60, and the patient was admitted to the gram and no enhancement with contrast administration on CTICU by cardiothoracic surgery for observation and close mon- scan. However, in some cases IMH can rupture into the aorticitoring. The patient was pain-free upon admission to the ICU. lumen, creating an aortic dissection. IMH can also progressHe was discharged on hospital day #6 with continued medical by rupturing outward into the adventitia or through the entiremanagement of his thoracic aortic intramural hematoma. aortic wall, leading to aortic rupture.3 Chest radiography is of limited value for diagnosing acute aortic syndrome (aortic dissection, nondissecting aneurysm,Aortic intramural hematomas intramural hematoma). In one study, board-certiﬁed radio-Intramural hematoma (IMH) of the aorta constitute 10– logists who were blinded to results from other diagnostic20% of acute aortic syndromes, with arterial hypertension procedures re-evaluated the admission chest radiograph forthe most frequent predisposing factor.1 IMH is classiﬁed as patients admitted with aortic disease.4 They evaluated each Figure 23.2 CT angiogram of the chest demonstrating IMH in the arch and descending thoracic aorta (arrows) in a 91-year-old male with sudden onset of sharp back pain.
Sudden onset of back pain in a 91-year-old male 93radiograph for the presence or absence of seven radiographic underwent prompt surgery versus 55% in those patients notfeatures of aortic disease: continuous or hump-like widening receiving surgery.6of the aortic contour; widening of the mediastinal shadow;tracheal shift to the right or distortion of the left mainstem KEY TEACHING POINTSbronchus; displacement of intimal calciﬁcation greater than 6mm into the aortic shadow; kinking or tortuosity of the aorta; 1. Intramural hematoma (IMH) of the aorta constitutes 10–opaciﬁcation of the pulmonary window between the aortic 20% of acute aortic syndromes, with arterial hypertensionknob and the left pulmonary artery; and blurring or double the most frequent predisposing factor.density of the aortic contour. Chest radiography had a sensi- 2. In some cases, IMH can rupture into the aortic lumen, cre-tivity of 64% and a speciﬁcity of 86% for aortic disease. Sensi- ating an aortic dissection.tivity was 67% for overt aortic dissection, 61% for nondissect- 3. The diagnostic test of choice for diagnosing IMH ising aneurysm, and 63% for intramural hemorrhage or pene- contrast-enhanced CT; MRI is useful to establish the agetrating ulcer. Sensitivity was lower for pathology conﬁned to of the hematoma and to monitor IMH over time.the proximal aorta (47%) than for disease involving distal aor- 4. Emergency treatment of IMH involves analgesia, stricttic segments (77%).4 blood pressure control and urgent cardiothoracic surgical On unenhanced chest CT, IMH is visible as a crescent consultation.of high-attenuation material within the aortic wall.5 This rim 5. Management for aortic IMH is similar to that for aortic dis-of high attenuation represents acute bleeding into the aortic section: surgical repair for type A hematomas and medicalwall, occasionally involving the entire circumference of management for type B hematomas.the aorta. Features reported as predictors that IMH willprogress to overt dissection include the presence of penetrat- REFERENCESing atherosclerotic ulcer, greater maximum thickness of the  Tatli S, Yucel EK, Lipton, MJ. CT and MR images of thehematoma, ﬂattening of the true lumen so that the short-axis thoracic aorta: current techniques and clinical applications.diameter is less than 75% of the long-axis diameter, involve- Radiol Clin N Am 2004;42:565–85.ment of the ascending aorta, and the presence of either peri-  Saborio DV, Sadeghi A, Burack JH, et al. Management ofcardial or pleural effusions.5 MRI allows detection of the age intramural hematoma of the ascending aorta and aortic arch:of the IMH, and may be useful to monitor IMH over time. the risks of limited surgery (case report). Tex Heart Inst J Emergency management of patients diagnosed with aortic 2003;30:325–7.IMH involves strict blood pressure control, pain manage-  Haro LH, Krajicek M, Lobl JK. Challenges, controversies,ment and urgent cardiothoracic surgery consultation. If and advances in aortic catastrophes. Emerg Med Clin N Amsurgery is not urgently indicated, these patients should be 2005;23:1159–77.  von Kodolitsch Y, Neinaber CA, Dieckmann C, et al. Chestadmitted to the ICU for close monitoring. Long-term manage- radiography for the diagnosis of acute aortic syndrome. Amment for aortic IMHs is similar to that for aortic dissection: J Med 2004;116:73–7.surgical repair for type A hematomas and medical manage-  Chiles C, Carr JJ. Vascular diseases of the thorax: evaluationment for type B hematomas.2 Although some authors have with multidetector CT. Radiol Clin N Am 2005;43:543–69.recommended medical management for type A IMHs, von  von Kodolitsch Y, Csosz SK, Koschyk DH, et al. IntramuralKodilitsch et al. found in a multicenter observational trial that hematoma of the aorta: predictors of progression to dissec-early mortality was 8% in patients with type A hematoma who tion and rupture. Circulation 2003;107:1158–63.
24Pleuritic chest pain in a 27-year-old maleHISTORY OF PRESENT ILLNESSA 27-year-old male presented to the ED complaining of fourdays of worsening right-sided chest pain, described as sharpand worse on inspiration. The pain began suddenly four daysprior following a severe coughing spell. He also describedincreased dyspnea but denied fevers, bloody sputum or recenttrauma.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient was a moderately obesemale in no acute distress, speaking full sentences.VITAL SIGNS Temperature 98.1◦ F (36.1◦ C) Pulse 88 beats/minute Blood pressure 120/80 mmHg Respirations 24 breaths/minute Oxygen saturation 96% on room airHEENT: UnremarkableNECK: Supple, no jugular venous distension, trachea midline.CARDIOVASCULAR: Regular rate and rhythm without rubs, Figure 24.1 Chest x-ray from a 27-year-old male with right-sided, pleuritic chest pain, demonstrating complete right-sided pneumo-murmurs or gallops. thorax.LUNGS: Absent breath sounds in the right lung ﬁeld, breathsounds clear to auscultation in the left lung ﬁeld. pneumothorax. A Thoravent R (thoracic vent and Heimlich valve) was placed in the right anterior chest, which resulted inABDOMEN: Soft, nontender, nondistended. a large, rapid rush of air escaping the catheter. After approx-EXTREMITIES: No clubbing, cyanosis or edema. imately 20 minutes, the patient described a “wave-like” sen- sation running through his right chest and became acutelyNEUROLOGIC: Nonfocal. dyspneic, tachypneic and diaphoretic, with oxygen saturations dropping to 87% on 2 liters oxygen by nasal canula. A repeatThe patient was placed on a cardiac monitor, supplemental portable chest radiograph was obtained (Figure 24.2).oxygen by nasal canula was administered and a peripheralintravenous line was placed. A chest radiograph was obtained(Figure 24.1), which demonstrated a complete right-sided What is your diagnosis? 97
98 Pulmonology ANSWERThe diagnosis is re-expansion pulmonary edema. The chestradiograph in Figure 24.2 demonstrates complete re-expansion of the collapsed right lung, with a ﬂuffy opacityin the right lung ﬁeld consistent with pulmonary edema.The patient was placed on high-ﬂow oxygen by face mask,received IV furosemide and was admitted to the telemetryunit for observation and repeat chest radiograph the follow-ing morning. The patient had good diuresis from the Lasix Rwith improvement in his respiratory symptoms; his repeatchest radiograph demonstrated substantial clearing of thepulmonary edema without evidence of residual pneumo-thorax. He was discharged home much improved with theThoravent R in place and instructions to follow up with thor-acic surgery in ﬁve days. Repeat chest radiograph at that timeshowed no evidence of pneumothorax, and the Thoravent Rwas removed. Figure 24.2 Chest x-ray from a 27-year-old male shortly after right chest wall Thoravent R placement for right-sided pneumothorax.Re-expansion pulmonary edema before chest tube thoracostomy should be performed for largeRe-expansion pulmonary edema (RPE) may develop in cer- pneumothoraces.2 Finally, chest tube thoracostomy or thora-tain patients whose lung has been rapidly re-inﬂated after a centesis should be terminated if the patient develops tightnessperiod of collapse, such as from a pneumothorax or a pleural of the chest or experiences coughing, as these symptoms mayeffusion.1 Patients with RPE have various degrees of hypoxia indicate the development of RPE.1,3and hypotension. The reported incidence of RPE ranges from1–14%.2 On rare occasions, the pulmonary edema is bilateraland the patient requires intubation and mechanical ventila- KEY TEACHING POINTStion. Even more rarely, RPE can be fatal. The risk factors for developing RPE include collapse of 1. Re-expansion pulmonary edema (RPE) can occur inthe affected lung for more than three days, large pneumoth- patients whose lung has been rapidly re-inﬂated after aorax, negative pleural pressure suction of greater than 20 cm period of collapse (usually more than 72 hours) secondaryH2 O and rapid re-expansion.2 The pathogenesis of RPE to a pneumothorax or pleural effusion.involves two main entities: alteration of capillary permeabil- 2. The risk factors for developing RPE include collapse ofity and increased hydrostatic pressure.3 Inﬂammatory medi- the affected lung for more than three days, large pneumo-ators, such as neutrophils, IL-8 and leukotrienes, may play a thorax, negative pleural pressure suction of greater thanrole in the development of RPE. Similarly, re-oxygenation of 20 cm H2 O and rapid lung re-expansion.the collapsed hypoxic lung may contribute to RPE through 3. Patients with RPE typically have coughing spells or chestoxygen free-radical generation and leukocyte inﬂux during re- tightness during or immediately after tube thoracostomyexpansion or re-oxygenation of the collapsed lung.4 or thoracentesis. Patients with RPE typically have coughing spells or chest 4. The symptoms of RPE usually progress for 12–24 hours;tightness during or immediately after tube thoracostomy or serial chest radiographs reveal progressive ipsilateral pul-thoracentesis. The symptoms usually progress for 12–24 hours monary edema, which may progress to involve the con-and serial chest radiographs reveal progressive ipsilateral tralateral lung.pulmonary edema, which may progress to involve the contra- 5. Treatment of RPE is primarily supportive with the admin-lateral lung.1 If the patient does not die within the ﬁrst 48 istration of supplemental oxygen and diuretics, and intuba-hours, recovery is usually complete. Treatment is primarily tion and mechanical ventilation when necessary.supportive, with the administration of supplemental oxygenand diuretics; intubation and mechanical ventilation may benecessary.1,3 Measures to prevent development of RPE include slow REFERENCESevacuation of the pneumothorax with intermittent clamping.2  Light RW, Lee YCG. Pneumothorax, chylothorax, hemo-An alternative to this may be simple repetitive aspiration of thorax, and ﬁbrothorax. In: Mason RJ, Murray JF, Broaddusless than 1000 mL air and the avoidance of negative pres- VC, et al. (eds). Murray and Nadel’s Textbook of Respiratorysure suction. Routine supplemental oxygen and hydration Medicine, 4th ed. Philadelphia: Elsevier, 2005:1507–8.
Pleuritic chest pain in a 27-year-old male 99 Beng ST, Mahadevan M. An uncommon life-threatening  Her C, Mandy S. Acute respiratory distress syndrome of the complication after chest tube drainage of pneumothorax in contralateral lung after reexpansion pulmonary edema of a the ED. Am J Emerg Med 2004;22:615–9. collapsed lung. J Clin Anesth 2004;16:244–50. Genofre EH, Vargas FS, Teixeira LR, et al. Reexpansion pulmonary edema. J Pneumol 2003;29:101–6.
25Acute onset of shortness of breath in a 30-year-old femaleHISTORY OF PRESENT ILLNESS CARDIOVASCULAR: Tachycardic rate, regular rhythm withoutA 30-year-old female presented to the ED complaining of rubs, murmurs or gallops.acute onset shortness of breath and a sensation of her heart LUNGS: Clear to auscultation bilaterally without rales, rhonchipounding approximately ﬁve hours prior to presentation. The or wheezes.patient was seen in the orthopedics clinic earlier in the dayfor a right knee injury she sustained playing soccer two weeks ABDOMEN: Soft, nontender, nondistended.previously. Shortly after the injury, she was placed in a right RECTAL: Normal tone, brown stool, hemoccult negative.knee brace, which she had been wearing for the past twoweeks. The patient was discharged from the clinic with the RIGHT LOWER EXTREMITY: Swelling and moderate effusion ofdiagnosis of possible right anterior cruciate ligament tear, and the knee, as well as mild swelling of the anterior shin and calf;was instructed to continue wearing her brace until her sched- tenderness to the anterior knee just below patella, anterioruled return to the clinic one week following an outpatient drawer sign noted, no popliteal mass. Dorsalis pedis pulse pal-MRI. pable. The patient reported that upon leaving the orthopedic NEUROLOGIC: Nonfocal.clinic, she began to experience difﬁculty breathing, madeworse with exertion, as well as the sensation of her heart The patient was placed on the cardiac monitor, 2 liters oxy-pounding. She denied chest pain, recent cough, fevers or gen by nasal cannula was administered, a peripheral intra-abdominal pain. She did feel lightheaded, and experienced venous line was placed, and blood was drawn and sent fornausea and vomited three times. She had noted signiﬁcant laboratory testing. A 12-lead ECG (Figure 25.1) and portableswelling to her right knee that had not dissipated since the AP chest radiograph (Figure 25.2) were obtained. Labora-injury, as well as some swelling to her shin and calf. The tory tests revealed a troponin I of 2.15 ng/mL (normal 0.00–patient had no signiﬁcant medical issues; her only medica- 0.09 ng/mL), leukocyte count of 16.3 K/μL (normal 3.5–tion was oral contraceptives. She drank alcohol and smoked 12.5 K/μL) with 88% neutrophils (normal 50–70%), andcigarettes on occasion, and denied any illicit drug use. hematocrit of 45%. The serum pregnancy test was negative, the glucose returned at 193 mg/dL (normal 60–159 mg/dL) andPHYSICAL EXAMINATION the remainder of the electrolytes and creatinine were withinGENERAL APPEARANCE: The patient appeared short of breath, normal limits.diaphoretic and somewhat anxious. Shortly after beginning the ED evaluation, the patientVITAL SIGNS began complaining of sharp, substernal chest pain, made Temperature 97.4◦ F (36.3◦ C) worse by deep inspiration. Her respiratory rate increased to Pulse 120 beats/minute 32 breaths/minute and her oxygen saturation declined to 92% Blood pressure 146/54 mmHg on 2 liters nasal cannula, at which time she was placed on a Respirations 24 breaths/minute 100% non-rebreather mask. Approximately one and a half Oxygen saturation 96% on room air hours after arrival in the ED, her blood pressure dropped to 88/54 mmHg despite receiving a 1-liter normal saline bolusHEENT: Unremarkable. intravenously.NECK: Supple, no jugular venous distension. What is your diagnosis? 101
102 Pulmonology Figure 25.1 12-lead ECG from a 30-year-old female with acute onset shortness of breath. Figure 25.2 Anteroposterior chest radiograph from a 30-year-old female with acute onset shortness of breath.
