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i

Emergency Management of
Infectious Diseases
Second Edition
ii
iii

Emergency Management of
Infectious Diseases
Second Edition
Edited by
Rachel L. Chin
Professor of Emergency Medicine
Department of Emergency Medicine
University of California, San Francisco School of Medicine
Zuckerberg San Francisco General Hospital and Trauma Center
San Francisco, CA

Bradley W. Frazee
Department of Emergency Medicine
Alameda Health System – Highland Hospital
Oakland, CA
Clinical Professor of Emergency Medicine
University of California, San Francisco School of Medicine
San Francisco, CA

Associate Editor
Zlatan Coralic
Assistant Clinical Professor of Emergency Medicine
Emergency Medicine Clinical Pharmacist
University of California, San Francisco
San Francisco, CA
iv

University Printing House, Cambridge CB2 8BS, United Kingdom

One Liberty Plaza, 20th Floor, New York, NY 10006, USA
477 Williamstown Road, Port Melbourne, VIC 3207, Australia
314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India
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Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the pursuit of
education, learning and research at the highest international levels of excellence.
www.cambridge.org
Information on this title: www.cambridge.org/9781107153158
DOI: 10.1017/9781316597095
© Cambridge University Press (2008) 2018
This publication is in copyright. Subject to statutory exception
and to the provisions of relevant collective licensing agreements,
no reproduction of any part may take place without the written
permission of Cambridge University Press.
First published: 2008
Second edition: 2018
Printed in the United Kingdom by Clays, St Ives plc
A catalogue record for this publication is available from the British Library
ISBN 978-1-107-15315-8 Hardback
Cambridge University Press has no responsibility for the persistence or accuracy of URLs
for external or third-party internet websites referred to in this publication, and does not
guarantee that any content on such websites is, or will remain, accurate or appropriate.

Every effort has been made in preparing this book to provide accurate and up-to-date
information which is in accord with accepted standards and practice at the time of publication.
Although case histories are drawn from actual cases, every effort has been made to disguise
the identities of the individuals involved. Nevertheless, the authors, editors and publishers
can make no warranties that the information contained herein is totally free from error, not
least because clinical standards are constantly changing through research and regulation.
The authors, editors and publishers therefore disclaim all liability for direct or consequential
damages resulting from the use of material contained in this book. Readers are strongly
advised to pay careful attention to information provided by the manufacturer of any drugs or
equipment that they plan to use.
v

Contents
Preface page ix
Contributors xi

1 Infective Endocarditis 1 17 Sinusitis 120

Jorge Fernandez and Jessica L. Osterman Aaron Kornblith
2 Pericarditis and Myocarditis 6 18 Supraglottitis (Epiglottis) 123
Jessica L. Osterman and Jorge Fernandez Aaron Kornblith
3 Cardiac Implantable Electronic Device 19 Parotitis 126
Infections 14 Nisa S. Atigapramoj
Jorge Fernandez and Nicholas Pokrajac
20 Pharyngitis and Peritonsillar Abscess 129
4 Altered Mental Status in HIV-Infected Patients 18 Bradley W. Frazee
Nisha Bhatia and Cheryl A. Jay
21 Deep Neck Space Infections 135
5 Botulism 26 Christopher Hahn and Bradley W. Frazee
David M. Stier and Mary P. Mercer
22 Dental and Odontogenic Infections 140
6 Fever and Focal Cerebral Dysfunction 33 Bradley W. Frazee
Serena S. Spudich and Leah T. Le
23 Infectious Biliary Diseases: Cholecystitis and
7 Infections Affecting the Spinal Cord 42 Cholangitis 146
Anh T. Nguyen and Debbie Yi Madhok Bryan Darger and Rachel L. Chin
8 Meningitis 50 24 Viral Hepatitis 155
Katherine C. Bonsell and Anita A. Koshy Kavita Radhakrishnan and Michele Tana
9 Rabies 64 25 Peritonitis 162
Fredrick M. Abrahamian and Jada L. Roe Tu Carol Nguyen and Mercedes Torres
10 Tetanus 69 26 Acute Infectious Diarrhea 169
Fredrick M. Abrahamian and Jada L. Roe Kimberly A. Schertzer and Gus M. Garmel
11 West Nile Encephalitis Virus 74 27 Diarrhea in HIV-Infected Patients 181
Michael S. Diamond Michael J. A. Reid and Phyllis C. Tien
12 Bacterial Skin and Soft-Tissue Infections 79 28 Clostridium Difficile Infection 188
Bradley W. Frazee Charles Hartis and Nicole Abolins
13 Ectoparasites 87 29 Male Genitourinary Infections 192
Jan Shoenberger, William Mallon, and R. James Salway Jonathan Schimmel and William D. Binder
14 Fever and Rash in Adults 98 30 Non-Ulcerative Sexually Transmitted Diseases 199
Catherine Marco, Janel Kittredge-Sterling, and Jaime Jordan
Rachel L. Chin
31 Ulcerative Sexually Transmitted Diseases 208
15 Otitis Externa 114 Jaime Jordan and Joseph Engelman
Jeffrey Bullard-Berent
32 Vulvovaginitis 220
16 Otitis Media 117 Jaime Jordan
Jeffrey Bullard-Berent

v
vi

Contents

33 Adult Septic Arthritis 225 54 Pediatric Respiratory Infections 354

Robert Goodnough and Christopher Fee Ghazala Sharieff
34 Diabetic Foot Infections 228 55 Pediatric Urinary Tract Infections 366
Tamara John and Melinda Sharkey Jeffrey Bullard-Berent and Steven Bin
35 Hand Infections: Fight Bite, Purulent 56 Bites (Dogs, Cats, Rodents, Lagomorphs) 369
Tenosynovitis, Felon, and Paronychia 233 Hugh West and Sukhjit S. Takhar
Michael Kohn
57 Blood or Body Fluid Exposure Management
36 Open Fractures 239 and Post-Exposure Prophylaxis for Hepatitis B
Robert Goodnough and Melinda Sharkey and HIV 375
Roland C. Merchant
37 Osteomyelitis 242
Melinda Sharkey 58 Fever in Pregnancy 385
Dominika Seidman and Deborah Cohan
38 Plantar Puncture Wounds 246
Bradley W. Frazee 59 Postpartum and Post-Abortion Infections 406
Lisa Rahangdale and Amy G. Bryant
39 Prosthetic Joint Infections 250
Elisabeth Giblin and Scott C. Sherman 60 Fever in the Returning Traveler 412
Bradley W. Frazee and Eric Snoey
40 Spine Infections 253
Scott C. Sherman and Elena Strunk 61 Infectious Complications of Injection
Drug Use 430
41 Conjunctival and Corneal Infections 258
Bradley W. Frazee and Daniel Schnorr
Michelle Y. Peng and Saras Ramanathan
62 Infections in Oncology Patients 442
42 Periocular Infections 265
Allison Nazinitsky and Erik R. Dubberke
Kareem Moussa and Saras Ramanathan
63 Post-Operative Infections 453
43 Infections of the Uvea, Vitreous, and Retina 274
Robert Brown and Siamak Moayedi
Greg Bever and Saras Ramanathan
64 The Febrile Post-Transplant Patient 458
44 Community-Acquired Pneumonia 280
Justin Bosley and Aparajita Sohoni
Bradley W. Frazee, Christopher Fee, and Rachel L. Chin
65 Sepsis 467
45 HIV-Associated Respiratory Infections 288
David Thompson
Rachel Greenblatt and Laurence Huang
66 Infections in Sickle Cell Disease 473
46 Influenza 299
Suzanne Lippert
Asim A. Jani and Timothy M. Uyeki
67 Anthrax 480
47 Tuberculosis 308
David M. Stier, Mary P. Mercer, and Rachel L. Chin
Robert Blount, Payam Nahid, and Adithya Cattamanchi
68 Plague 490
48 Lower Urinary Tract Infection in Adults 319
David M. Stier and Mary P. Mercer
Fredrick M. Abrahamian
69 Smallpox 498
49 Pyelonephritis in Adults 324
David M. Stier, Mary P. Mercer, and Rachel L. Chin
Fredrick M. Abrahamian
70 Tularemia 506
50 Fever in the Newborn 328
David M. Stier and Mary P. Mercer
Maureen McCollough
71 Hantavirus 514
51 The Febrile Child 334
Shruti Kant and Rachel L. Chin
Paul Ishimine
72 Ebola Virus Disease 521
52 Fever and Rash in the Pediatric Population 339
Edwin Dietrich, Bradley W. Frazee, and
Catherine Marco, Janel Kittredge-Sterling, and
Timothy M. Uyeki
Rachel L. Chin
73 Zika Virus 526
53 Pediatric Orthopedic Infections 348
Ashley Rider and Bradley W. Frazee
Cordelia W. Carter and Melinda S. Sharkey

vi
vii

Contents

74 Zoonotic Influenza (Novel Influenza A, including 77 Extended Spectrum Beta-Lactamase 552

Avian and Swine Influenza A Virus Infections) 531 Colgan Sloan and Christopher J. Edwards
Timothy M. Uyeki
78 Antimicrobial Overview 556
75 Methicillin-Resistant Staphylococcus Aureus Conan MacDougall and Camille Beauduy
(MRSA) 541
Tracy Trang and Bradley W. Frazee
76 Enterococci 548
Jill Logan and Megan Musselman Index 581

vii
viii
ix

Preface

The diagnosis and treatment of infectious disease represents a likely to be the first to encounter victims of biological weap-
large and very important part of emergency medicine practice. ons. In this edition, we include chapters on recent emerging
Challenges faced by acute care practitioners on a daily basis infections such as Ebola and Zika, as well as rare but deadly
range from the definitive treatment and discharge of a patient infectious agents that can be weaponized, such as anthrax
with a simple abscess, to recognition of a rare infection in a and smallpox.
traveler, to resuscitation and stabilization of a patient with We hope that our textbook can be of use to every type of
septic shock. practitioner that cares for patients with infectious diseases,
In this second edition of Emergency Management of including emergency physicians, primary care physicians and
Infectious Diseases, we have endeavored to produce a prac- specialists, nurse practitioners, physician assistants, residents,
tical, clinically oriented, systems-based overview of the most and medical students.
important infectious diseases encountered in emergency prac- We thank the many nationally and internationally
tice. Our textbook covers the gamut of common viral, bacterial, respected clinicians, educators, and researchers who con-
fungal, and parasitic infections. For each disease, we briefly dis- tributed, and hope that this second edition of Emergency
cuss microbiology, pathophysiology, and epidemiology, but the Management of Infectious Diseases will prove an invaluable
emphasis is on emergent diagnosis and treatment. The narra- reference for practitioners confronting the spectrum of infec-
tive is supplemented with photographs and tables highlighting tious disease.
key diagnostic findings and current antimicrobial recommen-
dations, including dosing. Bradley W. Frazee, MD
Acute care practitioners also act as sentinels for out- Rachel L. Chin, MD
breaks of communicable and emerging infections, and are Zlatan Coralic

ix
x
xi

Contributors

Nicole Abolins, PharmD, BCPS William D. Binder, MD

Medical Outcomes Specialist, Director Associate Professor of Emergency Medicine
Pfizer, Inc. Alpert School of Medicine, Brown University
Greensboro, NC Providence, RI