Acute onset of shortness of breath in a 30-year-old female 103 A repeat 12-lead ECG performed the following morning ANSWER in the ICU demonstrated resolution of the T-wave inversionsThe diagnosis is bilateral pulmonary emboli. The ECG in noted on the initial ECG (Figure 25.4). Doppler ultrasound ofFigure 25.1 demonstrates sinus tachycardia, rate 110 beats/ the right leg on hospital day #2 revealed a noncompressible,minute, with inverted T waves in leads III, aVF, V3 and V4 . occlusive thrombus in the distal right superﬁcial femoral veinThe chest radiograph in Figure 25.2 is normal. A CT angio- with extension into the popliteal vein.gram (CTA) of the chest was ordered along with the initiallaboratory tests as the patient was determined to be at high Pulmonary embolismrisk for pulmonary embolism. The patient initially receivedenoxaparin 1 mg/kg subcutaneously around the time her INCIDENCE AND ETIOLOGY: Although the exact incidence ofblood pressure began to drop, and a second peripheral IV pulmonary embolism (PE) is uncertain, it is estimated thatwas obtained. At the same time, as her blood pressure failed 600,000 episodes occur each year in the United States, result-to improve following a second liter NS bolus, a dopamine ing in 100,000 to 200,000 deaths.1 When the diagnosis of PEinfusion was started at 5 μg/kg/min, titrated to 10 μg/kg/min is conﬁrmed and effective therapy is initiated, recurrence ofwith improvement of her blood pressure to 104/68 (pulse PE is rare and death is uncommon – with the exception of112 beats/minute). Once the patient’s hemodynamic status patients who initially present with hemodynamic impairment,improved slightly, she was transported to the CT scanner with among whom the mortality approaches 30%.1 The majority ofa nurse, emergency physician and intubation equipment. preventable deaths associated with PE can be ascribed to a The resulting CTA demonstrated large bilateral pulmo- missed diagnosis rather than to a failure of existing therapies.nary emboli (Figure 25.3). Upon return from the CT scan- Most PEs arise from deep veins of the leg. Although deepner, the intensivist was consulted and a decision was made vein thrombosis (DVT) starts in calf veins, it has already prop-to discontinue the dopamine drip and begin Levophed R at agated above the knee in 87% of symptomatic patients before2 μg/min, titrating to maintain systolic blood pressure at 90– the diagnosis is made.2 Thrombosis in the veins is triggered by100 mmHg. An arterial blood gas obtained on a 100% non- venostasis, hypercoagulability and vessel wall inﬂammation,rebreather mask revealed a pH of 7.27 (normal 7.35–7.45), known as Virchow’s triad.2 All known clinical risk factors forpCO2 of 35 mmHg (normal 35–45 mmHg), pO2 of 60 mmHg DVT and PE have their basis in one or more elements of this(normal 80–95 mmHg) and bicarbonate of 16.2 mmol/L (nor- triad. These risk factors include previous DVT or PE, recentmal 23–28 mmol/L). A decision was made to administer surgery, prolonged immobilization, inherited forms of hyper-thrombolytics, and an infusion of tissue plasminogen activator coagulability (e.g., antiphospholipid syndrome, Factor V Lei-(t-PA) was given at 50 mg/hour IV over 2 hours (total 100 mg den deﬁciency), advanced age, malignancy, pregnancy, con-t-PA). At the completion of the t-PA infusion, the patient’s gestive heart failure, use of contraceptives/hormone replace-vital signs demonstrated a pulse of 79 beats/minute, blood ment therapy, and long air (or land) travel.3,4pressure of 110/76 and respirations of 26 breaths/minute, PE ranges from incidental, clinically unimportant throm-with an oxygen saturation of 100% on 15 L oxygen by non- boembolism to massive embolism with sudden death. Asrebreather mask. The Levophed R drip was discontinued and thrombi form in the deep veins of the leg, pelvis or arms,the patient was transferred to the ICU. they may dislodge and embolize to the pulmonary arteries A B Figure 25.3 CTA from a 30-year-old female with acute dyspnea, demonstrating large right (arrow, panel A) and left (arrow, panel B) pulmonary emboli.
104 Pulmonology Figure 25.4 12-lead ECG obtained from a 30-year-old female following treatment with t-PA for bilateral pulmonary emboli.with potentially serious consequences.5 Pulmonary arterial Despite its shortcomings as a single diagnostic step, theobstruction and the release by platelets of vasoactive agents presence of hypoxemia (pulse oximetry less than 95% breath-such as serotonin elevate pulmonary vascular resistance. The ing room air) that cannot be explained by a known diseaseresulting increase in alveolar dead space and redistribu- process increases the probability of PE.6 Conversely, lack oftion of blood ﬂow (which creates areas of decreased venti- hypoxemia can be used with other criteria to justify not pursu-lation to perfusion) impair gas exchange; stimulation of ing further evaluation for PE. Additionally, when PE is diag-irritant receptors causes alveolar hyperventilation.2 Reﬂex nosed the severity of hypoxemia represents a powerful inde-bronchoconstriction augments airway resistance. As right ven- pendent predictor of patient outcome.6tricular afterload increases, tension rises in the right ventricu- Wells et al. have published, reﬁned and internally vali-lar wall and may lead to dilatation, dysfunction and ischemia dated a clinical decision rule for pre-test probability of PE.7–10of the right ventricle.2 Wells Criteria for pre-test probability of PE consist of seven weighted criteria (Table 25.1). Summation of these point val-SIGNS AND SYMPTOMS: Symptoms that should invoke suspi- ues can be trichotomized into low (less than 2 points), moder-cion of PE include chest pain, shortness of breath, chest wall ate (2–6 points) or high (more than 6 points) pre-test probabil-tenderness, back pain, shoulder pain, upper abdominal pain, ities, with prevalences for PE of 2–4%, 19–21% and 50–67%,syncope, hemoptysis, painful respirations, new onset wheez- respectively. Alternatively, a total score can be dichotomizeding, any new cardiac dysrhythmia or other unexplained symp-tom referable to the thorax.2 Apprehension or anxiety are alsocommon symptoms in patients with PE. The classic ﬁndings of TABLE 25.1 Wells clinical prediction rule for pulmonaryhemoptysis, dyspnea and chest pain are neither sensitive nor embolismspeciﬁc for the diagnosis of PE; fewer than 20% of patientswith documented PE have this “classic triad.”3 Chest pain Clinical feature Pointsfrom noninfarcting PE can be highly variable and vague; as Clinical symptoms of DVT 3high as 30% of patients with deﬁnite PE deny any perception Other diagnosis less likely than PE 3of chest pain.6 Patients presenting with PE frequently com- Pulse >100 beats/minute 1.5 Immobilization or surgery within previous 4 weeks 1.5plain of dyspnea. Physical signs that should raise the clinical Previous DVT or PE 1.5suspicion of PE include tachypnea, tachycardia, rales, fever, Hemoptysis 1lower extremity edema, a cardiac murmur, S3 or S4, cyanosis, Malignancy treated within past 6 months or palliative 1hypotension and neck vein distention.2,3
Acute onset of shortness of breath in a 30-year-old female 105into a PE-unlikely (less than or equal to 4 points) or PE-likely also suggested a more severe clinical proﬁle. According to the(more than 4 points) pre-test probabilities, with prevalences authors, these ﬁndings support a link between the degree offor PE of 5–8% and 39–41%, respectively.7,8,10 troponin increase and the severity of clinical presentation.12 Most pulmonary emboli arise from the deep veins of theDIAGNOSTIC TESTS: ECG, chest radiography and arterial legs. Ultrasonography is positive in 10–20% of patients with-blood gas (ABG) analysis have limited roles in the evalua- out leg symptoms or signs who undergo evaluation, and intion of PE. The primary utility of ECG is its ability to point approximately 50% of patients with proven PE.1,13 Therefore,to an alternate diagnosis, such as acute coronary syndrome the possibility of PE cannot be ruled out on the basis of neg-or pericarditis.3 Sinus tachycardia is a common ECG ﬁnding ative ultrasonography.1 Moreover, positive ultrasonographicin patients with PE. The most frequent electrocardiographic ﬁndings in patients without symptoms or signs referable to theabnormality is T-wave inversion in the anterior leads, espe- legs should be interpreted with caution. Because ultrasono-cially leads V1 to V4 (found in 68% of patients with PE).3,5 graphic studies may be falsely positive or may detect resid-The classic ﬁnding of S1 Q3 T3 lacks sensitivity and speciﬁcity ual abnormalities related to previous VTE, only positive stud-(54% and 62%, respectively).3 New right-bundle branch block ies with appropriate clinical circumstances should serve as theor atrial ﬁbrillation may be seen but is uncommon.5 basis for initiating therapy. Chest radiography seldom provides speciﬁc information, Ventilation-perfusion (V/Q) scanning is a valuable tool inbut may be useful to suggest alternative diagnoses such as diagnosing PE when the results are deﬁnitive.1 A normal V/Qpneumonia, congestive heart failure or pneumothorax.6 Uni- scan essentially rules out PE, and a high-probability scan forlateral basilar atelectasis increases the probability of PE. If PE is strongly associated with its presence. Whereas normalsymptoms have been present three days or more, pulmonary results or results indicating a high probability of disease areinfarction sometimes shows an apex-central, pleural-based, extremely helpful, nondiagnostic results are difﬁcult to inter-wedge-shaped area of inﬁltrate (“Hampton’s hump”).6 Uni- pret and much more common.5 Rarely does the ventilationlateral lung oligemia (Westermark’s sign) is a rare radio- scanning clarify the interpretation of perfusion lung scans.graphic manifestation of a large PE. ABG analysis has a lim- Furthermore, in the presence of a high index of clinical sus-ited role in the evaluation of PE. The pO2 on ABG analysis picion, results of lung scanning indicating a low probabilityhas a zero or even negative predictive value in a typical pop- of PE may inadvertently steer clinicians away from the cor-ulation of patients in whom PE is suspected.2 It is a relatively rect diagnosis. Such results should instead be interpreted asinvasive procedure that lacks the sensitivity or speciﬁcity to nondiagnostic.5rule in or out disease.3 Most hospitals now employ CT angiography (CTA) as the The measurement of the degradation products of cross- primary method for evaluating PE.6 Images can be obtainedlinked ﬁbrin (D-dimer) circulating in plasma is a highly sensi- in a few seconds, so the time required for the test primarilytive but nonspeciﬁc screening test for suspected venous throm- depends upon scanner availability, transport time and radio-boembolism (VTE).1 Speciﬁcity is known to be low secondary logist interpretation time. For the most part, the radiologistto false-positive results from numerous causes, such as trauma, indicates the test is positive or negative, similar to resultspostoperative state, sepsis and myocardial infarction.3 It is of conventional catheter-based pulmonary angiography.6 Thisalso less likely to be helpful in elderly patients or patients binary output makes CTA easier to interpret and integratewith signiﬁcant co-morbid disease. The role of D-dimer gen- into medical decision-making, compared with the “probabil-erally has been reserved for ruling out PE or VTE in low-risk ity” result of V/Q scanning. In the case of CTA, the legs canpatients.3,5 Wells et al. found that patients with a low clinical also be scanned (CT venogram, or CTV), which allows eval-probability of VTE and a negative D-dimer assay could be dis- uation for DVT. More recently, multidetector CTA-CTV hascharged safely without further workup for PE, with only 0.4% been shown to have a higher diagnostic sensitivity than CTAfound to have VTE on follow-up examination.11 alone (90% vs. 83%, respectively), with a similar speciﬁcity Troponin I levels may be useful in predicting in-hospital (95% vs. 96%, respectively).13mortality in acute PE. La Vecchia et al. carried out a prospec- In hemodynamically unstable patients with large pulmo-tive clinical trial to assess the prevalence of cTnI positivity nary emboli, echocardiography (ECHO) is useful because itat various cut-off concentrations, and to evaluate the impact is noninvasive, can be performed at the bedside, can assistof increases on prognosis in a cohort of patients without in the recognition and differentiation of PE and is capable ofknown coronary artery disease.12 Their data indicated that an assessing the severity of the PE and the patient’s response toincreased cTnI concentration is associated with increased dis- therapy.14 Although predominantly employed to characterizeease severity. Increases were also associated with signiﬁcantly the presence and the extent of right ventricular pressure over-more extensive and proximal involvement of the pulmonary load, transthoracic ECHO (TTE) or transesophageal ECHOvasculature as assessed by spiral CT; many of the clinical (TEE) may detect emboli in transit or may provide alterna-parameters of these patients (oxygen saturation, blood pres- tive diagnoses, such as aortic dissection, pericardial disease,sure, heart rate, echocardiographic right ventricular abnor- hypovolemia, myocardial dysfunction or infarction, and valvu-malities and estimated pulmonary artery pressure elevations) lar insufﬁciency. ECHO also may be helpful in identifying
106 PulmonologyPE patients with a patent foramen ovale (PFO), which has the International Cooperative Pulmonary Embolism Registrybeen associated with increased mortality, ischemic stroke and (ICOPER) data, ﬁbrinolytics did not reduce the rate of mor-a complicated course.14 tality or recurrent PE at 90 days.20 In submassive PE, the Man- Ryu et al. provide a diagnostic algorithm for suspected PE agement Strategies and Prognosis of Pulmonary Embolism-3that incorporates clinical suspicion, D-dimer level and radio- Trial (MAPPET-3) demonstrated a reduction in the need forlogic testing.15,16 If the suspicion for PE is low, a normal D- escalation of therapy among patients receiving alteplase.22dimer level can exclude the diagnosis. If clinical suspicion is The management of patients with acute massive PE whomoderate to high (or the D-dimer is positive), the authors sug- do not respond to ﬁbrinolytic therapy remains unclear. In thegest CTA is an appropriate diagnostic approach. When con- setting of PE, the recovery of right ventricular function is antrast is contraindicated, V/Q scanning and sonography of the early marker of thrombolysis efﬁcacy, as well as a predictor oflower extremities are options. Pulmonary angiography should in-hospital course.23 Furthermore, residual pulmonary vascu-be considered if the results of the CTA are inadequate and the lar obstruction (more than 30% at 10 days) after thrombolyticsuspicion for PE remains high.15,16 therapy is associated with adverse outcomes and increased long-term mortality.24 Meneveau et al. compared rescue sur-TREATMENT OF PULMONARY EMBOLISM: Traditionally, the gical embolectomy and repeat thrombolysis in patients whotreatment of both PE and DVT had been anticoagulation with did not respond to thrombolysis for massive PE.23 In 40 non-unfractionated heparin and initiation of long-term oral anti- responders, rescue surgical embolectomy led to a better in-coagulation with Vitamin K antagonists, such as warfarin. hospital course when compared with repeat thrombolysis inHowever, data published over the last decade indicates patients with massive PE.23that treatment with low-molecular-weight heparin (LMWH)is superior to treatment with unfractionated heparin.4,17,18Treatment with Vitamin K antagonists should be initiated KEY TEACHING POINTSconcurrently with LMWH and continued until the Interna- 1. The classic ﬁndings of hemoptysis, dyspnea and chest paintional Normalized Ratio (INR) is stable (between 2.0 and are neither sensitive nor speciﬁc for a diagnosis of PE;3.0).4 In patients who have severe chronic kidney disease, fewer than 20% present with this “classic” triad.LMWH should not be used because of its renal clearance and 2. Thirty percent of patients with deﬁnite PE deny any per-the potential for bleeding complications. More recently, fon- ception of chest pain.daparinux (Arixtra R ) has been approved for the treatment 3. Wells Criteria for determining the pre-test probability ofof PE. Fondaparinux is a synthetic antithrombotic agent with PE are useful in stratifying patients into low, medium orspeciﬁc anti-factor Xa activity. Its pharmacologic properties high-risk likelihoods of PE.allow for a simple, ﬁxed-dose, once daily regimen of subcu- 4. ECG, chest radiography and ABG analysis each have lim-taneous injection without the need for monitoring.19 Fonda- ited roles in the evaluation of PE.parinux has been shown to be at least as effective and safe as 5. D-dimer is a useful test to rule out PE in low-risk patients.intravenous unfractionated heparin in the treatment of hemo- 6. Most hospitals employ CTA as the primary method ofdynamically stable patients with PE.19 For hemodynamically evaluation for PE, with multidetector CTA-CTV demon-unstable patients with PE, thrombolytic therapy is uniformly strating even greater sensitivity than conventional CTA foracknowledged as the treatment of choice.14 diagnosing PE. 7. Stable patients with PE should be treated with eitherTHROMBOLYSIS FOR MASSIVE PULMONARY EMBOLISM: The low-molecular-weight heparin or fondaparinux (Arixtra R )principal criterion to characterize acute PE as massive is while warfarin is initiated and reaching therapeutic levels.systemic arterial hypotension.20 Despite anticoagulation, the 8. Unstable patients with major pulmonary emboli shouldmortality rate doubles for submassive PE patients with pre- be treated with thrombolytic therapy (t-PA, 100 mg intra-served systemic arterial pressure and right ventricular dys- venous infusion over two hours) and admitted to the ICU.function. The mortality rate is even greater in patients whopresent with profound hypotension due to massive PE.20 Pri-mary therapy with ﬁbrinolysis or embolectomy is generally REFERENCESconsidered for patients presenting with either massive or sub-massive PE.21 The U.S. Food and Drug Administration has  Fedullo PF, Tapson VF. The evaluation of suspected pulmo-approved t-PA (alteplase) 100 mg administered as a contin- nary embolism. N Engl J Med 2003;349:1247–56.  Feied C, Handler JA. Pulmonary embolism. eMedicine Web-uous infusion over two hours for the ﬁbrinolysis of massive site. Available at http://www.emedicine.com/emerg/topic490.PE.21 Every patient being considered for ﬁbrinolysis requires htm. Accessed on June 25, 2008.meticulous screening for contraindications because the risk  Laack TA, Goyal DG. Pulmonary embolism: an unsuspectedof intracranial hemorrhage (ICH) may be as high as 3%. killer. Emerg Med Clin N Am 2004;22:961–83.Although ﬁbrinolysis is generally considered to be a lifesav-  Rogers RL. Venous thromboembolic disease in the elderlying intervention in patients with massive PE, the extent of patient: atypical, subtle, and enigmatic. Clin Geriatr Medthe clinical beneﬁt remains unclear.20 In a recent analysis of 2007;23:413–23.
Acute onset of shortness of breath in a 30-year-old female 107 Goldhaber SZ. Medical progress: pulmonary embolism. N  Ryu JH, Swensen SJ, Olson EJ, et al. Diagnosis of pulmonary Engl J Med 1998;339:93–104. embolism with use of computed tomographic angiography. Kline JA, Runyon MS. Pulmonary embolism and deep vein Mayo Clin Proc 2001;76:59–65. thrombosis. In: Marx JA, Hockberger RS, Walls RM, et al.  Makkar S. Tips from other journals: diagnostic approaches (eds). Rosen’s Emergency Medicine: Concepts and Clinical to possible pulmonary embolism. Am Fam Physician 2001; Practice, 6th ed. Philadelphia: Mosby, 2006:1371–81. 64:841. Wells PS, Ginsberg JS, Anderson DR, et al. Use of a clin-  van Dongen CJJ, Van Den Belt AGM, Prins MH, et al. ical model for safe management of patients with suspected Fixed dose subcutaneous low molecular weight heparins ver- pulmonary embolism. Ann Intern Med 1998;129:997–1005. sus adjusted dose unfractionated heparin for venous throm- Wells PS, Anderson DR, Rodger M, et al. Derivation of a boembolism. Cochrane Database Syst Rev 2004;4:CD001100. simple clinical model to categorize patients’ probability of DOI:10.1002/14651858. pulmonary embolism: increasing the model’s utility with the  Quinlan D, McQuillan A, Eikelboom J. Low-molecular- SimpliRED D-dimer. Thromb Haemost 2000;83:416–20. weight heparin compared with intravenous unfractionated Wells PS, Anderson DR, Rodger M, et al. Excluding pul- heparin for treatment of pulmonary embolism: a meta- monary embolism at the bedside without diagnostic imag- analysis of randomized, controlled trials. Ann Intern Med ing: management of patients with suspected pulmonary 2004;140:175–83. embolism presenting to the emergency department by using  Buller HR, Davidson BL, Decousus H, et al. Subcutaneous a simple clinical model and D-dimer. Ann Intern Med fondaparinux versus intravenous unfractionated heparin in 2001;135:98–107. the initial treatment of pulmonary embolism. N Engl J Med Wolf SJ, McCubbin TR, Feldhaus KM, et al. Prospective 2003;349:1695–702. validation of Wells criteria in the evaluation of patients with  Kucher N, Rossi E, De Rosa M, et al. Massive pulmonary suspected pulmonary embolism. Ann Emerg Med 2004;44: embolism. Circulation 2006;113:577–82. 503–10.  Piazza G, Goldhaber SZ. Acute pulmonary embolism. Part Wells PS, Anderson DR, Rodger M, et al. Evaluation of D- II: Treatment and prophylaxis. Circulation 2006;114:e42–7. dimer in the diagnosis of suspected deep-vein thrombosis.  Konstantinides S, Geibel A, Heusel G, et al. Heparin plus N Engl J Med 2003;349:1227–35. alteplase compared with heparin alone in patients with sub- La Vecchia L, Ottani F, Favero L, et al. Increased car- massive pulmonary embolism. N Engl J Med 2002;347:1143– diac troponin I on admission predicts in-hospital mortality 50. in acute pulmonary embolism. Heart 2004;90:633–7.  Meneveau N, Seronde MF, Blonde MC, et al. Management Stein PD, Fowler SE, Goodman LR, et al. Multidetector of unsuccessful thrombolysis in acute massive pulmonary tomography for acute pulmonary embolism. N Engl J Med embolism. Chest 2006;129:1043–50. 2006;354:2317–27.  Meneveau N, Ming LP, Seronde MF, et al. In-hospital and Wood KE. Major pulmonary embolism: review of a patho- long-term outcome after sub-massive and massive pulmo- physiologic approach to the golden hour of hemodynamically nary embolism submitted to thrombolytic therapy. Eur Heart signiﬁcant pulmonary embolism. Chest 2002;121:877–905. J 2003;24:1447–54.
26Recurrent pneumonias in a 37-year-old maleHISTORY OF PRESENT ILLNESS LUNGS: Scattered rhonchi, no rales or wheezes.A 37-year-old male a with medical history signiﬁcant for sleep ABDOMEN: Soft, nontender, nondistended.apnea and hydrocephalus (diagnosed as a child with place-ment of a ventriculoatrial shunt) presented to the ED com- EXTREMITIES: No clubbing, cyanosis or edema.plaining of nausea, vomiting, diarrhea and fevers for one day. NEUROLOGIC: Nonfocal.He denied chest pain, shortness of breath or cough. He wasinitially seen in a medical clinic and received IV hydration In the ED, the patient received an albuterol nebulizer treat-and promethazine with improvement of his symptoms. How- ment, a 1-liter normal saline IV bolus and an additionalever, he remained tachycardic and his oxygen saturation on dose of promethazine. A chest radiograph was obtained (Fig-room air was 93% while lying ﬂat, improving to 97% on sitting ure 26.1). Following treatment, his heart rate improved to 95upright. He was transferred to the ED for further evaluation beats/minute with oxygen saturation on room air improving toand treatment. 97%. At time of ED discharge, he was able to tolerate ﬂuids and ambulate without problems. His presumptive dischargePHYSICAL EXAMINATION diagnosis was acute gastroenteritis.GENERAL APPEARANCE: The patient appeared well nourished, The patient returned to the ED 24 hours later with per-well hydrated and in no acute respiratory distress. sistent vomiting, shortness of breath, dry cough, fevers andVITAL SIGNS fatigue. A repeat chest radiograph demonstrated an opaciﬁca- Temperature 99◦ F (37.2◦ C) tion at the right lung base as well as a small, right-sided pleu- Pulse 108 beats/minute ral effusion (Figure 26.2). The patient was given IV antibiotics Blood pressure 110/70 mmHg (moxiﬂoxacin) and admitted for pneumonia. His blood cul- Respirations 26 breaths/minute tures were negative during this hospitalization. The patient Oxygen saturation 96% on room air was re-admitted to the hospital on two more occasions over two consecutive months, with the diagnosis of unresolving ver-HEENT: Unremarkable. sus recurrent pneumonias. During the second hospitalization,NECK: Supple, no jugular venous distension. his blood cultures grew out Serratia marcescens.CARDIOVASCULAR: Tachycardic rate, regular rhythm withoutrubs, murmurs or gallops. What is your diagnosis? 109
110 Pulmonology A B Figure 26.1 Posteroanterior (panel A) and lateral (panel B) chest radiograph from a 37-year-old male with nausea, vomiting, diarrhea and fevers for one day. A B Figure 26.2 Posteroanterior (panel A) and lateral (panel B) chest radiograph from a 37-year-old male on return to ED one day following his initial visit for presumed gastroenteritis, demonstrating a right lower lobe inﬁltrate (arrows).
Recurrent pneumonias in a 37-year-old male 111 ANSWERThe diagnosis is recurrent pneumonias resulting from septicemboli and Serratia bacteremia arising from the fragmentedventriculoatrial shunt catheter. A transthoracic echocardio-gram was obtained that showed a linear density transversingfrom the right atrium to the right ventricle across the tricus-pid valve, likely the catheter (Figure 26.3). At the distal por-tion of the linear density, a ﬂuffy nodule consistent with eitherpossible thrombus or vegetation was seen. It was concludedthat the shunt catheter had dislodged from the original ven-triculoatrial shunt and was likely the source of recurrent septicemboli to the lungs. The patient was admitted to the thoracicsurgery service and underwent successful surgical removal ofthe catheter tip from the right side of the heart, with subse-quent resolution of his recurrent pneumonias. Figure 26.3 Transthoracic echocardiogram image demonstrating VA catheter tip (arrow) extending into the right ventricle in a 37-year-old male with recurrent pneumonias.Infections associated with ventriculoatrial shuntsThe frequency of long-term prosthetic device infection varies device-related infection. When suspecting endocarditis asso-with the type of implant, as do mortality rates associated with ciated with prosthetic valves, electrocardiac devices, or VAthese devices. Mortality rates are particularly high when infec- shunts, transthoracic or transesophageal echocardiographytion is associated with cardiovascular implants.1 Such pros- should be used, with the transesophageal technique yieldingtheses allow organisms to adhere to their surface and, in greater sensitivity.1some cases, produce a bioﬁlm. This bioﬁlm is an extracellular As with other types of cardiovascular device-related infec-polysaccharide matrix that protects the bacteria via physio- tions, foreign body removal of the VA shunt with antimi-logic as well as mechanical factors.2 In general, rates of infec- crobial therapy is the preferred treatment option.4 Infectedtion are greater after revision of a device than following pri- ventricular shunts are surgically managed in two stages. Themary device implantation procedures.1 Approximately 25,000 infected shunt is removed and an external ventricular cathetercerebrospinal ﬂuid shunt operations are performed each year is inserted to drain cerebrospinal ﬂuid and monitor intracra-in the United States, 18,000 of which are initial shunt place- nial pressure.5 The external ventricular catheter is usuallyments.1 Approximately 85% of individuals with cerebrospinal replaced every 5–10 days to prevent ventriculitis, and sys-ﬂuid shunts undergo at least two shunt revisions. Ventriculo- temic antibiotics are administered for 10–14 days. Repeatperitoneal (VP) shunts are the most common neurosurgical analysis of cerebrospinal ﬂuid is performed to ensure steril-shunts used, and are associated with less severe complications ity before a new ventricular shunt is inserted, preferably onthan ventriculoatrial (VA) shunts.3 the contralateral side, typically within two weeks of the initial The incidence of VA shunt infection in recent years has surgery.5averaged less than 10%.4 Clinical manifestations of VA shuntinfection vary and depend on many factors, including the siteof shunt infection, whether or not the infection site is prox- KEY TEACHING POINTSimal or distal, intraluminal or extraluminal, the virulence ofinfecting pathogens, and the presence or absence of shunt 1. Prosthetic indwelling device infections account for aboutmalfunction.4 Intraluminal infection can result in bacteremia half of the two million cases of nosocomial infection thatand sepsis; severe sepsis and septic shock are unusual. Right- occur in the United States each year.sided infective endocarditis and septic pulmonary emboli have 2. Ventriculoperitoneal (VP) shunts are the most commonbeen described.4 neurosurgical shunts used and are associated with less Blood cultures are usually positive when an intralumi- severe complications than ventriculoatrial (VA) shunts.nal infection is present and are important in diagnosing a 3. Intraluminal infection of VA shunts can result in bactere-VA shunt infection. The list of pathogens associated with mia and sepsis, right-sided infective endocarditis, septiccerebrospinal ﬂuid shunts includes (but is not limited to) pulmonary emboli and recurrent pneumonias.coagulase-negative staphylococci (e.g., S. aureus), Gram- 4. Blood cultures and transthoracic or transesophageal echo-negative bacilli (e.g., E. coli, Proteus mirabilis, P. aerugi- cardiography are essential diagnostic tools in evaluating fornosa, Klebsiella pneumoniae, H. inﬂuenzae), streptococci (e.g., VA shunt-related infections.group G and B), S. pneumoniae, and Propionibacterium 5. Treatment for VA shunt infections involves prompt anti-acnes.1 Imaging is an important tool used for the detection of microbial therapy and shunt removal.