Fredrick M. Abrahamian, DO, FACEP, FIDSA Robert Blount, MD

Health Sciences Clinical Professor of Emergency Medicine Pulmonary and Critical Care Medicine
David Geffen School of Medicine at UCLA University of Iowa
Los Angeles, CA Iowa City, IA

Nisa S. Atigapramoj, MD Katherine C. Bonsell, DO

Assistant Clinical Professor Neurological Care
Department of Emergency Medicine and Pediatrics Evergreen Health Neuroscience Institute
UCSF Benioff Children’s Hospital Kirkland, WA
Zuckerberg San Francisco General Hospital and
Justin Bosley, MD, CAQSM
Trauma Center
Emergency Medicine Attending Physician
University of California, San Francisco School of Medicine
The Permanente Medical Group
San Francisco, CA
Oakland, CA
Camille Beauduy, PharmD
Robert Brown, MD
Infectious Diseases Clinical Pharmacist
Department of Emergency Medicine
Department of Pharmacy Services
University of Maryland School of Medicine
Zuckerberg San Francisco General Hospital
Baltimore, MD
San Francisco, CA
Amy Bryant, MD, MSCR
Greg Bever, MD
Assistant Professor of Obstetrics and Gynecology
Department of Ophthalmology
Department of Obstetrics and Gynecology
University of California, San Francisco School of
Medicine University of North Carolina at Chapel Hill
San Francisco, CA Chapel Hill, NC

Nisha Bhatia, MD Jeffrey Bullard-Berent, MD, FAAP, FACEP

Neurology Attending Physician Professor Emergency Medicine and Pediatrics
The Permanente Medical Group Vice Chair Emergency Medicine
Vallejo, CA Medical Director, Child Ready
Steven Bin, MD Virtual Pediatric Emergency Department
Associate Clinical Professor University of New Mexico School of Medicine
Departments of Emergency Medicine and Pediatrics Albuquerque, NM
UCSF Benioff Children’s Hospital Cordelia W. Carter, MD
Zuckerberg San Francisco General Hospital and Assistant Professor of Orthopaedic Surgery
Trauma Center Yale Department of Orthopaedics and Rehabilitation
University of California, San Francisco School of Medicine Yale University School of Medicine
San Francisco, CA New Haven, CT

xi
xii

Contributors

Adithya Cattamanchi, MD Christopher J. Edwards, PharmD, BCPS

Associate Professor of Medicine Clinical Associate Professor – Department of Pharmacy
Zuckerberg San Francisco General Hospital and Practice
Trauma Center University of Arizona College of Pharmacy
University of California, San Francisco School of Medicine Marana, AZ
San Francisco, CA
Joseph Engelman, MD, MPH
Rachel L. Chin, MD Clinical Professor of Medicine
Professor of Emergency Medicine San Francisco Department of Public Health Physician
Department of Emergency Medicine Specialist
University of California, San Francisco School of Medicine University of California, San Francisco School of Medicine
Zuckerberg San Francisco General Hospital and Trauma Center San Francisco, CA
San Francisco, CA
Christopher Fee, MD
Deborah Cohan, MD, MPH Professor of Clinical Emergency Medicine
Professor of Obstetrics, Gynecology, and Associate Chair for Education
Reproductive Sciences Emergency Medicine Residency Program Director
University of California, San Francisco School of Medicine University of California, San Francisco School of Medicine
Medical Director, HIVE San Francisco, CA
Zuckerberg San Francisco General Hospital and Trauma Center
Jorge Fernandez, MD
San Francisco, CA
Assistant Clinical Professor of Emergency Medicine
Zlatan Coralic, PharmD Associate Residency Program Director
Assistant Clinical Professor of Emergency Medicine University of California, San Diego School of Medicine
Emergency Medicine Clinical Pharmacist San Diego, CA
University of California, San Francisco
Alexander C. Flint, MD, PhD
San Francisco, CA
Department of Neuroscience
Bryan Darger, MD Division of Research
Emergency Medicine Physician The Permanente Medical Group
Department of Emergency Medicine Redwood City, CA
University of California, San Francisco School of Medicine
Bradley W. Frazee, MD
Zuckerberg San Francisco General Hospital and Trauma
Department of Emergency Medicine
Center
Alameda Health System – Highland Hospital
San Francisco, CA
Oakland, CA
Michael S. Diamond, MD, PhD Clinical Professor of Emergency Medicine
The Herbert S. Gasser Professor University of California, San Francisco School of Medicine
Departments of Medicine, Molecular Microbiology, San Francisco, CA
Pathology, and Immunology
Associate Director, The Andrew M. and Jane M. Bursky Gus M. Garmel, MD
Center for Human Immunology and Immunotherapy Clinical Professor (Affiliate) of Emergency Medicine
Programs Stanford University School of Medicine
Washington University School of Medicine Stanford, CA
St. Louis, MO Senior Staff Emergency Physician, The Permanente
Medical Group
Edwin Dietrich, MD Santa Clara, CA
Emergency Medicine Attending Physician Senior Editor, The Permanente Journal
The Permanente Medical Group Portland, OR
Oakland, CA
Elisabeth Giblin, MD
Erik R. Dubberke, MD Attending Physician
Assistant Professor of Medicine Department of Emergency Medicine
Clinical Director, Transplant Infectious Diseases Northwest Community Hospital
Washington University School of Medicine Arlington Heights, IL
St. Louis, MO

xii
xiii

Contributors

Robert Goodnough, MD Jaime Jordan, MD

Emergency Medicine Physician Assistant Clinical Professor of Emergency Medicine
Department of Emergency Medicine Vice Chair, Acute Care College
University of California, San Francisco School of Medicine David Geffen School of Medicine at UCLA
Zuckerberg San Francisco General Hospital and Trauma Associate Director, Residency Training Program
Center Department of Emergency Medicine
San Francisco, CA Harbor-UCLA Medical Center
Torrance, CA
Christopher Hahn, MD
Assistant Professor of Emergency Medicine Shruti Kant, MD
Icahn School of Medicine at Mount Sinai Associate Clinical Professor
Assistant Program Director Departments of Emergency Medicine and Pediatrics
Department of Emergency Medicine UCSF Benioff Children’s Hospital
Mount Sinai St. Lukes-Roosevelt Zuckerberg San Francisco General Hospital and
New York, NY Trauma Center
University of California, San Francisco School of Medicine
Charles Hartis, PharmD, BCPS
San Francisco, CA
Clinical Pharmacy Specialist
Forsyth Medical Center Janel Kittredge-Sterling, DO
Davie Medical Center – Wake Forest Baptist Health St. Vincent Mercy Medical Center
Advance, NC Perrysburg, OH

Laurence Huang, MD, FCCP, ATSF Michael A. Kohn, MD, MPP

Professor of Medicine Professor of Epidemiology and Biostatistics
Chief, HIV/AIDS Chest Clinic University of California, San Francisco School of Medicine
Positive Health Program at San Francisco General San Francisco, CA
Zuckerberg San Francisco General Hospital and Attending Emergency Physician
Trauma Center Mills-Peninsula Medical Center
University of California, San Francisco School of Medicine Burlingame, CA
San Francisco, CA
Aaron Kornblith, MD
Paul Ishimine, MD Assistant Clinical Professor
Clinical Professor of Emergency Medicine and Pediatrics Departments of Emergency Medicine and Pediatrics
Program Director, Pediatric Emergency Medicine Fellowship UCSF Benioff Children’s Hospital
Division of Pediatric Emergency Medicine Zuckerberg San Francisco General Hospital and
Rady Children’s Hospital, San Diego Trauma Center
Department of Emergency Medicine University of California, San Francisco School of Medicine
University of California, San Diego School of Medicine San Francisco, CA
San Diego, CA
Anita A. Koshy, MD
Asim A. Jani, MD, MPH, FACP Associate Professor of Neurology
Hospital Epidemiologist Department of Neurology, Department of Immunobiology,
Orlando Health BIO5 Institute
Orlando, FL University of Arizona, College of Medicine
Tucson, AZ
Cheryl A. Jay, MD
Clinical Professor of Neurology Leah T. Le, MPH
University of California, San Francisco School of Medicine Research Coordinator
Zuckerberg San Francisco General Hospital and Trauma Department of Neurology
Center Yale University School of Medicine
San Francisco, CA New Haven, CT

Tamara John, MD Suzanne Lippert, MD, MS

Yale Department of Orthopaedics and Rehabilitation Emergency Medicine Attending Physician
Yale University School of Medicine The Permanente Medical Group
New Haven, CT Oakland, CA

xiii
xiv

Contributors

Jill Logan, PharmD, BCPS Siamak Moayedi, MD

Emergency Medicine Clinical Pharmacist Assistant Professor
Silver Spring, MD Department of Emergency Medicine
University of Maryland School of Medicine
Conan MacDougall, PharmD, MAS, BCPS-AQ ID
Baltimore, MD
Professor of Clinical Pharmacy
University of California, San Francisco School of Pharmacy Kareem Moussa, MD
San Francisco, CA Department of Ophthalmology
University of California, San Francisco School of
Debbie Yi Madhok, MD Medicine
Assistant Clinical Professor San Francisco, CA
Department of Emergency Medicine
Director, Emergency Stroke Program Megan Musselman, PharmD, MS, BCPS, BCCCP
Zuckerberg San Francisco General Hospital and Emergency Medicine Clinical Pharmacy Specialist
Trauma Center PGY1 Pharmacy Residency Coordinator
University of California, San Francisco School of Medicine North Kansas City Hospital
San Francisco, CA North Kansas City, MO
William Mallon, MD, DTMH, FACEP, FAAEM Payam Nahid, MD
Professor of Clinical Emergency Medicine Professor of Medicine
Director: Division of International Emergency Medicine University of California, San Francisco School of
Department of Emergency Medicine Medicine
Stony Brook University (SUNY) Zuckerberg San Francisco General Hospital and
Stony Brook, NY Trauma Center
San Francisco, CA
Catherine A. Marco, MD
Professor of Emergency Medicine Rachel Najafi, MD
Wright State University Boonshoft School of Medicine Hospitalist, Medical Service
Dayton, OH Veteran’s Hospital, Palo Alto
Clinical Instructor (Affiliated)
Maureen McCollough, MD, MPH, FACEP, FAAEM Stanford University School of Medicine
Assistant Professor of Emergency Medicine and Palo Alto, CA
Pediatrics
Director, Pediatric Emergency Department Allison Nazinitsky, MD
Department of Pediatrics Infectious Disease Physician
Medical Director, Department of Emergency Medicine Oklahoma City VA Health Care System
Los Angeles County+USC Medical Center Oklahoma City, OK
Keck School of Medicine
Anh T. Nguyen, MD, MS
University of Southern California
Department of Neurosurgery
Los Angeles, CA
Houston Methodist Neurocritical Care
Mary P. Mercer, MD, MPH, FAEMS Houston, TX
Associate Clinical Professor
Tu Carol Nguyen, MD
Department of Emergency Medicine
Clinical Instructor
University of California, San Francisco
Department of Emergency Medicine
Associate Director, EMS/Disaster Medicine Fellowship
University of Maryland School of Medicine
Zuckerberg San Francisco General Hospital and Trauma Center
Baltimore, MD
San Francisco, CA
Jessica L. Osterman, MD
Roland C. Merchant, MD, MPH
Assistant Professor of Clinical Emergency Medicine
Associate Professor
Assistant Program Director
Emergency Medicine and Epidemiology
Los Angeles County+USC Medical Center
Rhode Island Hospital
Keck School of Medicine
Alpert Medical School
University of Southern California
Brown University
Los Angeles, CA
Providence, RI

xiv
xv

Contributors

Michelle Y. Peng, MD Kimberly A. Schertzer, MD, FACEP

Department of Ophthalmology Associate Director of Simulation
University of California, San Francisco School of Medicine Simulation Fellowship Director
San Francisco, CA Department of Emergency Medicine
Stanford University School of Medicine
Nicholas Pokrajac, MD
Stanford, CA
Attending Physician
Department of Emergency Medicine Jonathan Schimmel, MD
University of California San Diego Health System Attending Physician
San Diego, CA Department of Emergency Medicine
University of Colorado School of Medicine
Kavita Radhakrishnan, MD
Aurora, CO
Department of Medicine, Division of Gastroenterology
University of California, San Francisco School of Daniel Schnorr, MD
Medicine Attending Physician
San Francisco, CA Department of Emergency Medicine
Harbor-UCLA Medical Center
Lisa Rahangdale, MD
Torrance, CA
Associate Professor of Obstetrics and Gynecology
Department of Obstetrics and Gynecology Dominika Seidman, MD, MAS
University of North Carolina School of Medicine Assistant Professor of Obstetrics, Gynecology and
Chapel Hill, NC Reproductive Sciences
Department of Obstetrics, Gynecology and
Saras Ramanathan, MD Reproductive Sciences
Associate Professor of Ophthalmology University of California, San Francisco School of Medicine
Department of Ophthalmology Zuckerberg San Francisco General Hospital and
University of California, San Francisco School of Trauma Center
Medicine San Francisco, CA
San Francisco, CA
Ghazala Sharieff, MD, MBA
Michael J. A. Reid, MD, MA, MPH Clinical Professor
Assistant Professor of Medicine University of California, San Diego School of Medicine
Division of HIV, Infectious Diseases, and Global Corporate Vice President, Chief Experience Officer,
Medicine Scripps Health
Zuckerberg San Francisco General Hospital San Diego, CA
University of California, San Francisco
San Francisco, CA Melinda Sharkey, MD
Associate Professor of Orthopaedic Surgery
Ashley Rider, MD Yale Department of Orthopaedics and Rehabilitation
Emergency Medicine Physician
Yale University School of Medicine
Department of Emergency Medicine New Haven, CT
Alameda Health System – Highland Hospital
Oakland, CA Scott C. Sherman, MD
Associate Professor of Emergency Medicine
Jada L. Roe, MD Department of Emergency Medicine
Emergency Medicine Physician Cook County (Stroger) Hospital
Department of Emergency Medicine Rush Medical College
David Geffen School of Medicine at UCLA Chicago, IL
Los Angeles, CA
Jan M. Shoenberger, MD
R. James Salway, MD Associate Professor of Clinical Emergency Medicine
Clinical Assistant Professor of Emergency Medicine Residency Program Director
Department of Emergency Medicine Los Angeles County+USC Medical Center
SUNY Downstate Medical Center / Kings County Hospital Keck School of Medicine
Center
University of Southern California
Brooklyn, NY
Los Angeles, CA

xv
xvi

Contributors

Colgan Sloan, PharmD, BCPS Michele M. Tana, MD, MHS

Clinical Pharmacy Specialist - Emergency Medicine Assistant Professor of Medicine
Department of Pharmacy Services Department of Medicine, Division of Gastroenterology
University of Utah Health University of California, San Francisco School of Medicine
Salt Lake City, UT Zuckerberg San Francisco General Hospital and Trauma
Center
Eric Snoey, MD San Francisco, CA
Vice Chair
Department of Emergency Medicine David Thompson, MD
Alameda Health System – Highland Hospital Clinical Associate Professor of Emergency Medicine
Oakland, California Department of Emergency Medicine
Clinical Professor of Emergency Medicine University of California, San Francisco School of Medicine
University of California, San Francisco School of Medicine Zuckerberg San Francisco General Hospital and Trauma
San Francisco, CA Center
San Francisco, CA
Aparajita Sohoni, MD
Attending Emergency Physician Phyllis C. Tien, MD, MPH
California Pacific Medical Center Professor of Medicine
San Francisco, CA University of California, San Francisco School of Medicine
UCSF Positive Health Program
Serena S. Spudich, MD Zuckerberg San Francisco General Hospital and Trauma
Professor of Neurology Center
Division Chief, Neurological Infections and Global San Francisco, CA
Neurology
Department of Neurology Mercedes Torres, MD
Yale University School of Medicine Clinical Assistant Professor
New Haven, CT Department of Emergency Medicine
University of Maryland School of Medicine
David M. Stier, MD Baltimore, MD
Director, Communicable Disease Prevention Unit
Medical Director, AITC Immunization and Travel Clinic Tracy Trang, PharmD, BCPS
Medical Epidemiologist, Communicable Disease Control Emergency Medicine and Infectious Disease Pharmacist
Unit Downey, CA
Population Health Division, San Francisco Department of
Timothy M. Uyeki, MD, MPH, MPP
Public Health
Chief Medical Officer, Influenza Division
San Francisco, CA
Centers for Disease Control and Prevention,
Elena Strunk, MD Atlanta, GA
Research Instructor Clinical Associate Professor
Department of Emergency Medicine Department of Pediatrics
George Washington University Hospital University of California, San Francisco School of Medicine
Washington, DC San Francisco, CA

Sukhjit S. Takhar, MD Hugh West, MD, FACEP, FAAEM

Attending Physician Associate Clinical Professor of Emergency Medicine
Mills-Peninsula Emergency Medical Associates University of California, San Francisco School of Medicine
Burlingame, CA San Francisco, CA

xvi
1

Chapter
Infective Endocarditis

1 Jorge Fernandez and Jessica L. Osterman

Outline Treatment and Prophylaxis 4

Complications and Admission Criteria 4
Introduction 1
Pearls and Pitfalls 5
Epidemiology and Microbiology 1
References 5
Clinical Features 1
Additional Readings 5
Differential Diagnosis 2
Laboratory and Radiographic Findings 3