112 PulmonologyREFERENCES  Baddour LM, Wilson WR. Infections of prosthetic valves and other cardiovascular devices. In: Mandell GL, Bennett Sampedro MF, Patel R. Infections associated with long-term JE, Dolin R (eds.). Principles of Infectious Disease, 6th ed. prosthetic devices. Infect Dis Clin N Am 2007;21:785–819. Philadelphia: Elselvier, 2005:1024–32. Schlossberg D. Clinical approach to antibiotic failure. Med  Darouiche RO. Current Concepts: treatment of infections Clin N Am 2006;90:1265–77. associated with surgical implants. N Engl J Med 2004;350: Lam CH, Villemure JG. Comparison between ventriculo- 1422–9. atrial and ventriculoperitoneal shunting in the adult popula- tion. Br J Neurosurg 1997;11:43–8.
27Hemoptysis in a 47-year-old maleHISTORY OF PRESENT ILLNESS HEENT: PERRL, EOMI, oropharynx pink and moist, noA 47-year-old male presented to the ED complaining of three lesions, mucosal ulcers or bleeding. Nares pink and moist with-episodes of coughing up 1–2 tablespoons of bright red blood out evidence of bleeding.earlier that day. He denied fevers, chills, night sweats, short-ness of breath, malaise, weight loss, abdominal pain, nausea or NECK: Supple, no cervical lymphadenopathy.vomiting; he also denied recent nosebleeds. His medical his-tory included open angle glaucoma, osteoarthritis and a previ- CARDIOVASCULAR: Regular rate and rhythm without rubs,ous lung infection diagnosed some years ago for which he was murmurs or gallops.prescribed antibiotics for six months, the name of which hecould not recall. He did not smoke cigarettes and denied per- LUNGS: Clear to auscultation bilaterally without rales, rhonchisonal or family history of cancer. He had not traveled outside or wheezes.the area recently but as a child grew up in Malaysia, and oneyear ago moved to Northern California from Arizona, where ABDOMEN: Soft, nontender, nondistended.he had spent most of his adult life. EXTREMITIES: No clubbing, cyanosis or edema.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient was a well-nourished, SKIN: Warm and dry without pallor, no rashes or lesions.well-hydrated male who appeared comfortable and in noacute discomfort. NEUROLOGIC: Nonfocal.VITAL SIGNS A chest radiograph (posteroanterior and lateral views) was Temperature 97.7◦ F (36.5◦ C) obtained (Figure 27.1). Pulse 87 beats/minute Blood pressure 165/100 mmHg Respirations 18 breaths/minute What is your diagnosis? Oxygen saturation 98% on room air A B Figure 27.1 Posteroanterior (panel A) and lateral (panel B) views of chest radiograph from a 47-year-old male with hemoptysis. 113
114 Pulmonology Coccidioidomycosis is not a contagious disease. Patients with ANSWER coccidioidomycosis do not require isolation if hospitalized,The diagnosis is bacterial infection of a cavitary lesion from although care must be taken in disposing of materials contam-previous coccidioidomycosis infection. The chest radiograph inated with secretions.2demonstrates a 2.5-cm cavitary lesion in the apex of the left Sixty percent of people infected with C. immitis have nolung (arrows, Figure 27.2). Upon further investigation, the symptoms or have an illness indistinguishable from an upperpatient’s previous lung infection turned out to be coccidio- respiratory infection.2 In others, symptoms develop one toidomycosis, for which he was prescribed ﬂuconazole for six three weeks after exposure. The typical presentation is amonths. Following the chest radiograph, the patient under- lower respiratory infection accompanied by systemic symp-went a CT scan of the chest with intravenous contrast, which toms, such as fever, sweating, anorexia, weakness, arthral-also demonstrated a 2-cm spherical, thick-walled cavitary gias, cough, sputum production and chest pain.2 Erythemalesion in the anterior left upper lobe (Figure 27.3). The patient nodosum or erythema multiforme may develop. The main-was admitted to the medical service and treated with intra- stays of diagnosis are sputum culture and serologic testing.venous ampicillin/sulbactam for possible bacterial infection of Chest radiographic ﬁndings may include inﬁltrates, pleuralthis cavitary lesion. Coccidioidomycosis IgG antibody serolo- effusion and hilar adenopathy.2 The acute infection almostgies returned positive, whereas acid-fast bacilli tests of the always resolves without speciﬁc therapy, although the ill-sputum were negative. The patient’s hemoptysis resolved, and ness may last several weeks. Disseminated disease occurs inhe was discharged on hospital day #2 with follow up arranged approximately 1% of infected persons.3 Dissemination occurswith a pulmonologist. more frequently in the very young or very old, certain racial or ethnic groups, individuals with AIDS or other immuno- suppressive disorders, and during the second half of preg-Coccidioidomycosis nancy or postpartum.4 Aside from pulmonary involvement,Coccidioidomycosis is an infection caused by inhalation of tissues most commonly involved are skin, bone, joints andarthroconidia of dimorphic fungi of the genus Coccidioides.1 meninges; tenosynovitis and sinus tract formation have beenTwo species of this genus, C. immitis (isolated from Califor- reported.4 In patients with severe primary infection or dis-nia) and C. posadasii (isolated outside of California) produce seminated disease, therapy with amphotericin B (intravenous)identical diseases.1 These soil-dwelling fungi have an endemic or one of the azoles (e.g., itraconazole, ﬂuconazole) is recom-range that encompasses semi-arid to arid life zones, princi- mended, with treatment for six months.1–4pally in the southwestern United States and northern Mexico. Several types of pulmonary disease can develop after ini-Coccidioides is also found in parts of Argentina, Brazil, tial infection. These include the formation of pulmonaryColumbia, Guatemala, Honduras, Nicaragua, Paraguay and nodules (coccidioidomas), cavitary disease and progressiveVenezuela.1 Hyperendemic areas include Kern, Tulare and pneumonia.4 The nodules are typically solitary, measuring 2–3Fresno counties in the San Joaquin Valley of California, and cm in diameter, representing areas of granulomatous organi-Pima, Pinal and Maricopa counties in Arizona. There are ap- zation of coccidioidal pneumonia and raising concern for lungproximately 150,000 infections per year in the United States.1 cancer. Thin-walled cavities are seen in approximately 0.1% A B Figure 27.2 Posteroanterior (panel A) and lateral (panel B) views of chest radiograph from a 47-year-old male with cavitary lesion (arrows) from previous coccidioidomycosis infection.
Hemoptysis in a 47-year-old male 115 empyemas, close persistent bronchopleural ﬁstulas or expand lungs that are restricted by residual disease. KEY TEACHING POINTS 1. Coccidioidomycosis is caused by inhalation of soil-dwelling fungi of the Coccidioides genus; it is endemic to the San Joaquin Valley, California and several counties in Arizona. 2. There are approximately 150,000 cases of coccidioido- mycosis per year in the United States; the typical presen- tation of signiﬁcant Coccidioides infection is a lower respi- ratory infection accompanied by systemic symptoms, such as fever, sweating, anorexia, weakness, arthralgias, cough, sputum production and chest pain. 3. Several types of pulmonary disease can develop after the initial infection, including the formation of pulmonary nodules (coccidioidomas), cavitary disease and progressive pneumonia.Figure 27.3 Chest CT from a 47-year-old male with hemoptysis,demonstrating a cavitary lesion in the left upper lung ﬁeld (arrow). 4. Hemoptysis occurs in one-third of cases of cavitary cocci- dioidomycosis, usually caused by a secondary bacterial or fungal infection.of all patients, which often spontaneously resolve within two 5. In patients with severe primary infection or disseminatedyears.4 Thick-walled cavities are more likely to remain present disease, IV therapy with amphotericin B or one of thefor prolonged periods. Chronic ﬁbrocavitary infection with azoles is recommended for six months.progressive ﬁbrosis similar to that seen with histoplasmosis 6. Pulmonary resection may play a role in managing severemay also be seen in coccidioidomycosis, occurring primarily hemoptysis or cavities that enlarge or rupture duringin those with underlying emphysema.4 pharmacologic therapy. Hemoptysis occurs in one-third of cases of cavitary cocci-dioidomycosis, usually not life-threatening.5 When the cavity REFERENCESis in the periphery of the lung, it may rupture into thepleural space causing a hydropneumothorax. Ninety percent  Anstead GM, Graybill JR. Coccidioidomycosis. Infect Disof the cavities are solitary, 70% are in the upper lung ﬁeld, Clin N Am 2006;20:621–43.and about 60% are 2–4 cm in diameter.5 Once a cavity has  Stevens DA. Current concepts: coccidioidomycosis. N Englformed, further spread of the infection is unlikely, presumably J Med 1995;332:1077–82.because cell-mediated immunity is well established. Symp-  Spinello IM, Johnson RH. A 19-year-old pregnant woman with a skin lesion and respiratory failure. Chest 2006;130:toms in patients with cavitation are due to complications, such 611–5.as hemoptysis and secondary infection, which can be bacterial  Wheat LJ. Endemic mycosis. In: Cohen J, Powderly WG,or fungal; aspergillus mycetoma is the most common.5 How- Berkley SF, et al. (eds.). Cohen & Powderly: Infectious Dis-ever, C. immitis itself can proliferate in its mycelial form, pro- eases, 2nd ed. Philadelphia: Mosby, 2004:434–6.ducing a similar mycetoma. Pulmonary resection has a role in  Nardell EA, Kucyj G. Case 21-1994: a 20-year-old Mexicanmanaging severe hemoptysis or cavities that enlarge or rup- immigrant with recurrent hemoptysis and a pulmonary cavi-ture during chemotherapy.2 Surgery is also indicated to drain tary lesion. N Engl J Med 1994;330:1516–22.
28Cough, fever and shortness of breath in a 62-year-old maleHISTORY OF PRESENT ILLNESSA 62-year-old male with a medical history signiﬁcant forchronic alcohol abuse presented to the ED complaining ofpersistent cough productive of green sputum, fevers to 104◦ F(40◦ C), chills and rigors, shortness of breath, and sharp chestpain with cough and deep inspiration for three days. Hereported nausea and vomiting but denied abdominal pain ordiarrhea. He also denied recent travel, leg swelling or tobaccouse. His last alcoholic drink was 24 hours prior to presentation.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient looked older than hisstated age. He was a cachectic and ill-appearing male, in mod-erate respiratory distress, speaking only three- or four-wordsentences.VITAL SIGNS Temperature 104◦ F (40◦ C) Pulse 120 beats/minute Blood pressure 110/65 mmHg Respirations 30 breaths/minute Oxygen saturation 96% on room airHEENT: PERRL, EOMI, sclera anicteric, oropharynx dry.NECK: Supple, no jugular venous distension.CARDIOVASCULAR: Tachycardic rate, regular rhythm without Figure 28.1 Portable chest radiograph from a 62-year-old male withrubs, murmurs or gallops. cough, fever and shortness of breath for three days.LUNGS: Mild expiratory wheezes throughout all lung ﬁelds,scattered rhonchi, crackles and egophony at the right lower peripheral intravenous line was placed, and blood was drawnand mid-lung ﬁelds. and sent for cultures and laboratory testing. A 12-lead ECG demonstrated sinus tachycardia, rate 120 without acute ST-ABDOMEN: Soft, nontender, nondistended. T wave changes. A 1-liter bolus of normal saline was admin-EXTREMITIES: No clubbing, cyanosis or edema; no calf istered IV, as well as acetaminophen orally for the fever; aswelling. portable chest radiograph was obtained (Figure 28.1). Labo- ratory tests were signiﬁcant for a leukocyte count of 20 K/μLNEUROLOGIC: Nonfocal. (normal 3.5–12.5 K/μL), with 35% immature bands (presence of bands abnormal) and sodium of 125 mEq/L (normal 137–The patient was placed on the cardiac monitor with continu- 145 mEq/L).ous pulse oximetry and supplemental oxygen (2 liters by nasalcannula), which increased his oxygen saturation to 98%. A What is your diagnosis? 117
118 Pulmonology ANSWERThe diagnosis is community-acquired pneumonia (CAP). Thechest radiograph demonstrated a right middle lobe inﬁltrate(arrow, Figure 28.2). The patient’s calculated PneumoniaSeverity Index (PSI) score was 117 (62 points for male age,10 points for respiratory rate greater than 29, 15 points fortemperature greater than or equal to 40◦ C and 20 points forsodium less than 130 mEq/L), which placed him in Risk ClassIV. This estimated his 30-day mortality risk at 9.3%. Thepatient received moxiﬂoxacin 400 mg IV, albuterol nebulizedtreatments and was admitted to the medicine service. Intra-venous antibiotics were continued, and the patient’s symp-toms improved by hospital day #3, at which time he wasafebrile with a room air oxygen saturation of 98%. He wasdischarged on hospital day #4 to complete a ten-day course oforal moxiﬂoxacin, with close follow up arranged with his pri-mary care provider. He was encouraged to stop drinking, andwas given resources to assist him.Community-acquired pneumoniaPneumonia is an important cause of morbidity and mortal-ity in adults; more than 5 million cases occur annually in theUnited States.1 Patients with CAP are most often managedin an outpatient setting. The mortality rate in this patient Figure 28.2 Portable chest radiograph from a 62-year-old male with apopulation is low (less than 1%), in contrast to patients who right middle lobe inﬁltrate consistent with pneumonia (arrow).require hospitalization (mortality rate approximates 15%).2CAP is usually acquired by inhalation or aspiration of pul-monary pathogenic organisms into a lung segment or lobe.3 usually a feature of atypical pathogens with the exception ofLess commonly, CAP may result from secondary bacteremia Legionnaires’ disease (caused by L. pneumophila).3from a distant source, such as an Escherichia coli urinary tract Chest radiography is typically the most important test forinfection or bacteremia. CAP due to aspiration or oropha- establishing the diagnosis of pneumonia. Routine chest radio-ryngeal contents is the only form of CAP that typically has graphy is not necessary for all patients who present withmultiple pathogens.3 Streptococcus pneumoniae is the most cough. It can be reserved for patients without a history ofcommonly diagnosed etiology of CAP among hospitalized asthma who have ﬁndings suggestive of pneumonia (e.g.,patients.1 Common bacterial etiologies of CAP and their asso- fever, tachycardia, decreased oxygen saturation or focalciated severities are listed in Table 28.1. abnormality on lung examination).2 Among patients sus- Cough is a common presenting complaint of patients diag- pected of having pneumonia, these clinical ﬁndings have beennosed with pneumonia; however, only a small fraction of prospectively validated and better predict the presence ofpatients who present with cough are diagnosed with pneu- an inﬁltrate than physician judgment.5 Patients with seriousmonia (4% in one large series).2,4 Patients with respiratory underlying disease or severe sepsis/septic shock for whomcomplaints should be screened at triage with pulse oximetry hospitalization is considered should have a chest radiographbecause hypoxia is an important diagnostic clue to the pres- performed.2ence of pneumonia.2 Typically, patients with bacterial CAP Laboratory studies are of limited use to establish the diag-present with variable degrees of fever, usually with productive nosis and speciﬁc cause of pneumonia. For the patient withcough, and often with pleuritic chest pain.3 The clinical pre- mild disease who is to be treated at home, little or no labo-sentation of patients with CAP due to atypical pathogens (e.g., ratory data is needed.1 Although a white blood cell (WBC)M. pneumoniae, C. pneumoniae, L. pneumophila) is usually count greater than 15,000/mm3 increases the probability thatless acute than the presentation of typical bacterial pathogens the pneumonia is bacterial rather than viral or atypical in ori-(e.g., S. pneumoniae, H. inﬂuenzae).3 With typical bacterial gin, leukocytosis is neither sensitive or speciﬁc enough to aidCAP, abnormal physical ﬁndings are generally conﬁned to the in therapeutic decisions.2 A WBC count may be helpful if itchest. Rales on auscultation of the chest over the involved reveals evidence of neutropenia or lymphopenia, which mightlobe or segment are common. If consolidation is present, occur in immunosuppression. In sicker patients who requireincreased tactile fremitus, bronchial breathing and “E-to-A” admission, electrolytes, blood urea nitrogen, serum glucosechanges may be present.3 Purulent sputum is characteristic of and a complete blood count (CBC) should be obtained. Serumpneumonia caused by typical bacterial pathogens, and is not lactate levels are useful in identifying septic patients and
Cough, fever and shortness of breath in a 62-year-old male 119 TABLE 28.1 Bacterial etiologies of CAP1 Mild (Outpatient) Moderate (Medical ward) Severe (ICU) Mycoplasma pneumoniae Streptococcus pneumoniae Streptococcus pneumoniae Chlamydia pneumoniae Mycoplasma pneumoniae Legionella pneumophila Streptococcus pneumoniae Chlamydia pneumoniae Staphylococcus aureus Haemophilus inﬂuenzae Haemophilus inﬂuenzae Gram-negative bacilli Legionella pneumophila Anaerobestheir response to therapy, as well as evaluating for possible patient’s psychosocial characteristics.10 Disease-speciﬁc pre-Pneumocystis carinii pneumonia (PCP) in patients known or diction rules are available that can be used to assess the ini-suspected to have HIV infection. tial severity of pneumonia and predict the risk of death. The Gram stain and culture of the sputum is not routinely done most widely used and rigorously studied prediction rule – thein the ED. This is controversial because of the time it takes to Pneumonia Severity Index (PSI) – has been validated in moreinduce a good sample, as well as the possibility of ED patients than 50,000 patients from a variety of inpatient and outpatientpresenting with cough having TB. Furthermore, uncontam- populations.11,12 The PSI is based on data commonly availableinated specimens with a single etiologic agent are rare. If upon presentation (Table 28.2), and stratiﬁes patients into ﬁveobtained, these should be reserved for the subset of patients risk classes in which 30-day mortality rates range from 0.1–with serious illness (e.g., requiring ICU admission) in whom 27.0%. The greater the PSI score, the greater the risk of death,the bacteriologic diagnosis is highly uncertain or an unusualpathogen is suspected, and for those in whom the outcomemay depend on optimal antimicrobial therapy.2 The need for TABLE 28.2 Pneumonia severity index for CAP11routine blood cultures among patients admitted for pneumo- Characteristic Points assignednia is also controversial.6,7 Routine blood cultures for patientsadmitted with pneumonia have shown mixed results in terms Demographic Factor Age (in years)of improved diagnostic accuracy or ability to guide therapy.8 It Men Ageis considered best practice to obtain blood cultures in seriously Women Age – 10ill patients before antibiotics are initiatiated.2 Bacteremia Nursing home resident +10occurs in approximately 25–30% of hospitalized pneumococ- Coexisting illnessescal pneumonia cases but the diagnosis and therapy are usual- Neoplastic disease +30 Liver disease +20ly well established before blood culture results are available.2 Congestive heart failure +10 Outpatients diagnosed with CAP who are otherwise Cerebrovascular disease +10healthy can be treated with a macrolide (erythromycin, Renal disease +10azithromycin or clarithromycin) or doxycycline as monother- Findings on Physical Examinationapy.9 Those who have had recent antibiotic exposure may be Altered mental status +20offered a ﬂuoroquinolone alone (levoﬂoxacin, moxiﬂoxacin Respiratory rate ≥30/min +20or gatiﬂoxacin), amoxicillin-clavulanate, or the combination Systolic blood pressure <90 mmHg +20 Temperature <35◦ C or ≥40◦ C +15of azithromycin or clarithromycin plus high-dose amoxicillin. Pulse ≥125 beats/min +10Although the ﬂuoroquinolones offer convenient once-daily Laboratory and X-ray Findingsdosing, increasing resistance among isolates to this class of Arterial pH <7.35 +30agents has been recently demonstrated.9 Inpatients requiring Blood urea nitrogen ≥30 mg/dL +20treatment of CAP but who are not admitted to the ICU should Sodium <130 mmol/liter +20be offered azithromycin or clarithromycin plus a β-lactam Glucose ≥250 mg/dL +10 Hematocrit <30% +10agent or a third-generation cephalosporin (e.g., ceftriaxone). Partial pressure of arterial oxygenRespiratory ﬂuoroquinolones may be offered as monother- <60 mmHg or O2 saturation <90% +10apy. For ICU patients with a concern for pseudomonas Pleural effusion +10infection, an antipseudomonal agent plus ciproﬂoxacin, or PSI Class 30-day mortalityantipseudomonal agents with an aminoglycoside plus a respir- ∗atory ﬂuoroquinolone or a macrolide are recommended.9 I 0.10% Between 30–50% of patients hospitalized with pneumonia II (less than 70 points) 0.60% III (71–90 points) 0.90%are placed in low-risk categories, many of whom could poten- IV (91–130 points) 9.30%tially be managed at home.10 The decision regarding hospi- V (more than 130 points) 27%talization should be based on the stability of the patient’s ∗ For class I, age less than 50 years; no cancer, congestive heart failure,clinical condition, the risk of death and complications, the cerebrovascular, renal or liver disease; normal vital signs/examination.presence or absence of other active medical problems, and the
120 Pulmonologyadmission to the ICU, readmission and the longer the length severity of pneumonia, predict the risk of death and aid inof hospitalization. deciding which patients diagnosed with CAP require hos- Mortality is sufﬁciently low in PSI classes I–III (less pital admission.than 1%) that outpatient management is appropriate in theabsence of extenuating circumstances. Some low-risk patients,especially those who are elderly or PSI class III, may look sick REFERENCESor be reluctant to be treated at home. Many of these patients  Plouffe JF, Martin DR. Pneumonia in the emergency depart-may be appropriate candidates for a short hospitalization or ment. Emerg Med Clin N Am 2008;26:389–411.23 hours of observation.10 Mortality increases to 9–27% in PSI  Moran GJ, Talan DA, Abrahamain FM. Diagnosis and man-classes IV–V, suggesting that these higher-risk patients should agement of pneumonia in the emergency department. Infectbe hospitalized. Dis Clin N Am 2008;22:53–72. A similar tool to the PSI that is easier to use is the CURB-  Cunha BA. Pneumonia, community-acquired. eMedicine65 rule.13 This rule uses only ﬁve criteria to determine patients Website. Available at http://www.emedicine.com/med/at lower risk for adverse events: confusion, uremia (blood urea topic3162.htm. Accessed August 19, 2008.nitrogen greater than or equal to 20 mg/dL), respiratory rate  Metley JP, Stafford RS, Singer DE. National trends ingreater than or equal to 30 breaths/minute, blood pressure less the use of antibiotics by primary care physicians for adult patients with cough. Arch Intern Med 1998;158:1813–8.than 90 mmHg systolic or 60 mmHg diastolic, and age greater  Emerman CL, Dawson N, Speroff T, et al. Comparisonthan or equal to 65. The risk of 30-day mortality increases with of physician judgment and decision aids for ordering chesta greater number of these factors present: 0.7% with no fac- radiographs for pneumonia in outpatients. Ann Emerg Medtors, 9.2% with two factors and 57% with ﬁve factors. It is sug- 1991;20:1215–9.gested that patients with zero to one feature may receive treat-  Moran GJ, Abrahamian FM. Blood cultures for pneumonia:ment as an outpatient, patients with two features be admitted, can we hit the target without a shotgun? Ann Intern Medand ICU-level care be considered for patients with three or 2005;46:407–8.more factors.2,13  Walls RM, Resnick J. The Joint Commission on Accred- itation of Healthcare Organizations and Center for Medi- care and Medicaid Services community-acquired pneumo-KEY TEACHING POINTS nia initiative: what went wrong? Ann Emerg Med 2005;46: 409–11.1. Patients with community-acquired pneumonia (CAP)  Kennedy M, Bates DW, Wright SB, et al. Do emergency appropriate for the outpatient setting have a low mortal- department blood cultures change practice in patients with ity (less than 1%) compared to hospitalized patients, who pneumonia? Ann Emerg Med 2005;46:393–400. have a mortality rate of approximately 15%.  Patel SM, Saravolatz LD. Monotherapy versus combination2. Streptococcus pneumoniae is the most commonly diag- therapy. Med Clin N Am 2006;90:1183–95. nosed etiology of CAP among hospitalized patients.  Halm EA, Teirstein AS. Clinical practice: management of3. Typically, patients with bacterial CAP present with vari- community-acquired pneumonia. N Engl J Med 2002;347: able degrees of fever, productive cough and pleuritic chest 2039–45. pain.  Fine MJ, Auble TE, Yealy DM, et al. A prediction rule to4. Laboratory tests have little use in outpatient management identify low-risk patients with community-acquired pneumo- of patients with CAP, whereas tests obtained on admitted nia. N Engl J Med 1997;336:243–50.  Auble TE, Yealy DM, Fine MJ. Assessing prognosis and patients should include electrolytes, blood urea nitrogen, selecting an initial site of care for adults with community- serum glucose and complete blood count (CBC). acquired pneumonia. Infect Dis Clin North Am 1998;12:741–5. Blood cultures should be obtained in seriously ill and 59. admitted patients with CAP, preferably before the initia-  Lim WS, Van Der Eerden MM, Liang R, et al. Deﬁning tion of antibiotics. community-acquired pneumonia severity on presentation to6. Disease-speciﬁc prediction rules (e.g., Pneumonia Sever- hospital: an international derivation and validation study. ity Index and CURB-65) can be used to assess the initial Thorax 2003;58:377–82.
29Abdominal pain and dysuria in a 16-year-old maleHISTORY OF PRESENT ILLNESS HEENT: Unremarkable.A 16-year-old male presented to the ED complaining of supra- NECK: Supple.pubic pain radiating to the right testicle, dysuria, urgency andfrequency for eight days. The patient was seen one week CARDIOVASCULAR: Regular rate and rhythm without rubs,prior to his ED visit by his primary care provider (PCP), at murmurs or gallops.which time he described the previous complaints as well as LUNGS: Clear to auscultation bilaterally.subjective fevers. At that time, the patient’s temperature was99.2◦ F (37.3◦ C). He was noted to be well appearing and in no ABDOMEN: Soft, nondistended; suprapubic, periumbilical andacute discomfort. The abdominal examination revealed mild right lower quadrant tenderness to palpation without reboundsuprapubic tenderness to palpation without the presence of or guarding (maximal point of tenderness over suprapubicrebound or guarding, no costovertebral angle tenderness area). No CVAT.(CVAT) was noted and his genitourinary (GU) examination RECTAL: Normal tone, brown stool, hemoccult negative.was normal. A urinalysis was negative for infection and thepatient was diagnosed with a viral syndrome. GENITOURINARY: Circumcised, no penile discharge, testes de- Three days prior to his ED presentation, the patient re- scended bilaterally, no testicular swelling or tenderness, noported a temperature of 103◦ F (39.4◦ C) and severe supra- hernias.pubic pain. The following day, the intensity of his pain dimin- EXTREMITIES: No clubbing, cyanosis or edema.ished somewhat and his fever resolved. In the ED, the patientcontinued to complain of crampy abdominal pain at a level of NEUROLOGIC: Nonfocal.6 (on a scale of 0 to 10), with associated dysuria, urgency andfrequency. He denied nausea, vomiting, diarrhea, constipation A peripheral intravenous line was placed, and blood wasor penile discharge, and was tolerating oral liquids. drawn and sent for laboratory testing. Laboratory tests re- vealed a leukocyte count of 16 K/μL (normal 3.5–12.5 K/μL)PHYSICAL EXAMINATION with 84% neutrophils (normal 50–70%); electrolytes, creati-GENERAL APPEARANCE: The patient was lying supine on the nine, glucose and urinalysis were within normal limits.gurney, appeared comfortable and in no acute discomfort.VITAL SIGNS What is your diagnosis? Temperature 98.7◦ F (37.1◦ C) Pulse 88 beats/minute Blood pressure 120/80 mmHg Respirations 20 breaths/minute Oxygen saturation 100% on room air 123
124 Gastroenterology Symptoms of appendicitis usually begin with abdominal ANSWER pain, often in the periumbilical area. Classically, the painThe diagnosis is intra-abdominal abscess from perforated migrates to McBurney’s point (two-thirds the distance fromappendicitis. The patient underwent a CT scan of the abdo- the umbilicus along a straight line toward the anterior supe-men and pelvis with oral and intravenous contrast, which rior iliac spine of the pelvis), 6–18 hours from onset.4 Thedemonstrated a 7 cm × 4 cm intra-abdominal abscess in the pain steadily worsens until the appendix perforates if not diag-right lower quadrant (Figure 29.1), resulting from a perfor- nosed in a timely manner. At the time of perforation, localizedated appendix. The patient was admitted to the surgery ser- pain may decrease but the more generalized pain of periton-vice, received intravenous ciproﬂoxacin and metronidazole, itis predominates. Anorexia is the next most common symp-and subsequently underwent percutaneous drainage of the tom after pain, occurring in about 95% of patients. Nauseaabscess by interventional radiology on hospital day #2. The is seen in approximately 75% of cases, whereas vomiting ispatient was discharged on hospital day #4 with instructions seen in 60–70% of cases. Diarrhea, or more accurately tenes-to continue his oral antibiotics for two weeks. The patient mus, may occur but is usually seen late in the clinical courseunderwent successful interval appendectomy approximately of appendicitis, when the sigmoid colon becomes irritated byfour months following percutaneous abscess drainage. a severely inﬂamed or perforated appendix.4 About 75% of patients have a low-grade fever, but a higher fever or the absence of fever does not eliminate the diagnosis.5Appendicitis The most common ﬁnding on physical examination is local-Appendicitis occurs when a fecalith, fecal matter or lymph- ized abdominal tenderness, usually in the right lower quad-oid hyperplasia obstructs the appendix.1 Obstruction leads rant. Pain may be noted over McBurney’s point; however,to inﬂammation, rising intraluminal pressures, and ultimately because only 35% of patients have the base of their appendixischemia. Subsequently, the appendix enlarges and incites within 5 cm of this point, the pain of appendicitis can be local-inﬂammatory changes in the surrounding tissues, such as in the ized over other areas of the abdomen.3 Direct rebound tender-pericecal fat and peritoneal cavity. If untreated, the inﬂamed ness is a response to the inﬂamed appendix and its proximityappendix may eventually perforate.1 Appendectomy is the to the peritoneal surface.2 This localized peritoneal irritationmost common emergent operation in the world.2 More than may also be demonstrated by indirect referred tenderness in250,000 appendicitis-related admissions occur annually in the the right lower quadrant elicited during left lower quadrantUnited States, totaling nearly $3 billion in hospital charges.2 palpation (i.e., Rovsing’s sign). Involuntary guarding refersThe current incidence of appendicitis is 86 per 100,000 patients to muscle contraction in response to the inﬂamed parietalper year, with a lifetime risk of 6.7% for females and 8.6% for peritoneum. This ﬁnding, along with rebound tenderness, aremales.1,2 independent predictors of appendicitis.6 A positive psoas sign The anatomic location of the appendix affects the clini- occurs when a patient experiences pain while on their left sidecal presentation as well as the subsequent risk of developing and an examiner slowly extends the right thigh. Pain occurs asappendicitis. In a study of 10,000 autopsies, the appendix was the iliopsoas is irritated by the inﬂamed appendix.2 The obtu-located behind the cecum in the retrocecal fossa in 65% of rator sign may be elicited when an examiner internally rotatescases, and in the pelvis in 31% of cases.3 This ratio is reversed the ﬂexed right thigh while the patient is supine. This bringsin patients who undergo an operation for appendicitis. A the obturator internus muscle in contact with an irritatedretrocecal location of the appendix is less likely to become pelvis, which produces hypogastric pain. The patient’s temp-obstructed due to the position of its lumen.3 erature is a poor predictor of appendicitis; however, when Figure 29.1 CT of the pelvis from a 16-year-old male with suprapubic pain, demonstrating abscess in the right lower quadrant (arrows) resulting from a perforated appendix.