Introduction and heart block. Large, mobile vegetations are associated with
embolization and metastatic infection (see below).
Infectious endocarditis (IE) is a difficult diagnosis to make The list of pathogens that have been reported to cause
in the emergency setting. Early diagnosis and management IE is enormous and includes fungi and protozoa. The most
requires an understanding of endocarditis risk factors, typical common etiolgies, however, are gram-positive cocci, including
and atypical clinical presentations, and current diagnostic and Staphylococcus species, both S. aureus and coagulase nega-
empiric treatment strategies. tive Staphylococcus, and Streptococcal species, particularly
viridans Streptococci and group D Streptococcus. S. aureus
Epidemiology and Microbiology is both the most common etiology and the pathogen most
In developed countries, the incidence of IE is roughly 5 cases often associated with metastatic complications. Enterococcus
per 100,000 persons per year. It more commonly affects males is common in the elderly. The clinical setting may suggest the
(2:1). Well-recognized risk factors for IE include presence of pathogen involved: S. aureus is the most common in injection
a prosthetic heart valve (which carry an annual incidence of drug users, viridans Streptococci in patients with recent dental
approximately 1%), congenital heart disease, endocardiac procedures, and gram-negative bacilli in patients that have
devices, injection drug use (see Chapter 61), and a prior history undergone invasive genitourinary procedures.
of endocarditis. Rheumatic heart disease is now an uncommon Pathogens that are less commonly implicated in IE include
predisposing risk factor in the United States. However, in the “HACEK” (Haemophilus aphrophilus, Haemophilus
modern series, there is no easily identifiable risk factor for paraphrophilus, Haemophilus parainfluenzae, Actinobacillus
underlying valve damage in approximately 50% of endocarditis actinomycetemcomitans, Cardiobacterium hominis, Eikenella
cases. Such cases are believed to be due to age-related degener- corrodens, and Kingella kingae) group of fastidious bacteria,
ative valve disease and subtle immunosuppresion from diabetic Bartonella, chlamydia, Legionella, and fungi. Infections with
endocarditis and other factors. Health-care associated cases, these organisms may be difficult to detect because they do not
often in the elderly, account for a growing proportion of endo- always grow in routine blood cultures.
carditis in the United States.
Infective endocarditis occurs when circulating pathogens
adhere to damaged endothelium and form a vegetation, usu- Clinical Features
ally on or around a cardiac valve. Abnormal turbulent flow and The presentation of IE (see Table 1.1 and Figure 1.1) ranges
damaged endothelium lead to fibrin and platelete deposition from the well-appearing patient with non-specific symptoms
which presents a nidus for bacterial infection during bacter- to the toxic patient in severe septic shock with multi-organ
emia. In the setting of frequent bacteremia, such as intravenous failure. Symptoms are often frustratingly non-specific, and
drug use and dental infection, IE may occur even without an may include low-grade fever, malaise, myalgias, headache, and
identifiable pathologic valvular lesion. Growth of the infected anorexia. Patients with mild symptoms are often misdiagnosed
vegetation eventually leads to valve destruction and impaired as having a viral syndrome. Approximately 80% of patients
function, typically regurgitation, and eventually heart failure. with IE will have a fever during their initial emergency depart-
Invasion of the myocardium can lead to paravalvular abscess ment stay. The presence of a new murmur may be helpful;

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Chapter 1: Infective Endocarditis

Table 1.1 Clinical Features: Infective Endocarditis

Pathogens Staphylococcus aureus
Staphylococcus epidermidis
Viridans
Streptococcus bovis
Enterococcus spp.
HACEK
Immuno-compromised: fungal, rickettsial, protozoan
Signs and symptoms Fever, malaise, weight loss, night sweats, myalgias, headache, chest/neck/back pain, cough, dyspnea,
hepatosplenomegaly, hematuria, arthritis, edema, neurologic symptoms, jaundice, rash.
Laboratory and radiologic findings Duke Clinical Criteria:
2 Major
or
1 Major + 3 Minor
or
5 Minor
Major (microbiology):
Typical organisms × 2 blood cultures (S. viridans, S. bovis, HACEK, S. aureus, or Enterococcus)
Persistent bacteremia (≥ 12 hours)
3/3 or 3/4 positive blood cultures
Major (valve):
Positive echocardiogram
New valve regurgitation
Minor:
Predisposing heart condition or IDU
Fever ≥ 38 °C (100.4 °F)
Vascular phenomenon (arterial embolism, mycotic aneurysm, intracerebral bleed, conjunctival hemorrhage,
Janeway lesions)
Immune phenomenon (glomerulonephritis, Osler node, Roth spot, rheumatoid factor)
Positive blood culture not meeting above criteria
Echocardiogram – abnormal but not diagnostic

IDU – intravenous drug use.

however, the high prevalence of a baseline murmur in older may present with septic pulmonary emboli, which cause respi-
adults makes this finding non-specific. ratory symptoms that may be mistaken for pneumonia or
Patients with a more indolent or subacute presentation may pulmonary embolism. Mechanical failure of the pulmonic or
display physical findings that result from the deposition of tricuspid valves can cause signs and symptoms of acute right-
immune complexes in end-vessels throughout the body. These sided heart failure.
findings include the classic stigmata of IE: Roth spots (exuda- Other serious sequelae of endocarditis include intravas-
tive lesions on the retina), Janeway lesions (painless erythema- cular hemolysis, and disseminated intravascular coagulation.
tous lesions on the palms and soles), and Osler nodes (painful Abscesses around the annulae of the cardiac valves may result
violet lesions on the fingers or toes), as well as hematuria (due in conduction blocks and bradydysrhythmias. Ventricular wall
to glomerulonephritis), subungual splinter hemorrhages, or rupture may lead to cardiac tamponade or hemorrhagic shock,
petechiae of the palate and conjunctiva. These subtle signs of and extension into the coronary arteries may cause acute cor-
IE should be sought on examination; however, they are actually onary syndrome.
quite uncommon and their absence does not rule out IE.
In left-sided endocarditis, arterial embolization may occur Differential Diagnosis
in any organ system. The central nervous system is the most
The differential diagnosis of IE includes both acute and chronic
common location. Infections that initially appear to be focal
infections, malignancies, and a wide spectrum of inflammatory
or localized, particularly when due to S. aureus, may actu-
and autoimmune disorders. However, IE should be suspected
ally be the result of septic emboli from IE. Examples include
in any febrile patient with the following risk factors:
stroke and spinal cord syndromes, mycotic aneurysms, osteo-
myelitis, epidural abscesses, septic arthropathies, necrotic skin • injection drug use
lesions, and cold, pulseless extremities. Mycotic aneurysms • rheumatic heart disease
may cause meningitis, headaches, or focal neurological deficits. • valvular insufficiency
Destruction of the mitral or aortic valve can cause acute respi- • indwelling catheter
ratory failure and cardiogenic shock. Right-sided endocarditis • pacemaker

2
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Chapter 1: Infective Endocarditis

B D

Figure 1.1 Classic physical examination findings in IE. Splinter hemorrhages (A); conjunctival petechiae (B); Osler nodes (C); and Janeway lesions (D).
Images from E. Mylonakis and S. B. Calderwood, Infective endocarditis in adults. N. Engl. J. Med., 2001; 345(18): 1318–30.
Copyright © 2008 Massachusetts Medical Society. All rights reserved.

• prosthetic heart valve • systemic embolization: carotid stenosis, vascular dissection,

• congenital heart disease or cardiac dysrhythmias
• prior endocarditis • altered mental status with fever: meningitis, encephalitis,
In more severe cases, the differential diagnosis will depend brain abscess
on the presenting signs and symptoms:
• severe sepsis with end-organ dysfunction: pneumonia, uri- Laboratory and Radiographic Findings
nary tract infection, peritonitis, soft-tissue infections, and Blood cultures are a crucial basis for the definitive diag-
meningitis nosis of IE. Thus, it is important for emergency providers
• left- or right-sided heart failure: myocardial infarction, to obtain blood cultures prior to giving antibiotics when-
acute myocarditis, decompensated valvular disease, pulmo- ever IE is suspected. At least two and preferably three sets of
nary embolism, or aortic dissection blood cultures should be drawn with aseptic technique, be of

3
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Chapter 1: Infective Endocarditis

sufficient volume (10 mL), and be drawn at multiple sites. The Table 1.2 Empiric Treatment for Infective Endocarditis
sensitivity of three sets of blood cultures approaches 90% in
Patient Category Empiric Therapy Recommendation*
patients who have not received antibiotics. Serologies for
Adults Native valve:
Bartonella, Brucella, and Coxiella Burnetii (Q fever) may be
Vancomycin 15–20 mg/kg/dose IV every
indicated if standard cultures are negative. Other routine blood 8–12 hours
tests such as inflammatory markers (complete blood count and
[CBC], erythrocyte sedimentation rate [ESR], C-reactive pro- Ceftriaxone 2 g IV every 24 hours
tein [CRP]) lack specificity. (alternate: ciprofloxacin 400 mg IV every
Endocarditis produces abnormal findings on standard diag- 12 hours)
nostic tests that can lead the clinician to an incorrect initial Prosthetic valve:
diagnosis. For example, an abnormal urinalysis may lead to a Vancomycin 15–20 mg/kg/dose IV every
8–12 hours
diagnosis of cystitis or glomerulonephritis, infiltrates on a chest
and
X-ray may be interpreted as pneumonia, or abnormalities on a Gentamicin 1 mg/kg IV every 8 hours
lumbar puncture may lead to a diagnosis of primary meningitis. and
Electrocardiography (ECG) is seldom helpful in Rifampin 300 mg PO/IV every 8 hours
establishing the diagnosis of IE. The most common ECG Children Vancomycin 15–20 mg/kg/dose IV every
abnormality in IE is sinus tachycardia. A valve ring abscess 6 hours
can produce heart block, particularly an elongating PR and
interval. Cardiac ischemia may result if IE extends into a cor- Gentamicin 1.5–2.5 mg/kg IV every 8 hours
onary artery lumen. Pregnant women Vancomycin 15–20 mg/kg/dose IV every
Like blood cultures, echocardiography is an essential test 8–12 hours
in establishing the definitive diagnosis of IE. However, its and
main utility in the emergency setting is in the detection of life- Ceftriaxone 2 g IV every 24 hours
threatening complications such as pericardial effusion, cardiac and
Rifampin 300 mg PO/IV every 8 hours (if
tamponade, and valvular rupture. Transthoracic echocardiog-
prosthetic heart valve)
raphy is useful if positive for a clear-cut vegetation; however,
Immunocompromised As above, depending on age and pregnancy
transesophageal echocardiography has higher sensitivity and is status
generally required in suspected IE if the transthoracic echocar-
diogram is negative. * Vancomycin and gentamicin dosing may need to be adjusted based
on renal function and ideal body weight. Trough monitoring with both
The Duke Criteria (see Table 1.1) are a widely accepted, agents is strongly recommended. Rifampin has many clinically important
structured diagnostic tool for assisting in the often challenging drug–drug interactions and may require other drug-level monitoring.
diagnosis of IE. However, these criteria have limited utility in IV – intravenous.
the emergency setting. Emergency providers must maintain
constant vigilance for IE, have a low threshold for obtaining
blood cultures and echocardiography in suspicious cases, and skin infections (with vancomycin 20mg/kg IV × 1) in very high
must exercise judgment in when to admit patients for empiric risk patients: those with a prior history of IE; prosthetic valve;
therapy. heart transplant with abnormal valve function; repaired con-
genital heart disease.
Treatment and Prophylaxis
Empiric therapy targeting common IE bacterial pathogens Complications and Admission Criteria
is indicated when the diagnosis is strongly suspected. The The treatment of septic and mechanical complications of
empiric regimen should be tailored to whether or not there is endocarditis can be challenging. In cases of suspected acute
a prosthetic valve, and, when possible, to the current hospital valvular dysfunction with pump failure, emergent echocardi-
antibiogram (see Table 1.2). The duration of therapy is typi- ography and consultation with a cardiothoracic surgeon and
cally 4 to 6 weeks. It may be appropriate to withhold antibiotics cardiologist are indicated. Anticoagulation with heparin is not
pending culture results in patients with chronic, intermittent recommended for septic emboli because it does not reduce fur-
fevers who otherwise appear well, provided that close follow- ther embolization and the risk of hemorrhagic transformation
up is available. is very high. Limb-threatening emboli (e.g. a cold, pulseless
Antibiotic prophylaxis was previously recommended to all extremity) may require revascularization with interventional
patients at risk from IE prior to certain invasive dental, gastro- or surgical techniques, such as the administration of local
intestinal, and genitourinary procedures; however, this prac- fibrinolytics.
tice has now become controversial, with conflicting guidelines Patients for whom the diagnosis of IE is suspected should
in the United States and Europe. While most procedures rou- generally be admitted for further work-up and empiric intra-
tinely performed in the emergency department do not require venous antibiotics. In selected cases, it may be appropriate to
prophylaxis, prophylaxis should be strongly considered for discharge febrile but otherwise well-appearing patients home
dental or skin abscess incision and drainage (see Table 1.3) or with blood cultures pending, provided that reliable, urgent