Abdominal pain and dysuria in a 16-year-old male 125high and accompanied by tachycardia a ruptured appendix pediatric population ranges from 20–40%.4 These patientswith intra-abdominal abscess should be suspected.2,7 often present dehydrated and toxic-appearing, with obvious About 80–90% of patients with acute appendicitis have physical signs of peritonitis; they should immediately be ﬂuidan elevated white blood cell (WBC) count above 10,000/mm3 resuscitated and treated with antibiotics before taken to the(this percentage is slightly lower in elderly and very young operating room.patients). Unfortunately, the WBC count is nonspeciﬁc and There is a small subgroup of patients with appendicealoften elevated with other etiologies of abdominal pain.3 The perforations in whom the diagnosis is missed or who do notsensitivity of C-reactive protein (CRP) varies from 40–99%, present for medical evaluation until late in the course of theirdepending on the study. A urinalysis is helpful in differentiat- illness. Many of these patients may have been ill for 7–10ing urinary tract disease from acute appendicitis; mild sterile days; CT often reveals a walled-off abscess or phlegmon inpyuria may be seen in patients with appendicitis due to irri- the right lower quadrant.4 These patients can often be treatedtation of the ureter by the appendix. However, signiﬁcant medically and have their abscesses drained percutaneously bypyuria (more than 20 WBC per high-power ﬁeld) suggests an interventional radiologist. After stabilization and recov-urinary tract pathology.3 All women of childbearing age with ery, patients who have undergone successful percutaneousabdominal pain should be tested for pregnancy, as a positive drainage are discharged home. These patients should be fol-test expands the differential diagnosis of right lower quadrant lowed closely, complete a course of antibiotics and be sched-pain. uled to return for interval appendectomy.2 In patients where the history, physical examination andlaboratory ﬁndings do not clearly suggest the diagnosis ofappendicitis, imaging studies are indicated. A plain ﬁlm radio- KEY TEACHING POINTSgraph of the abdomen may reveal a fecalith; however, a 1. The current incidence of appendicitis is 86 per 100,000fecalith is present in only 10% of the cases of appendicitis.4 patients per year, with a lifetime risk of 6.7% for femalesGraded compression ultrasonography has been prospectively and 8.6% for males.demonstrated to improve the clinical accuracy of the diagno- 2. Classic signs and symptoms of acute appendicitis includesis of acute appendicitis.3 It may be particularly helpful in periumbilical pain migrating to the right lower quadrant,women of childbearing age, in whom pelvic conditions can anorexia, nausea, vomiting and fever.mimic appendicitis. It is often advocated as the initial imaging 3. The most common ﬁnding on physical examination is local-modality in children and pregnant patients to spare them radi- ized abdominal tenderness, usually in the right lower quad-ation exposure. The sensitivity and speciﬁcity of ultrasono- rant; additional ﬁndings may include rebound tenderness,graphy for acute appendicitis in most studies is 75–90% and as well as the presence of a Rovsing’s, obturator or psoas85–95%, respectively.3 signs. Abdominal CT has become the most important imaging 4. In patients where the history, physical examination andstudy in the evaluation of patients with atypical presentations laboratory ﬁndings are not consistent with the diagnosisof appendicitis.8 Studies have demonstrated a decreased neg- of appendicitis, imaging studies (abdominal CT or ultra-ative laparotomy rate and appendiceal perforation rate when sound) are indicated.pelvic CT was used in selected patients with suspected appen- 5. A small subgroup of patients with appendiceal rupture maydicitis. Advantages of CT scanning include its superior sensi- present late in the disease process, and may have a walled-tivity and accuracy compared to other imaging techniques, off phlegmon or abscess.availability, lack of invasiveness and potential to reveal alter-native diagnoses. Disadvantages include radiation exposure,potential for anaphylactic reaction if intravenous contrast isused, lengthy acquisition time if oral contrast is used and REFERENCESpatient discomfort if rectal contrast is used.8  Rybkin AV, Thoeni RF. Current concepts in imaging of Appendiceal rupture puts patients at risk for serious seque- appendicitis. Radiol Clin N Am 2007;45:411–22.lae, including peritonitis, sepsis and even death. It remains a  Dominguez EP, Sweeney JF, Choi YU. Diagnosis and man-persistent problem. Increased time between symptom onset agement of diverticulitis and appendicitis. Gastroenterol Clinand surgical treatment may be a risk factor for ruptured N Am 2006;35:367–91.appendicitis. Bickell et al. demonstrated that the risk of rup-  Wolfe JM, Henneman PL. Acute appendicitis. In: Marx JA,ture after 36 hours of untreated symptoms is approximately Hockberger RS, Walls RM, et al. (eds.). Rosen’s Emergency5%, which increases by 5% for each ensuing 12-hour period Medicine: Concepts and Clinical Practice, 6th ed. Philadel- phia: Mosby, 2006:1451–8.after 36 hours.9 They concluded that physicians should be  Halter JM, Baesl T, Nicolette L, et al. Common gastrointes-cautious about delaying surgery beyond 36 hours from symp- tinal problems and emergencies in neonates and children.tom onset in patients with appendicitis.9 The perforation rate Clin Fam Pract 2004;6:731–54.in cases of appendicitis has varied from 10–85% depending  Pearl RH, Hale DA, Molloy M, et al. Pediatric appendec-upon age, gender and whether or not the institution where the tomy. J Ped Surg 1995;30:173–81.patient is evaluated is located in the inner city.4 In most major  Andersson RE, Hugander AP, Ghazi SH, et al. Diag-hospital centers, the incidence of perforation in the general nostic value of disease history, clinical presentation, and
126 Gastroenterology inﬂammatory parameters of appendicitis. World J Surg  Craig S. Appendicitis, acute. eMedicine Website. Available 1999;23:133–40. at http://www.emedicine.com/emerg/topic41.htm. Accessed Cardall T, Glasser J, Guss DA. Clinical value of the total June 24, 2008. white blood cell count and temperature in the evaluation  Bickell NA, Aufses AH, Rojas M, et al. How time affects of patients with suspected appendicitis. Acad Emerg Med the risk of rupture in appendicitis. J Am Coll Surg 2006;202: 2004;11:1021–7. 401–6.
30Left upper quadrant abdominal pain in an 18-year-old maleHISTORY OF PRESENT ILLNESSAn 18-year-old male presented to the ED with a one-day his-tory of severe left upper quadrant abdominal pain. The paincame on suddenly while sitting and was described as sharp,constant and radiating to the back. The pain worsened oninspiration, and was rated at a level of 8 (on a scale of 0 to10). He denied nausea or vomiting, fevers, diarrhea, consti-pation or dysuria, as well as recent trauma. Six weeks priorto these current symptoms, the patient developed fevers, asore throat, generalized malaise and mild, diffuse abdominalpain. These symptoms gradually resolved with rest, ﬂuids andacetaminophen. A throat swab for group A strep at that timewas negative.PHYSICAL EXAMINATIONGENERAL APPEARANCE: The patient appeared well nourished,well hydrated and in no acute discomfort.VITAL SIGNS Temperature 98◦ F (36.6◦ C) Pulse 90 beats/minute Blood pressure 117/78 mmHg Figure 30.1 CT of the abdomen with IV contrast from an 18-year-old Respirations 20 breaths/minute male with left upper quadrant abdominal pain. Oxygen saturation 100% on room airHEENT: PERRL, EOMI, sclera anicteric, oropharynx pink and EXTREMITIES: No clubbing, cyanosis or edema.moist without exudates. SKIN: No rashes.NECK: Supple, no jugular venous distension. A peripheral intravenous line was placed, morphine sulfateCARDIOVASCULAR: Regular rate and rhythm without rubs, IV was administered for pain, and blood was drawn and sentmurmurs or gallops. for laboratory testing. Laboratory tests, including a completeLUNGS: Clear to auscultation bilaterally. blood count, creatinine, PT, aPTT and INR, were within nor- mal limits. A CT scan of the abdomen with intravenous con-ABDOMEN: Soft, nondistended, active bowel sounds present. trast was obtained (Figure 30.1).Palpable spleen with left upper quadrant tenderness to deeppalpation; no rebound or guarding noted. What is your diagnosis? 127
128 Gastroenterology ANSWERThe diagnosis is a grade I spontaneous splenic lacerationsecondary to infectious mononucleosis. The CT scan demon-strated some irregular, band-shaped areas of nonenhancingsplenic parenchyma at the posterior and lateral aspects ofthe spleen, compatible with splenic laceration (arrow, Fig-ure 30.2). During the patient’s initial illness eight weeks prior,his laboratory results demonstrated a complete blood countwith 16% atypical lymphocytes and a positive monospot test.Following the diagnosis of grade I splenic laceration, thepatient was admitted to the surgical service for close observa-tion and nonoperative management (serial examinations andhematocrit testing). The patient’s hematocrit and vital signsremained stable, his pain improved and he was discharged onhospital day #3 with instructions to avoid strenuous physicalactivity and contact sports for a minimum of three weeks.Infectious mononucleosis and splenic injuryInfectious mononucleosis (IM), a common entity caused bythe Epstein-Barr virus (EBV), is a self-limiting viral illness Figure 30.2 Grade I splenic laceration (arrow) in an 18-year-old malemost common in children and young adults. It is character- with spontaneous onset of sharp, left upper quadrant abdominal pain.ized by a triad of fever, pharyngitis and lymphadenopathyassociated with atypical lymphocytes and heterophil antibod-ies, as well as myalgias and reversible splenomegaly.1,2 More Patients with spontaneous splenic laceration or rupturethan 90% of adults eventually acquire EBV, establishing a secondary to IM often present with acute onset of severelatent infection of B-lymphocytes, thereby acquiring a life- abdominal pain that may be diffuse or localized to the left side.long infection typical of members of the herpes virus family.3 Splenomegaly alone (without splenic rupture) rarely causesEBV is probably acquired during childhood by salivary con- pain.2 Abdominal symptoms of spontaneous splenic lacera-tact as a consequence of intermittent, asymptomatic shed- tion or rupture secondary to IM may be accompanied by pal-ding of the virus into oropharyngeal secretions among family lor, tachycardia, hypotension, oliguria, orthostasis and syn-members. The individual immune response to EBV is highly cope. Abnormal laboratory studies include low hematocritvariable, and likely determines its severity or whether EBV and leukocytosis with or without the presence of atypicalcauses symptomatic disease.4 This depends on the prolifer- lymphocytes. Up to 90% of patients may also have abnormallyation and activation of T cells in response to infection. For elevated liver function studies.2 Ultrasound is an effectivereasons that remain unexplained, infection acquired during bedside tool for visualizing the spleen and any free ﬂuid in thechildhood is usually asymptomatic or yields nonspeciﬁc symp- abdomen. CT scan is conﬁrmatory and allows for grading thetoms. In developed societies, primary EBV infection is shifted severity of splenic damage. Splenomegaly, splenic lacerations,to later ages, in which 50–74% of individuals develop symp- subcapsular hematomas and hemoperitoneum are readily vi-toms consistent with IM.3 The risk of developing symptomatic sualized with contrast-enhanced CT.2 The presence of acuteinfection drops 100-fold by age 35 or older.5 bleeding may also be seen in some instances. Serious complications of IM usually come after the illness. There is debate over surgical versus conservative treat-The rare deaths that occur are mostly attributed to neurologic ment for splenic lacerations/rupture in IM.1–3 Patients who aresequelae and splenic rupture.3 EBV infection results in the hemodynamically compromised warrant early surgical inter-proliferation of mononuclear cells, which collect in the reser- vention with total splenectomy. More recent recommenda-voirs of lymphoid tissue, including the spleen. As a result, the tions state that splenic laceration/rupture may be managedspleen becomes congested and enlarged, causing thinning of conservatively if bleeding is not profuse (deﬁned by some asthe splenic capsule; splenomegaly occurs in 50% of patients requiring less than two units of transfused blood).3 Nonoper-with IM.2 Although relatively rare, complaints of signiﬁcant ative percutaneous drainage may be an alternative to laparo-left upper quadrant abdominal pain in IM should invoke con- tomy in some cases. Spleen preservation will avoid the poten-sideration of spontaneous splenic laceration or rupture, which tial for long-term complications of asplenia, including the riskoccurs in 0.1–0.5% of patients.3,6 Presence of severe left shoul- of severe sepsis due to encapsulated bacteria.2,3 Finally, ander pain, known as Kehr’s sign, indicates splenic injury with enlarged spleen in IM may remain susceptible to delayedblood irritating diaphragmatic nerves.3 rupture for several weeks, although the exact period is
Left upper quadrant abdominal pain in an 18-year-old male 129unknown. Therefore, a patient considered for conservative 5. Patients with splenic injury secondary to IM should be ad-treatment should be advised to avoid physical activities for mitted to the surgical service for either conservative man-a considerable time, at least until the spleen has returned to agement or splenectomy based on hemodynamic stability,normal size (e.g., four to six weeks).2 type and grade of injury, and numerous other factors.KEY TEACHING POINTS REFERENCES1. Spontaneous splenic laceration/rupture is a rare but serious  Rothwell S, McAuley D. Case report: Spontaneous splenic sequelae of infectious mononucleosis (IM), affecting less rupture in infectious mononucleosis. Emerg Med 2001;13: than 1% of patients. 364–6.2. Symptoms and signs of spontaneous splenic laceration/  Brichkov I, Cummings L, Fazylov R, et al. Nonoperative rupture may include diffuse or left upper quadrant abdom- management of spontaneous splenic rupture in infectious inal pain, left shoulder pain, pallor, tachycardia, hypo- mononucleosis: the role of emerging diagnostic and treat- tension, orthostasis and syncope. ment modalities. Am Surg 2006;72:401–4.3. Laboratory abnormalities seen with spontaneous splenic  Auwaerter PG. Infectious mononucleosis: return to play. Clin Sports Med 2004;23:485–97. rupture associated with IM may include leukocytosis, pres-  Baumgarten E, Herbst H, Schmitt M, et al. Life-threatening ence of atypical lymphocytes, low hematocrit and abnor- infectious mononucleosis: is it correlated with virus-induced mal liver function tests. T cell proliferation? Clin Infect Dis 1994;19:152–6.4. Bedside ultrasound is useful in identifying free ﬂuid in  Auwaerter PG. Infectious mononucleosis in middle age the abdomen associated with spontaneous splenic rupture. [clinical conference]. JAMA 1999;281:454–9. Abdominal CT scan is conﬁrmatory and useful in grading  Farley DR, Zietlow SP, Bannon MP, et al. Spontaneous rup- the severity of splenic damage in hemodynamically stable ture of the spleen due to infectious mononucleosis. Mayo patients. Clin Proc 1992;67:846–53.
31Abdominal pain and vomiting in a 29-year-old femaleHISTORY OF PRESENT ILLNESS VITAL SIGNSA 29-year-old female presented to the ED with several days Temperature 98.6◦ F (37◦ C)of mild, diffuse abdominal pain, nausea and vomiting. Eight Pulse 90 beats/minutedays prior to presentation she had undergone a lower abdo- Blood pressure 130/90 mmHgminal cesarean section. The patient denied diarrhea or consti- Respirations 18 breaths/minutepation, dysuria, fevers, chills, chest pain or shortness of breath. Oxygen saturation 98% on room airShe described her pain as crampy and constant, rated at a HEENT: Unremarkable.level of 4 (on a scale of 0 to 10), which was not relieved withacetaminophen. On examination she was afebrile, with nor- NECK: Supple.mal pulse and blood pressure. She appeared to be in no acute CARDIOVASCULAR: Regular rate and rhythm without rubs,distress. Abdominal examination revealed a soft, slightly dis- murmurs or gallops.tended abdomen with mild, diffuse tenderness to palpationwithout associated rebound or guarding. Her incision was LUNGS: Clear to auscultation bilaterally.healing well without associated erythema or discharge. A ABDOMEN: Soft, mildly distended, with diffuse tenderness toperipheral intravenous line was placed, blood was drawn palpation without associated rebound or guarding. Boweland sent for laboratory testing, and intravenous ﬂuids were sounds were absent. The surgical incision was healing welladministered along with an antiemetic. An abdominal radio- without erythema or discharge.graph (kidney, ureter, and bladder, or KUB) was obtained(Figure 31.1). RECTAL: Normal tone, paucity of stool, hemoccult negative. The radiograph demonstrated a nonspeciﬁc bowel gas pat- EXTREMITIES: No clubbing, cyanosis or edema.tern without the presence of free air or air-ﬂuid levels. Lab-oratory tests, including a complete blood count, electrolytes, NEUROLOGIC: Nonfocal.creatinine, glucose, liver function tests, amylase and urin-alysis, were normal. The patient’s symptoms improved after Laboratory tests on this repeat visit revealed a leukocyteIV hydration and antiemetics. She was discharged home with count of 13.1 K/μL (normal 3.5–12.5 K/μL) with 77% neutro-precautions to return for worsening symptoms. phils (normal 50–70%) and a creatinine of 1.7 mg/dL Three days later, the patient returned to the ED complain- (increased from 0.8 mg/dL on the previous visit). Intravenousing of persistent nausea, vomiting and worsening abdominal ﬂuids and antiemetics were administered, and a CT scan of thepain. She denied fevers or diarrhea but reported no ﬂatus for abdomen and pelvis with oral and intravenous contrast wasthe past 24 hours. obtained (Figure 31.2).PHYSICAL EXAMINATION What is your diagnosis?GENERAL APPEARANCE: The patient appeared well nourished,slightly dehydrated and in mild discomfort. 131
Figure 31.1 Abdominal radiograph (KUB) from a 29-year-old female with abdominal pain, nausea and vomiting following a cesarean section. A B C DFigure 31.2 CT of the abdomen and pelvis in a 29-year-old female with several days of nausea, vomiting andabdominal pain (panels A–D from superior to inferior transverse images).
Abdominal pain and vomiting in a 29-year-old female 133 report acute episodes of agonizing abdominal pain.4 Symp- ANSWER toms may arise from acute or chronic intestinal obstructionThe diagnosis is malrotation of the midgut. The CT scan caused by the presence of abnormal peritoneal bands (e.g.,revealed moderate dilatation of the proximal duodenum, a Ladd’s bands) or a volvulus. The presence of Ladd’s bandsdistended stomach, and mesenteric swirling in the right upper in patients with anomalies of intestinal rotation can lead toabdomen (arrows, Figure 31.3). These ﬁndings were signiﬁ- vomiting due to compression of the duodenum by these peri-cant for a partial obstruction secondary to an internal hernia toneal bands between the abnormally positioned cecum andor mesenteric volvulus. The patient was taken to the oper- the right retroperitoneum.2 Patients with Ladd’s bands andating room and underwent an exploratory laparotomy with anomalies of intestinal rotation frequently present with a his-a Ladd’s procedure (division of Ladd’s band with appen- tory of chronic vomiting (often bilious) associated with failuredectomy). Intraoperative ﬁndings included a signiﬁcant band to gain weight.2from the cecum and right colon crossing over the malrotated The diagnosis of rotational anomaly can be identiﬁed fromduodenum, which was divided; the duodenum was freed with- radiographic studies. In the absence of volvulus, a plain radio-out evidence of volvulus. The bowel was healthy without evi- graph of the abdomen is of little diagnostic value.4 The absentdence of ischemia. The patient was discharged home on post- cecal gas shadow or the localization of small intestinal loopsoperative day #3 with an uneventful recovery. predominantly on the right side should arouse suspicion of malrotation.4 The accuracy of the upper gastrointestinal series (UGI) is reported to be over 80%.5 The ﬁnding on UGIMalrotation of the midgut of a right-sided duodenojejunal junction or proximal jejunalMalrotation of the midgut is a term used to describe abnormal loops is highly suggestive of malrotation.5 CT scan of therotation of the fetal intestines around the axis of the superior abdomen is the radiographic test of choice for diagnosingmesenteric artery.1 These congenital anomalies include non- malrotation. Malrotation can be diagnosed on CT by therotation, incomplete rotation, reversed rotation, and ﬁxation anatomic location of a right-sided small bowel, a left-sidedabnormalities of the mesentery.1,2 Rotational anomalies may colon, an abnormal relationship of the superior mesentericbecome symptomatic at any age, including late in adult life. vessels, and aplasia of the pancreatic uncinate process.4 Ultra-However, 80% of patients who become symptomatic do so in sonography can be used to diagnose malrotation with midgutthe ﬁrst month of life.2 The true incidence of malrotation is volvulus by detecting the superior mesenteric vein (SMV)unknown. Estimates in the literature range from 1 in 200 to 1 rotated around the superior mesenteric artery (SMA). Thisin 6000 live births.3 Autopsy studies suggest that some form sonographic sign, known as the whirlpool sign, corresponds toof malrotation may exist in 0.5–1% of the population.2,3 The a clockwise wrapping of the SMV and mesentery around themost feared complication associated with anomalies of intesti- SMA.6 The appearance of this characteristic sign can facili-nal rotation is ischemic necrosis of the intestines with midgut tate the preoperative diagnosis of midgut volvulus and mal-volvulus.2 rotation. The disadvantage of ultrasonography is that it is Not all patients with malrotation present with symptoms.4 operator-dependent.6Many live without any complaints, with the anomaly discov- The classic treatment for incomplete intestinal rotationered incidentally at autopsy. Some may present with chronic is the Ladd’s procedure, which involves immobilization ofand unexplained abdominal discomfort, and even fewer may the right colon, division of Ladd’s bands and mobilization Figure 31.3 CT of the abdomen and pelvis in a 29-year-old female with midgut volvulus, demonstrating dis- tended stomach with mesenteric swirling in the right upper abdomen (mesenteric swirling, arrows).
134 Gastroenterologyof the duodenum, division of adhesions around the SMA to abdomen or ultrasonography. CT scan of the abdomen isbroaden the mesenteric base, and appendectomy.4 Gener- the radiographic test of choice.ally, symptomatic patients with malrotation require surgical 5. The classic treatment for incomplete intestinal rotation isintervention. Treatment for patients discovered to have mal- the Ladd’s procedure, which involves immobilization of therotation (e.g., incidental radiologic ﬁnding) who are asympto- right colon, division of Ladd’s bands and mobilization ofmatic is more controversial, although some surgeons recom- the duodenum, division of adhesions around the SMA, andmend that all patients with malrotation receive laparotomy.4 appendectomy.Intestinal rotation abnormalities without the presence ofvolvulus have been successfully managed using laparoscopic REFERENCESsurgical techniques.7  Wai C-T, Cheah W-K. Gastrointestinal: midgut malrotation in an adult. J Gastroent Hepatol 2006;21:917.KEY TEACHING POINTS  Gosche JR, Vick L, Boulanger SC, et al. Midgut abnormali- ties. Surg Clin N Am 2006;86:285–99.1. Midgut malrotation, an anomaly of fetal intestinal rotation  Kapfer SA, Rappold JF. Intestinal malrotation – not just the usually presenting in the ﬁrst month of life, may present in pediatric surgeon’s problem. J Am Coll Surg 2004;199:628– adulthood. 35.2. Symptomatic patients present either acutely, with symp-  Gamblin TC, Stephens RE, Johnson RK, et al. Adult mal- toms of bowel obstruction and intestinal ischemia from rotation: a case report and review of the literature. Curr Surg 2003;60:517–20. midgut or cecal volvulus, or more chronically, with vague  Kanazawa T, Kasugai K, Miyata M, et al. Case report: midgut abdominal pain with or without vomiting. malrotation in adulthood. Intern Med 200;39:626–31.3. Patients with compression of the duodenum by Ladd’s  Chin L-W, Wang H-P. Ultrasonographic diagnosis of elderly bands may present with bilious emesis and abdominal pain, midgut volvulus in the ED. Am J Emerg Med 2006;24:900–2. even in the absence of midgut volvulus.  Mazziotti MV, Stasberg SM, Langer JC. Intestinal rota-4. Radiographic diagnosis of midgut malrotation can be made tion abnormalities without volvulus: the role of laparoscopy. by upper gastrointestinal series (UGI), CT scan of the J Am Coll Surg 1997;185:172–6.
32Right lower quadrant abdominal pain and fever in a 36-year-old maleHISTORY OF PRESENT ILLNESS EXTREMITIES: No clubbing, cyanosis or edema.A 36-year-old male with a medical history signiﬁcant for poly- NEUROLOGIC: Nonfocal.cystic kidney disease and a known right inguinal hernia pre-sented to the ED complaining of one day of fever and right A peripheral intravenous line was placed, blood was drawnlower quadrant abdominal pain. The patient described the and sent for laboratory testing, and morphine sulfate andpain as cramping and constant, with radiation to the right groin. Zofran R were administered IV for pain and nausea, respec-He reported nausea without vomiting, and denied diarrhea, tively. A 1-liter bolus of normal saline was also given. Labora-constipation, dysuria, hematuria or anorexia. He reported that tory tests were signiﬁcant for a leukocyte count of 11.8 K/μLhis right inguinal hernia had been present for many years (normal 3.5–12.5 K/μL) with 82% neutrophils (normal 50–with swelling into the right scrotum, which was unchanged. He 70%); the electrolytes, creatinine glucose, liver function testsdenied any redness to the skin overlying the hernia. and urinalysis were all within normal limits. A CT scan of the abdomen and pelvis with intravenous and oral contrast wasPHYSICAL EXAMINATION obtained (Figure 32.1).GENERAL APPEARANCE: The patient appeared well hydrated The CT scan interpreted by the radiologist demonstrated aand well developed but in moderate discomfort. normal appendix and presence of a right inguinal hernia withVITAL SIGNS small bowel extending within it, without evidence of strangu- Temperature 100.9◦ F (38.3◦ C) lation or localized inﬂammation. Because the patient was still Pulse 87 beats per minute having discomfort despite pain medication, a surgical consul- Blood pressure 148/100 mmHg tation was obtained in the ED. The hernia was noted to be Respirations 18 breaths per minute reducible and no acute surgical issue was determined to be Oxygen saturation 98% on room air present. The patient was therefore discharged from the ED with a prescription for hydrocodone and an outpatient surgeryHEENT: Unremarkable. clinic referral to evaluate for elective right inguinal hernior-NECK: Supple. rhaphy. Approximately 36 hours after discharge, the patient re-CARDIOVASCULAR: Regular rate and rhythm without rubs, turned to the ED complaining of worsening lower abdomi-murmurs or gallops. nal pain not controlled with hydrocodone. The patient wasLUNGS: Clear to auscultation bilaterally. afebrile with normal vital signs and appeared in moderate dis- tress. Abdominal examination demonstrated bilateral lowerABDOMEN: Soft, nondistended, active bowel sounds present. abdominal tenderness, right greater than left, with guardingTenderness noted in the right lower quadrant and suprapubic and rebound tenderness. Laboratory tests were essentially un-regions, with voluntary guarding but no rebound tenderness. changed from his prior visit. A second CT scan of the abdo-No masses present. men and pelvis with intravenous and oral contrast was ob-GENITOURINARY: A large hernia sac was present in the right tained (Figure 32.2).scrotum; the area was mildly tender but easily reducible.There was neither erythema nor increased warmth over the What is your diagnosis?sac. 135
136 Gastroenterology A B Figure 32.1 CT of the abdomen and pelvis from a 36-year-old male with one day of right lower quadrant abdominal pain, demonstrating a normal air-ﬁlled appendix (arrow, panel A) and a large right inguinal hernia sac (arrow, panel B). A B Figure 32.2 Repeat CT of the abdomen and pelvis from a 36-year-old male with two days of right lower quadrant abdominal pain.