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Chapter 1: Infective Endocarditis

Table 1.3 Antibiotic Prophylaxis for Invasive Procedures in Highest Risk Habib, G., Hoen, B., Tornos, P., et al., Guidelines on the preven-
Patients tion, diagnosis, and treatment of infective endocarditis (new
version 2009): the Task Force on the Prevention, Diagnosis, and
Patient Category Recommended Antibiotic for Treatment of Infective Endocarditis of the European Society of
ED Dental Procedures Cardiology (ESC). Eur. Heart J. 2009; 30(19): 2369–2413.
Adults Amoxicillin 2 g PO × 1 Li, J. S., Sexton, D. J., Mick, N., et al., Proposed modifications to the
if PCN allergy Duke Criteria for the diagnosis of infective endocarditis. Clin.
Clindamycin 600 mg PO × 1 Infect. Dis. 2000; 30(4): 633–8.
Unable to take oral medications:
Mitchell, R. S., Kumar, V., Robbins, S. L., Abbas, A. K., and Fausto, N.
Ceftriaxone 1 g IV/IM × 1
Robbins Basic Pathology, 8th edn. (Philadelphia, PA: Saunders/
if PCN allergy
Elsevier, 2007), pp. 406–8.
Clindamycin 600 mg IV/IM × 1
Olaison L. and Pettersson G., Current best practices and guidelines
Children Amoxicillin 50 mg/kg PO × 1 (max. 2 g/dose)
indications for surgical intervention in infective endocarditis.
if PCN allergy
Infect. Dis. Clin. North Am. 2002; 16(2): 453–75.
Clindamycin 20 mg/kg PO × 1 (max. 600 mg/
dose) Pawsat, D. E. and Lee, J. Y., Inflammatory disorders for the heart.
Unable to take oral medications: Pericarditis, myocarditis, and endocarditis. Emerg. Med. Clin.
Ceftriaxone 50 mg/kg IV/IM × 1 (max. 1 g/dose) North Am. 1998; 16(3): 665–81.
if PCN allergy Samet, J. H., Shevitz, A., and Fowle J., Hospitalization decision in
Clindamycin 20 mg/kg IV/IM × 1 (max. 600 mg/ febrile intravenous drug users. Am. J. Med. 1990; 89(1): 53–7.
dose) Sandre, R. M. and Shafran, S. D., Infective endocarditis: review of 135
Pregnant women As above cases over 9 years. Clin. Infect. Dis. 1996; 22(2): 276–86.
Immunocompromised As above Sexton, D. J. and Spelman, D., Current best practices and guidelines.
Assessment and management of complications in infective endo-
IM – intramuscular; IV – intravenous; PCN – penicillin; PO – by mouth.
carditis. Infect. Dis. Clin. North Am. 2002; 16(2): 507–21.
Thornhill, M. H., Dayer, M. J., Forde, J. M., et al., Impact of the NICE
follow-up is available. Patients with septic or mechanical guideline recommending cessation of antibiotic prophylaxis for
complications of IE should be managed in a closely monitored prevention of infective endocarditis: before and after study. BMJ
setting, preferably one in which cardiothoracic surgical inter- 2011; 342: d2392.
vention is readily available. Towns, M. L. and Reller, L. B., Diagnostic methods current best
practices and guidelines for isolation of bacteria and fungi in infec-
Pearls and Pitfalls tive endocarditis. Infect. Dis. Clin. North Am. 2002; 16(2): 363–76.
1. Endocarditis is important to consider in any febrile patient Wilson, L. E., Thomas, D. L., Astemborski, J., et al., Prospective study
with a predisposing valve disease or other risk factors. of infective endocarditis among injection drug users. J. Infect.
Dis. 2002; 185(12): 1761–6.
2. Emergency providers can play an essential role in IE diag-
nosis by obtaining blood cultures prior to empiric antibiotics. Wilson, W., Taubert, K. A., Gewitz, M., et al., Prevention of infective
endocarditis: guidelines from the American Heart Association: a
3. Mechanical complications of IE may require emergent car- guideline from the American Heart Association Rheumatic Fever,
diovascular surgery. Endocarditis, and Kawasaki Disease Committee, Council on
4. Do not heparinize patients with septic emboli and Cardiovascular Disease in the Young, and the Council on Clinical
endocarditis. Cardiology, Council on Cardiovascular Surgery and Anesthesia,
and the Quality of Care and Outcomes Research Interdisciplinary
Working Group. Circulation 2007; 116(15): 1736–54.
References Young, G. P., Hedges, J. R., Dixon, L., et al., Inability to validate a pre-
Alexiou, C., Langley, S. M., Stafford, H., et al., Surgery for active dictive score for infective endocarditis in intravenous drug users.
culture-positive endocarditis: determinants of early and late out- J. Emerg. Med. 1993; 11(1): 1–7.
come. Ann. Thorac. Surg. 2000; 69(5): 1448–54.
Cabell, C. H., Jollis, J. G., Peterson, G. E., et al., Changing patient Additional Readings
characteristics and the effect on mortality in endocarditis. Arch.
Intern. Med. 2002; 162(1): 90–4. Baddour, L. M., Wilson, W. R., Bayer, A. S., et al., Infective endocarditi
in adults: diagnosis, antimicrobial therapy, and management of
Calder, K. K. and Severyn, F.A., Surgical emergencies in the intravenous
complications. A scientific statement for healthcare professionals
drug user. Emerg. Med. Clin. North. Am. 2003; 21(4): 1089–116.
from the American Heart Association. Circulation 2015; 132(15):
Cresti, A., Chiavarelli, M., Scalese, M., et al., Epidemiology and mor- 1435–86.
tality trends in infective endocarditis, a 17-year population-based
Hoen, B. and Duval, X., Infective endocarditis. N. Engl. J. Med. 2013;
prospective study. Cardiovasc. Diagn. Ther. 2017; 7(1): 27–35.
368(15): 1425–33.

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Chapter
Pericarditis and Myocarditis

2 Jessica L. Osterman and Jorge Fernandez

Outline Myocarditis 11
Epidemiology and Microbiology 11
Introduction 6
Clinical Features 11
Pericarditis 6
Differential Diagnosis 11
Epidemiology and Microbiology 6 Laboratory and Radiographic Findings 12
Clinical Features 7 Treatment and Prophylaxis 12
Differential Diagnosis 7 Complications and Admission Criteria 12
Laboratory and Radiographic Findings 8 Pearls and Pitfalls 13
Treatment and Prophylaxis 9
References 13
Complications and Admission Criteria 10
Additional Readings 13