Right lower quadrant abdominal pain and fever in a 36-year-old male 137 length, it is usually found within 2 feet of the ileocecal valve, ANSWER it is often found in children under 2 years of age, and it affectsThe diagnosis is perforated Meckel’s diverticulitis. The repeat males twice as often as females.3CT scan demonstrated bowel wall thickening in the right lower A person with Meckel’s diverticulum has a 4–6% lifetimequadrant, with one segment of bowel wall appearing to rep- risk of developing a complication.4 The major complicationsresent the appendix. Stranding and inﬁltration of adjacent are hemorrhage, obstruction, intussusception, diverticulitisfat was noted, along with the presence of small amounts of and perforation. Bleeding is the most common complicationpneumoperitoneum (Figure 32.3). The bowel loops within the occurring in childhood, whereas most adults present with ob-hernia did not show inﬂammation or thickening. The ﬁnd- struction, diverticulitis or both.4 Although rare, Meckel’sings were suspicious for ruptured appendicitis. Intravenous diverticulum can be part of a hernia’s contents.antibiotics were given and the patient was taken to the OR. Various imaging techniques have been used to diagnoseA laparotomy was performed; upon surgical exploration of Meckel’s diverticulum. Plain ﬁlms are of limited value; how-the right lower quadrant, a Meckel’s diverticulum that had ever, they may show enteroliths, bowel obstruction, or theperforated into the small bowel mesentery was discovered. presence of gas or a gas-ﬂuid level in the diverticulum.5Although the appendix itself appeared normal, periappen- Meckel’s diverticulum is not often seen on routine bariumdiceal changes were noted. A small bowel resection to remove studies because of its small ostium, it is often ﬁlled with intesti-the perforated Meckel’s diverticulum was performed, as well nal contents, and peristalsis results in rapid emptying. Meti-as an appendectomy. The patient’s recovery was uneventful. culous examination with enteroclysis has been reported to be more sensitive.5 Although of limited value, sonography has been used for the investigation of Meckel’s diverticulum.6Meckel’s diverticulum High-resolution sonography usually shows a ﬂuid-ﬁlled struc-Meckel’s diverticulum is the most common congenital ture in the right lower quadrant having the appearance of aanomaly of the GI tract (1–3% of the population), result- blind-ending, thick-walled loop of bowel, with the typical guting from failure of the omphalomesenteric duct to become signature and a clear connection to a peristaltic, normal smallobliterated.1 As a congenital variant, Meckel’s diverticula are bowel loop.often found in children and are much less common in the adult On CT, Meckel’s diverticulum is difﬁcult to distinguishpopulation. Anatomically, this structure is located within from normal small bowel in uncomplicated cases.5 However, a75 cm of the ileocecal valve in 75% of cases.2 The vascular blind-ending ﬂuid- or gas-ﬁlled structure in continuity with thesupply to a Meckel’s diverticulum is a vestige of the vitelline small bowel may be seen. CT may also show enteroliths, intus-artery and arises directly from the mesentery. There is ectopic susception, diverticulitis or small bowel obstruction. CT ente-gastric and pancreatic mucosa found in a Meckel’s diverticu- roclysis (CTE) combines the advantages of CT and bariumlum in 95% of resected specimens for gastrointestinal bleed- enteroclysis, and has resulted in better visualization of theing and in 30–65% of asymptomatic patients.2 A commonly small bowel and higher sensitivity in the diagnosis of Meckel’squoted “rule of 2s” applies to Meckel’s diverticula: 2% of the diverticulum.7 CTE combines the improved spatial and tem-population have the anomaly, it is approximately 2 inches in poral resolution of multidetector CT with large volumes of A B Figure 32.3 Repeat CT of the abdomen and pelvis from a 36-year-old male with right lower quadrant abdo- minal pain, demonstrating small areas of pneumoperitoneum (arrow, panel A) and appendix with stranding and inﬁltration of adjacent fat (arrow, panel B).
138 Gastroenterologyingested neutral enteric contrast material to permit visualiza- rhage, obstruction, intussusception, diverticulitis or perfor-tion of the small bowel wall.7 The potential drawbacks to using ation.CTE in the ED include requiring placement of a nasogas- 3. CT enteroclysis (CTE) combines the advantages of CTtric tube for enteral contrast infusion as well as ﬂuoroscopy and barium enteroclysis, resulting in better visualization ofto determine the placement of the nasogastric tube prior to the small bowel and higher sensitivity in the diagnosis ofcontrast infusion and CT. Meckel’s diverticulum. Scintigraphy with 99m Tc-Na-pertechnetate has only minor 4. Meckel’s diverticulitis may mimic appendicitis; the correctdiagnostic value and a limited sensitivity (60%) in diagnosing diagnosis is usually established at laparotomy or laparo-Meckel’s diverticulum.5 However, it aids in the diagnosis of scopy.diverticula with ectopic gastric mucosa. Pertechnetate is taken 5. Complications from a Meckel’s diverticulum should beup by mucin-secreting cells of the gastric mucosa and ectopic considered as one of the differential diagnoses of an acutegastric tissue. Higher sensitivity in pediatric (85–90%) than abdomen in patients of any age.adult (60%) patients occurs, possibly due to earlier symptoms(such as hemorrhage) in patients with ectopic gastric mucosa.5 REFERENCES Meckel’s diverticulitis may mimic appendicitis. The correctdiagnosis is usually established at laparotomy or laparoscopy.  Kaltenback T, Nguyen C, Lau J, et al. Multidetector CTNo clinical features are pathognomonic, and the diagnosis is enteroclysis localized a Meckel’s diverticulum in a case ofrarely made preoperatively.8 Routine laboratory studies, such obscure GI bleeding. Gastrointest Endosc 2006;64:441–2.  Gosche JR, Vick L, Boulanger SC, et al. Midgut abnormali-as leukocyte and erythrocyte counts, serum electrolytes, blood ties. Surg Clin N Am 2006;86:285–99.glucose, serum creatinine and coagulation screen, are help-  Dumper J, Mackenzie S, Mitchell P, et al. Complications offul. CT and ultrasonography have been used for the diagno- Meckel’s diverticula in adults. Can J Surg 2006;49:353–7.sis of Meckel’s diverticulitis; despite the availability of these  Zacharakis E, Papadopoulos V, Athanasiou T, et al. Anmodern imaging techniques, the diagnosis remains challeng- unusual presentation of Meckel diverticulum as strangulateding. Rangarajan et al. described a case similar to this in which femoral hernia. South Med J 2008;101:96–8.the clinical diagnosis was appendicular perforation, whereas  Elsayes KM, Menias CO, Harvin HJ, et al. Imaging man-laparoscopy revealed a perforated Meckel’s diverticulum.8 ifestations of Meckel’s diverticulum. Am J RoentgenolMeckel’s diverticulitis should be kept in mind in the differ- 2007;189:81–8.ential diagnosis of an acute abdomen.  Mostbeck GH, Liskutin J, Dorffner R, et al. Ultrasono- graphic diagnosis of a bleeding Meckel’s diverticulum. Pedi- atr Radiol 2000;30:382.KEY TEACHING POINTS  Maglinte DDT, Sandrasegaran K, Lappas JC. CT entero- clysis: techniques and applications. Radiol Clin N Am 2007;1. Meckel’s diverticulum, the most common congenital ano- 45:289–301. maly of the GI tract, is best described by the “rule of 2s.”  Rangarajan M, Palanivelu C, Senthilkumar R, et al. Laparo-2. A person with Meckel’s diverticulum has a 4–6% life- scopic surgery for perforation of Meckel’s diverticulum. time risk of developing a complication such as hemor- Singapore Med J 2007;48:e102–5.
33Abdominal pain and diarrhea in a 64-year-old femaleHISTORY OF PRESENT ILLNESS CARDIOVASCULAR: Regular rate and rhythm without rubs,A 64-year-old female with a remote surgical history signiﬁcant murmurs or gallops.for a total abdominal hysterectomy presented to the ED com- LUNGS: Clear to auscultation bilaterally.plaining of four days of diffuse abdominal pain and multipleepisodes of watery diarrhea. She described her pain initially as ABDOMEN: A low, horizontal scar was noted; the abdomenintermittent and crampy, becoming constant on the day of pre- was moderately distended with hypoactive bowel sounds. Pal-sentation. She rated the pain at a level of 7 (on a scale of 0 to pation demonstrated diffuse tenderness with both rebound10). She denied fevers or chills but reported signiﬁcant nausea and guarding.without vomiting. She also reported at least 10 episodes of RECTAL: Normal tone, brown stool, hemoccult negative.nonbloody diarrhea per day beginning four days ago. Herdiarrhea stopped on the day of presentation, and she was not EXTREMITIES: No clubbing, cyanosis or edema.passing gas. NEUROLOGIC: Nonfocal.PHYSICAL EXAMINATION A peripheral intravenous line was placed, blood was drawnGENERAL APPEARANCE: The patient appeared well nourished, and sent for laboratory testing, and the patient was givensomewhat dehydrated and in moderate discomfort. morphine sulfate and Phenergan R IV for pain and nausea, respectively. She also received a 500 mL normal saline IV ﬂuidVITAL SIGNS bolus. Laboratory tests revealed a leukocyte count of 8.3 K/μL Temperature 97.8◦ F (36.5◦ C) (normal 3.5–12.5 K/μL) with 83% neutrophils (normal 50– Pulse 95 beats/minute 70%), hematocrit of 47% (normal 34–46%), BUN of 24 mg/ Blood pressure 165/90 mmHg dL (normal 7–17 mg/dL) and creatinine of 1.2 mg/dL (normal Respirations 20 breaths/minute <1.3 mg/dL). An abdominal radiograph series was obtained Oxygen saturation 98% on room air (Figure 33.1).HEENT: Unremarkable.NECK: Supple, no jugular venous distension. What is your diagnosis? A B Figure 33.1 Supine (panel A) and upright (panel B) abdominal radiographs from a 64-year-old female with four days of diffuse abdominal pain and diarrhea. 139
140 Gastroenterology shows a dilated loop of bowel with a “coffee bean” appear- ANSWER ance in the left upper quadrant, although this characteristicThe diagnosis is bowel obstruction with perforated viscus sec- ﬁnding is not always seen on plain radiographs.4,5ondary to cecal volvulus. The abdominal radiograph series CT reveals the presence and location of the volvulus anddemonstrates multiple dilated small bowel loops in the mid- has the added beneﬁt of allowing early identiﬁcation of poten-to-upper abdomen, as well as a dilated large bowel loop in the tially fatal complications, such as ischemia or perforation.6left upper abdomen (upright view, panel B, Figure 33.1). No A CT sign speciﬁc for volvulus is the “whirl,” which hasfree air was identiﬁed on the plain ﬁlms. A CT of the abdomen been described as volvulus of the midgut, cecum and sigmoidand pelvis with oral and intravenous contrast (Figure 33.2) colon.6 The “whirl” is composed of spiral loops of collapsedrevealed the presence of a markedly dilated cecum positioned cecum and sigmoid colon. Low-attenuating fatty mesenteryin the left upper abdomen, associated dilatation of the small with enhancing engorged vessels radiate from the twistedbowel to 3 cm, several foci of free air, and a swirling pattern in bowel. In the central eye of the “whirl,” a soft-tissue densitythe mesentery. These ﬁndings were consistent with a perfo- pinpoints the source of the twist. The degree of cecal rotationrated cecal volvulus. The patient was taken to the OR and can even be predicted by the “whirl’s” tightness.6upon laparotomy, a massively distended cecum was identiﬁed Emergency management of patients with cecal volvulusas well as tears in the bowel wall taenia, with a small perfo- includes pain control, aggressive intravenous hydration withration site. No adhesions from her previous hysterectomy normal saline, nasogastric suctioning and prompt surgical con-were identiﬁed. The patient underwent a right hemicolectomy sultation. The rates of reduction in cecal volvulus achievedwith side-to-side anastomosis between the ileum and the distal through colonoscopy are much lower than those achieved inascending colon. Her recovery was uneventful. sigmoid volvulus. Furthermore, in patients with cecal volvulus the recurrence rate exceeds 50%.6 Although successful reduc- tion by barium enema has been reported, high rates of per-Cecal volvulus foration may occur; therefore, the standard of care for treat-Cecal volvulus is an axial twist of the cecum, ascending colon ment of cecal volvulus is almost always operative, with eitherand terminal ileum around a mesenteric pedicle.1 Cecal volvu- cecopexy or right-sided hemicolectomy.5lus is relatively uncommon, with an incidence of 2.8–7.1 per1 million people per year. It accounts for approximately 1% KEY TEACHING POINTSof acute intestinal obstruction in British, Western Europeanand American series.1 It also causes proximal colonic obstruc- 1. Cecal volvulus involves an axial twist of the cecum, ascend-tion and secondary small bowel dilatation. Recognition of the ing colon and terminal ileum around a mesenteric pedicle,distended cecum on imaging studies is the key to differentiat- leading to large bowel obstruction.ing volvulus from an isolated small bowel obstruction.2 2. Cecal volvulus usually occurs in the sixth decade of life Patients with cecal volvulus are usually in the sixth decade and typically presents with acute onset of abdominal pain,of life; many have underlying congenital or acquired abnor- nausea and vomiting.malities that lead to increased cecal mobility.3 Cecal volvu- 3. In cases of cecal volvulus, plain abdominal radiographslus typically presents with acute onset of pain, nausea and may show the characteristic “coffee bean” appearance ofvomiting.4 On abdominal plain ﬁlms, cecal volvulus usually the dilated large bowel. A B Figure 33.2 CT of the abdomen and pelvis from a 64-year-old female with cecal volvulus, demonstrating a massively distended cecum (dark arrow, panel A) with several small foci of free air (white arrows, panel A), as well as dilated loops of small bowel and a swirling pattern of the mesentery (panel B).
Abdominal pain and diarrhea in a 64-year-old female 1414. Management of patients with cecal volvulus should include  Qalbani A, Paushter D, Dachman AH. Multidetector row pain control, intravenous hydration, nasogastric suctioning CT of small bowel obstruction. Radiol Clin N Am 2007; and prompt surgical consultation. 45:499–512.5. Deﬁnitive treatment of cecal volvulus is predominantly sur-  Kahi CJ, Rex DK. Bowel obstruction and pseudo-obstruc- gical, with either cecopexy or right-sided hemicolectomy; tion. Gastroenterol Clin N Am 2003;32:1229–47.  Martinez JP, Mattu A. Abdominal pain in the elderly. Emerg attempts at reduction by colonoscopy or contrast enemas Med Clin N Am 2006;24:371–88. lead to low success rates and the potential for perforation.  Hsia R, Chiao A, Law-Courter J. Images in emergency medicine. Ann Emerg Med 2007;49:272, 281.REFERENCES  Moore CJ, Corl FM, Fishman EK. Pictorial essay. CT of cecal volvulus: unraveling the image. Am J Roentgen Majeski J. Operative therapy for cecal volvulus combining 2001;177:95–8. resection with colopexy. Am J Surg 2005;189:211–3.
34Rectal and abdominal pain in a 70-year-old maleHISTORY OF PRESENT ILLNESSA 70-year-old male with a history of anemia presented to theED complaining of several hours of lower abdominal and rec-tal pain. The pain started suddenly, was describe