Introduction endocarditis, can also occur. There are also numerous non-
infectious causes of both pericarditis and myocarditis.
Cardiac infections are classified by the affected site: pericar-
dium, myocardium, or endocardium. Since pericarditis and
myocarditis often coexist, and the infectious etiologies are very
Epidemiology and Microbiology
similar, these will be discussed together here. Endocarditis is While the epidemiology of pericarditis is not well described, it
a fundamentally different type of infection that is covered in is clearly a common condition, estimated to account for 5% of
Chapter 1. Pericarditis is a common cause of chest pain that has non-ischemic chest pain cases seen in emergency departments
the potential to result in significant morbidity and mortality. (EDs). Pericarditis commonly affects young men, for reasons
Acute care providers should be well versed in the identifica- that are not well understood.
tion, risk stratification, and evidence-based management of this Acute pericarditis is often idiopathic, in that routine eval-
common condition. uation reveals no definite cause; the majority of such cases are
presumed to be viral. When a pathogen is identified, viruses
predominate, including coxsackieviruses, echoviruses, influ-
Pericarditis enza, EBV, VZV, mumps, and hepatitis. Human immunodefi-
The pericardium is composed of two layers of fibrous tissue, ciency virus (HIV) can cause pericarditis and myocarditis and
the visceral and parietal, which envelop and protect the remains a common cause of pericardial disease in developing
heart. The visceral layer is firmly attached to the epicardium, countries where HIV is prevalent.
whereas the parietal layer moves freely within the medias- Bacterial pericarditis, termed purulent pericarditis, is for-
tinum. Approximately 15 to 50 mL of fluid is normally present tunately rare. It can result from hematogenous seeding or
within the pericardial sac. direct spread, usually from pneumonia. Myriad bacteria have
Pericarditis is defined as inflammation of the pericar- been reported to cause pericarditis, with the most common
dium. It frequently causes a small pathologic pericardial pathogens being Staphyloccus aureus and Streptococcus
effusion and may be associated with adjacent myocardial pneumoniae. Pneumococcal pneumonia and empyema and
inflammation or infection, termed myopericarditis. Large S. aureus endocarditis (via endomyocardial abscess) are the
pericardial fluid accumulations may occur in pericarditis, infections that classically spread directly to the pericardium.
which can result in cardiac tamponade, if they develop Mediastinitis, penetrating trauma, and thoracic surgery can
rapidly. also lead to purulent pericarditis. S. aureus is the predominant
The majority of infectious pericarditis and myocarditis are pathogen in hematogenous cases.
due to direct viral infection or less commonly bacterial seeding Mycobacterium tuberculosis is considered to be the most
of the pericardium. Contiguous spread to the pericardium uncommon etiology of infectious endocarditis in devel-
from pleural, pulmonary, or mediastinal infections, or from oping countries. Fungi are a relatively uncommon cause of

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Chapter 2: Pericarditis and Myocarditis

Table 2.1 Important Causes of Pericarditis and Myocarditis

Idiopathic Fungal infections Malignancy
Viral infections Histoplasma capsulatum Medications
Coxsackievirus A and B Aspergillus species Penicillin
Echoviruses Mycobacterial infections Sulfa drugs
Adenoviruses M. tuberculosis Procainamide
HIV Parasitic infections Hydralazine
Bacterial infections Chagas disease Isoniazid
Gram-positive species Trichinosis Phenytoin
Gram-negative species Toxoplasmosis Chemotherapeutic agents
Anaerobes Autoimmune-mediated Metabolic disorders
Mycoplasma Acute rheumatic fever Hypothyroidism
Rickettsial infections Dressler’s syndrome Uremia (dialysis-related)
RMSF Systemic lupus erythematosus Radiation exposure
Q fever Rheumatoid arthritis toxins/environmental
Scrub typhus Vasculitis (e.g. Kawasaki) Cocaine
Spirochetes Sarcoidosis Amphetamines
Lyme disease Postvaccination Carbon monoxide
Syphilis Postpericardiotomy syndrome Lead
Stings/bites
Trauma or surgery

Adapted from A. M. Ross and S. E. Grauer, Acute pericarditis. Evaluation and treatment of infectious and other
causes. Postgrad Med. 2004 March; 115(3): 67–75.
RMSF – Rocky Mountain spotted fever.

pericarditis. Histoplasomosi pericarditis is seen in endemic limited hemodynamics signs. Those with rapidly accumulating
regions of the United States and Candida species are a common effusions may present with tamponade and shock. This clas-
etiology in nosocomial cases. sically occurs from malignancy, in patients on anticoagulants
The list of non-infectious causes of acute pericarditis is and in purulent pericarditis. Associated myocarditis can lead
very long (see Table 2.1). These include uremia, trauma, malig- to rapid heart failure, cardiogenic shock, and arrythmias.
nancy (lymphoma, cancers of the breast, lung, and kidney), Patients with purulent pericarditis usually appear toxic with
radiation, chemotherapy, drug reactions (penicillin, minox- an acute febrile illness and may have evidence of pneumonia,
idil), post-cardiotomy or thoracic surgery, and autoimmune empyema, endocarditis, or mediastinal infection. Tuberculous
disorders (systemic lupus erythematosus [SLE], rheumatoid pericarditis generally presents as an indolent illness with non-
arthritis [RA], Dressler’s syndrome after myocardial infarction specific symptoms such as fever, night sweats, weight loss, and
postpericardiotomy syndrome). fatigue.
The classic physical finding in acute pericarditis is a peri-
Clinical Features cardial friction rub, which is typically a three-phase “scratchy”
The clinical presentation of infectious pericarditis varies heart sound that comes and goes, best heard while the patient
depending on the pathogen and the the host immune response leans forward. Signs of pericardial tamponade are discussed
(see Table 2.2). Most patients with acute viral (or ideopathic) under “Complications and Admission Criteria.”
pericarditis have mild symptoms, which include low-grade
fever, malaise, and substernal chest pain. There may be a his- Differential Diagnosis
tory of a preceeding viral respiratory or gastrointestinal illness. The differential diagnosis of a patient complaining of chest
The pain is typically described as sharp or stabbing, but may pain or dyspnea in an emergent or urgent setting includes the
be squeezing. It usually has a pleuritic quality – worsened by following:
inspiration and cough. The pain is commonly postural: lying
• aortic dissection
supine exacerbates the pain, whereas sitting upright or leaning
• pulmonary embolism
slightly forward relieves it. The phrenic nerve traverses the
pericardium, so the pain of pericarditis is often described as • pneumothorax and tension pneumothorax
radiating to the trapezial ridges. Patients with pericarditis may • acute coronary syndrome
also complain of cough, odynophagia, or dysphagia, presum- • esophageal perforation
ably secondary to the spread of the inflammatory process to • myopericarditis
adjacent structures. • mediastinitis
Patients with slowly accumulating effusions, such as in • pneumonia
uremic or autoimmune pericarditis, may have no chest pain and • pleurisy

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Chapter 2: Pericarditis and Myocarditis

Table 2.2 Clinical Features: Pericarditis and Myocarditis

Pericarditis Myocarditis
Signs and symptoms: • Fever, malaise, night sweats • Fever, malaise, night sweats
adults • Chest pain (typically sharp, pleuritic) • Chest pain uncommon unless associated pericarditis
• Pericardial friction rub • Dyspnea, orthopnea
• Tamponade: tachycardia, Beck’s triad, pulsus • Left and right-sided heart failure signs: lung crackles,
paradoxus hypoxemia, hypotension, JVD, HSM, peripheral edema
• Dysrhythmia or conduction disturbance
Signs and symptoms: • As above • As above
infants • Non-specific – lethargy, poor feeding, cyanosis • Non-specific – lethargy, poor feeding, cyanosis
Laboratory and ECG findings • Elevated WBC, CRP, ESR • Elevated WBC, CRP, ESR, and cardiac biomarkers
• ECG findings include: • ECG findings non-specific:
• Sinus tachycardia and non-specific ST-T changes • Sinus tachycardia and non-specific ST-T changes
• Diffuse ST-segment elevation • ST-segment elevation or depression
• PR depression • Decreased QRS amplitude and Q waves
• T wave inversion without Q wave formation • Atrial or ventricular ectopy
• Ultrasound – pericardial effusion, possible signs of • Bundle branch blocks
tamponade • Ultrasound – decreased left ventricular function

CRP – C-reactive protein; DOE – dyspnea on exertion; ECG – electrocardiography; ESR – erythrocyte sedimentation rate; JVD – jugular venous distention;
HSM – hepatosplenomegaly; TB – tuberculosis; WBC – white blood (cell) count.

• gastroesophageal reflux disease A single set of biomarkers is recommended; elevated cardiac

• costochondritis biomarkers suggest associated myocarditis (myopericarditis).
• panic attack Blood culture should be drawn in patients with a high fever or
• herpes zoster signs of toxicity. Skin testing and sputum testing for acid-fast
• cholecystitis bacilli should be considered in the appropriate setting.
Chest X-ray is useful in excluding pneumonia and pneu-
The diagnosis of pericarditis and/or myocarditis should
mothorax, and it may reveal a pleural effusion, lung mass, or
be considered when chest pain, dyspnea, dysrhythmias, heart
infiltrate suggestive of active tuberculosis, which can focus the
failure, or cardiac tamponade accompanies a recent viral-
differential diagnosis. A large pericardial effusion or severe
seeming upper respiratory or gastrointestinal illness, or in
myocarditis with heart failure will cause cardiomegaly (see
the setting of an underlying autoimmune disorder, malig-
Figure 2.1).
nancy, renal failure, recent cardiac surgery, or exposure to
Electrocardiography is a cornerstone of pericarditis diag-
tuberculosis.
nosis. Typical findings are shown in Figure 2.2. Acute peri-
Acute pericarditis can be mistaken for ST-segment elevation
carditis causes a characteristic progression of ECG findings
myocardial infarction resulting in inappropriate treatment with
through four distinct phases. Stage one lasts for days and is
fibrinolytic agents and/or anticoagulants. Electrocardiographic
characterized by diffuse ST elevation in all leads except avR and
findings should distinguish these disorders: ST elevations of
V1 and PR segment depression. Stage two is normalization of
pericarditis generally occur diffusely, whereas acute coronary
the ST and PR segments. Stage 3 is characterized by diffuse T
syndrome (ACS) involves a specific coronary artery territory.
wave inversion without Q wave formation, and stage 4 is ECG
Likewise, pericarditis can be difficult to distinguish from other
normalization. In the case of a large effusion, these signs are
pain syndromes associated with underlying immunologic dis-
usually not seen; rather, there may be tachycardia, loss of QRS
ease, or from pulmonary embolism in a patient with under-
voltage, and electrical alternans.
lying cancer.
Echocardiography is recommended for risk stratification
in suspected pericarditis (See Figure 2.4). In typical acute
Laboratory and Radiographic Findings idiopathic pericarditis, a small effusion may or may not be
In the acute care setting, routine studies in patients presenting seen. An effusion greater than 20 mm is considered high risk,
with chest pain or dyspnea include pulse oximetry, chest X-ray, generally necessitating admission. Echocardiographic evi-
and electrocardiography. Echocardiography is recommended dence of tamponade (discussed below under “Complications
in all cases of suspected pericardial disease. and Admission Criteria”) or decreased ventricular function,
While blood tests may not always be necessary in an oth- suggesting associated myocarditis, also necessitate admission.
erwise healthy patient presenting with typical findings of acute Diagnostic pericardiocentesis should be considered in
pericarditis and normal vital signs, most patients require fur- patients with a significant effusion and fever, to rule out puru-
ther risk stratification. Laboratory findings in pericarditis lent pericarditis, in those with tamponade or impending
may include leukocytosis, elevated CRP, and increased ESR. tamponade, and to work up suspected malignant pericardial
Negative inflammatory markers argue against pericarditis. effusion.

8
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Chapter 2: Pericarditis and Myocarditis

Figure 2.1 Chest X-ray findings in pericarditis and myocarditis. (A) Cardiomegaly from pericardial effusion. (B) Acute pulmonary edema in myocarditis.
Reprinted with permission from W. J. Brady, J. D. Ferguson, E. A. Ullman, and A. D. Perron, Myocarditis: emergency department recognition and management.
Emerg. Med. Clin. North Am. 2004; 22(4): 865–85.

I aVR V1 V4

II aVL V2 V5

III aVF V3 V6

V1

II

V5
Figure 2.2 Electrocardiography in acute pericarditis. Stage 1, showing diffuse ST segment elevation.
Reprinted with permission from A. M. Ross and S. E. Grauer, Acute pericarditis. Evaluation and treatment of infectious and
other causes. Porstgrad. Med. 2004; 115(3): 67–75.

Treatment and Prophylaxis now recommended for acute uncomplicated pericarditis.

No definitive treatment benefit of corticosteroids has been
Symptomatic treatment of pericarditis should be under- documented, except when there is an underlying collagen
taken after ruling out other life-threatening causes of chest vascular disease such as SLE or RA. Additionally, the use of
pain and life-threatening complications of pericarditis steroids in acute pericarditis appears to increase the risk of
(see Table 2.3). Treatment of pain and inflammation with recurrent or chronic pericarditis. Exercise restriction until
aspirin or non-steroidal agents like ibuprofen is the main- symptom resolution and normalization of inflammatory
stay of pericarditis treatment. Based on trial data showing markers is recommended in young patients with idiopathic
a reduction in recurrence, routine addition of colchicine is or viral pericarditis.

9
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Chapter 2: Pericarditis and Myocarditis

Complications and Admission Criteria purulent or tuberculous pericarditis are at risk from progres-
sion of the infection itself. Signs of myocarditis should always
Important complications of pericarditis include myocarditis, be sought.
tamponade, and recurrence (see Table 2.4). Patients with Evaluation of a patient with suspected pericarditis should
routinely include assessment for signs of hemodynamic com-
Table 2.3 Initial Treatment for Pericarditis promise and pericardial tamponade. These signs include pulsus
paradoxus, tachycardia, and Beck’s triad of hypotension, JVD,
Patient Category Therapy Recommendation and muffled heart sounds. Electrical alternans, characterized by
Adults Non-steroidal anti-inflammatories alternating voltage of the P wave, QRS segment, and T wave, is
(avoid if isolated myocarditis): pathognomonic of a large, hemodynamically significant peri-
Aspirin 650–1000 mg PO TID
cardial effusion. Echocardiography is the gold standard test
or
for diagnosis. Diagnostic findings include pericardial effusion,
Ibuprofen 600–800 mg PO TID
or
inferior vena cava dilation, diastolic collapse of the right atrial
Indomethacin 50 mg PO TID or ventricular, and leftward bowing of the septum with inspi-
plus ration (see Figure 2.3). Cardiac tamponade requires aggressive
Colchicine 0.6 mg PO BID fluid resuscitation followed by emergent pericardiocentesis if a
Children Non-steroidal anti-inflammatories patient does not immediately improve with IV fluids.
(avoid if isolated myocarditis): Recurrence occurs in up to 38% of patients with idiopathic
Ibuprofen 5–10 mg/kg PO QID pericarditis who are not treated with colchicine and 17% of
or those who are. Recurrecnt of pericarditis is thought to be auto-
Naproxen 5–10 mg/kg PO BID immune and can prove difficult to manage.
plus In the setting of a normal echocardiogram, patients
Colchicine 0.3–0.6 mg PO daily
with acute pericarditis who are well appearing may be safely
Pregnant women Acetaminophen 500 mg PO every 6 hours discharged. Small or moderate effusions can be followed
Immunocompromised As above, depending on age and pregnancy with serial echocardiograms; large effusions may require
status pericardiocentesis or placement of a pericardial window.
PO – by mouth.

A B

Figure 2.3 Echocardiographic evidence of cardiac tamponade. Echocardiographic images of large pericardial effusion with features of tamponade. (A) Apical
four-chamber view of LV, LA, and RV that shows large PE with diastolic right-atrial collapse (arrow). (B) M-mode image with cursor placed through RV, IVS, and LV in
parasternal long axis. The view shows circumferential PE with diastolic collapse of RV free wall (arrow) during expiration. (C) M-mode image from subcostal window
in same patient that shows IVC plethora without inspiratory collapse. Reprinted with permission from Elsevier (The Lancet, 2004, vol. 363, pp. 717–27).
Photo and text from R. W. Troughton, C. R. Asher, and A. L. Klein, Pericarditis. Lancet 2004; 363(9410): 717–27.
IVC – inferior vena cava; IVS – interventricular septum; LA – left atrium; LV – left ventricle; PE – pericardial effusion; RV – right ventricle.

10
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Chapter 2: Pericarditis and Myocarditis

Guidelines recommend hospitalization for pericarditis patients (Lyme disease) have all been associated with myocar-
with any of the following high risk features: ditis. Lyme myocarditis should be suspected in patients
• temperature >38 °C from endemic areas presenting with atrioventricular block.
• subacute onset Similarly, in patients from rural South and Central America
• pericardial effusion >20 mm presenting with heart block or regional wall motion abnormal-
ities or ventricular aneurisms, Chagas cardiomyopathy, caused
• cardiac tamponade
by the parasite Trypanosoma cruzi, should be suspected.
• lack of response to anti-inflammatory treatment after 1 week
Immunocompromised patients may develop myocarditis sec-
• evidence of myopericarditis ondary to toxoplasmosis.
• immunosuppression There are a variety of non-infectious causes of myocarditis,
• trauma including autoimmune disorders, medications, and environ-
• oral anticoagulant therapy mental toxins. Autoimmune causes include systemic lupus ery-
thematosus (SLE), rheumatoid arthritis (RA), sarcoidosis, and
Myocarditis various vasculitides (Kawasaki disease and giant cell arteritis).
Myocarditis, inflammation of the myocardium, can occur on A variety of drugs and chemotherapeutics can directly induce
its own or be associated with concurrent pericarditis. Though myocardial inflammation, including cocaine, amphetamines,
most cases are infectious, there are many non-infectious forms lithium, phenothiazines, zidovudine (AZT), chloroquine,
of myocarditis too. Generally speaking, idiopathic, viral, and and doxorubicin. Hypersensitivity reactions to penicillin and
lymphocytic myocarditis are synonymous. Manifestations sulfonamides may trigger inflammatory changes in the myo-
range from mild dyspnea and chest pain in the setting cardium, resulting in myocarditis. Environmental toxins such
of a viral illness to sudden, progressive heart failure and as carbon monoxide, lead, and arsenic, as well as stings from
cardiogenic shock. spiders, scorpions, and wasps, can also result in myocardial
inflammation.

Epidemiology and Microbiology Clinical Features

The epidemiology of myocarditis is difficult to gauge, since
Like pericarditis, the virulence of the pathogen and the host
the majority of cases are mild, self limited, and often associ-
immune response dictate the clinical course in myocarditis,
ated with generalized viral syndrome. Studies of coxsackievirus
resulting in a wide spectrum of severity. Typically, myocarditis
outbreaks suggest myocarditis may occur in up to 5% of
presents with symptoms such as fatigue, dyspnea on exertion,
patients. Evidence of myocarditis is found in 5–10% of young
palpitations, syncope, and occasionally chest pain. There will
athletes with sudden death and approximately 10% of cases of
often be a history of a viral syndrome that may include fever,
unexplained dilated cardiomyopathy in children and adults.
upper respiratory symptoms, gastrointestinal symptoms, or
Myocarditis is obviously a much more common cause of car-
myalgias. Chest pain, particulary if pleuritic, suggests concur-
diomyopathy in children than adults.
rent pericarditis, but coronary-artery spasm can also occur.
Etiologies of mycarditis mirror those of endocarditis or
Dyspnea on exertion is common; dyspnea at rest and orthopnea
pericarditis (see Table 2.1). Infectious causes include viruses,
suggest severe disease. Palpitations, light-headedness, or syn-
bacteria, fungi, rickettsia, spirochetes, and parasites. In all
cope suggest associated dysrhythmia. Neonates and infants
types of infection, myocardial damage may result from direct
frequently present with non-specific symptoms, such as fever,
effects of the invasive pathogen, or from immune-mediated
respiratory distress, cyanosis, or poor feeding.
lysis of infected cells. In developed nations, viruses represent
Physical exam findings in myocarditis may include signs
the most common infectious cause. In North America, the most
of left-sided heart failure such as tachypnea, hypoxemia, and
common viral pathogens are coxsackievirus, adenovirus, and
pulmonary rales. Right-sided heart failure presents with JVD,
parvovirus B 19. Other viral etiolgies include influenza virus,
hepatosplenomegaly, and peripheral edema. Some patients,
echovirus, herpes simplex virus (HSV), varicella-zoster virus
including children, present with fulminant cardiomyopathy
(VZV), Epstein-Barr virus (EBV), cytomegalovirus (CMV), and
characterized by pulmonary edema and/or cardiogenic shock.
the hepatitis viruses. Human immunodeficiency virus (HIV)
Tachyarhythmias, bradyarhythmias, and heart block can occur.
infection may also cause myocarditis, either directly from HIV-
Myocarditis can be the cause of sudden cardiac death.
induced cytotoxicity during any phase of the infection, or indi-
rectly as a result of other opportunistic infections. Most cases of
viral myocarditis are preceded by an upper respiratory infection Differential Diagnosis
or gastrointestinal illness by 1 to 2 weeks. In the case of myopericarditis with chest pain, the differential
Bacterial myocarditis is unusual and most often caused diagnosis includes the diseases listed in the pericarditis section.
by direct extension from infected endocardial or pericardial In the case of new onset heart failure in an adult, the main
tissue. Certain exotoxin-mediated bacterial illnesses, such as considerations are ischemic cardiomyopathy and hypertensive
diphtheria, may also cause myocarditis. cardiomyopathy. Lack of risk factors or pre-existing hyperten-
Tick-borne illnesses caused by rickettsia (Rocky Mountain sion, and a preceeding viral illness, favor myocarditis. A his-
spotted fever, Q fever, and scrub typhus) and spirochetes tory of immunologic disease, prior chemotherapy or radiation

11
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Chapter 2: Pericarditis and Myocarditis

A magnetic resonance imaging (MRI) has emerged as an alterna-

tive to endomyocardial biopsy. MRI is increasingly being used
to detect occult myocarditis in younger patients who present
with idiopathic dysrhythmias and have normal electrophysi-
B ology testing.

Treatment and Prophylaxis

The treatment of myocarditis is primarily supportive, with
cardiac monitoring, cardiovascular support, and diuresis as
C indicated. Congestive heart failure with acute pulmonary
edema may require aggressive treatment with vasodilators
such as nitrates and angiotensin-converting enzyme
inhibitors. Beta-blockers should be avoided, as they are not
D only contraindicated in acute congestive heart failure, but
have also been shown to worsen cardiac inflammation in
animal models. While non-steroidal agents are a mainstay
of treatment for cases of pericarditis, some studies suggest
Figure 2.4 Rhythm disturbances in acute myocarditis. (A) Sinus tachycardia.
(B) Atrial fibrillation with bundle-branch block morphology. (C) Third-degree that these drugs are potentially harmful in cases of iso-
(complete) atrioventricular block with wide QRS complex escape. (D) Wide lated myocarditis. As with pericarditis, no definitive benefit
QRS complex tachycardia. of corticosteroids or intravenous gamma globulin has been
Reprinted with permission from W. J. Brady, J. D. Ferguson, E. A. Ullman, documented in myocarditis, except when caused by a spe-
and A. D. Perron, Myocarditis: emergency department recognition and
management. Emerg. Med. Clin. North Am. 2004; 22(4): 865–85. cific collagen vascular disease such as SLE or Kawasaki’s dis-
ease. Other specific immunomodulator and antiviral drugs
have yet to be proven beneficial. Antitrypanosomal therapy
therapy, or heavy alcohol, cocaine, or amphetamine use should is not recommended in established Chagas cardiomyopathy.
be sought. A careful medication history is crucial, looking for Patients with suspected or diagnosed myocarditis should
potentially cardiotoxic agents. limit activity for 6 months.

Laboratory and Radiographic Findings Complications and Admission Criteria

Myocarditis will present with the diagnostic test findings of All cases of suspected myocarditis should be admitted, pref-
heart failure. The chest X-ray will demonstrate cardiomegaly erably to a telemetry or intensive care unit setting for cardiac
and signs of pulmonary congestions (see Figure 2.1). Brain monitoring.
natiuretic peptide (BNP) may be elevated. Cardiac biomarkers In the emergent setting, the main complications of myocar-
are often elevated reflecting myocardial necrosis. While these ditis are dysrhythmias, pulmonary edema, respiratory failure,
findings confirm the diagnosis of heart failure, they are obvi- cardiogenic shock, and tamponade due to concommitant
ously not specific for infectious myocarditis. pericarditis (see Table 2.4). For the emergency management
ECG findings are likewise non-specific. Sinus tachycardia, of bradycardia or tachydysrhythmias, standard advanced car-
ectopic beats, and non-specific ST-T changes are the rule (see diovascular life support (ACLS) protocols should be followed.
Figure 2.4). Lyme carditis classically presents with heart block. Because conduction disturbances are generally transient,
ST segment elevation, when present, can be diffuse if there is insertion of a transvenous pacemaker is usually not necessary
associated pericarditis, or regional. in cases of myocarditis-induced bradycardia.
Echocardiography is a crucial diagnostic test in cases of Hemodynamic support with vasopressors and/or
suspected myocarditis, since it is the gold standard for ventric- inotropes may be needed. Intubation is frequently needed
ular dysfunction. Wall motion abormalities are typically global, in patients with fulminant myocarditis. Emergent placement
but can be regional. Echocardiography may demonstrate con- of an intra-aortic balloon pump or left-ventricular assist
comitant pericardial involvement. device in adults may serve as a bridge to transplantation.
Myocarditis, as the cause of ventricular dysfunction, par- Extracorporial membrane oxygenation is used frequently in
ticularly in adults, is a diagnosis of exclusion. In adults, normal children as a bridge to recovery or transplantation. Cardiac
coronary angiography is generally required prior to diagnosis transplantation may be life saving in cases of fulminant myo-
of myocarditis. While endomyocardial biopsy is considered carditis; however, these patients are at high risk of recurrent
the gold standard test to establish the diagnosis of myocar- myocarditis or rejection.
ditis, and to help determine the underlying etiology, many Most cases of viral myocarditis, particularly those with clin-
patients with presumed myocarditis never undergo this inva- ical myopericarditis, have a benign course and resolve spontane-
sive test. A diagnostic biopsy will show mononuclear inflam- ously without sequelae. Cases with severe and biopsy-proven
matory infiltrate and necrosis of the myocardium. The added cardiomyopathy, however, have an approximately 20% 1 year
diagnostic value of viral genome PCR is uncertain. Cardiac mortality. Unfortunately, a subset of both children and adults

12
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Chapter 2: Pericarditis and Myocarditis

Table 2.4 Complications of Pericarditis and Myocarditis and European Association for Cardio-Thoracic Surgery (EACTS).
Recommended Treatment Eur. Heart J. 2015; 36: 2921–64.
Complication Recommended Therapy Barbaro, G., Fisher, S. D., Gaincaspro, G., and Lipshultz, S. E. HIV-
associated cardiovascular complications: a new challenge for
Congestive heart failure Nitroglycerin 5–300 mcg/min IV drip titrated
emergency physicians. Am. J. Emerg. Med. 2001; 19(7): 566–74.
to effect, and
Captopril 25 mg SL/PO × 1, and Caforio, A. L. P., Pankuweit, S., Arbustini, E., et al. Curent state of
Furosemide 0.5–1 mg/kg IV × 1, and knowledge on aetiology, diagnosis, management, and therapy
BiPAP of myocarditis: a position statement of the European Society
Note: Beta-blockers are contraindicated.
of Cardiology Working Group on Myocardial and Pericardial
Diseases. Eur. Heart J. 2013; 34: 2636–48.
Cardiac tamponade Aggressive fluid resuscitation
Pericardiocentesis
Carapetis, J. R., McDonald, M., and Wilson, N. J. Acute rheumatic
fever. Lancet 2005; 366(9480): 155–68.
Heart block and As per ACLS or APLS protocols
tachydysrhythmias Cilliers, A. M., Manyemba, J., and Saloojee, H. Anti-inflammatory
treatment for carditis in acute rheumatic fever. Cochrane
Cardiogenic dhock Dobutamine 1–20 mcg/kg/min IV drip
Database Syst. Rev. 2003; (2): CD003176.
titrated to effect (may need additional pressor
support) Imazio, M., Spodick, D. H., Brucato, A., and Trinchero, R.
Intra-aortic balloon pump Controversial issues in the management of pericardial diseases.
Extracorporeal membrane oxygenation Circulation 2010; 121(7): 916–28.
Cardiac transplantation Imazio, M. and Trinchero, R. Myopericarditis: etiology, management
and prognosis. Int. J. Cardiol. 2008; 127(1): 17–26.
APLS – advanced pulmonary life support; BiPAP – bilevel positive airway
pressure; IV – intravenous; PO – by mouth. Klein, A. L., Abbara, S., Agler, D. A., et al. American Society of
Echocardiography clinical recommendations for multimodality
cardiovascular imaging of patients with pericardial disease. J.
with infectious cardiomyopathy will go on to develop chronic Am. Soc. Echocardiogr. 2013; 26(9): 965–1012.
dilated cardiomyopathy and/require transplantation. Meune, C., Spaulding, C., Lebon, P., and Bergman, J. F. Risks
versus benefits of NSAIDs including aspirin in myocarditis: a
Pearls and Pitfalls review of the evidence from animal studies. Drug Saf. 2003;
26(13): 975–81.
1. Most cases of myocarditis and pericarditis are viral and Pawsat, D. E. and Lee, J. Y. Inflammatory disorders for the heart.
have a benign course; consider alternative causes in toxic Pericarditis, myocarditis, and endocarditis. Emerg. Med. Clin.
appearing patients. North Am. 1998; 16(3): 665–81.
2. Serious complications of myocarditis include con- Ross, A. M. and Grauer, S. E. Acute pericarditis. Evaluation and
gestive heart failure, conduction disturbances, and treatment of infectious and other causes. Postgrad. Med. 2004;
tachydysrhythmias. 115(3): 67–75.
3. Echocardiography is recommended for all patients with newly Stollerman, G. H. Rheumatic fever in the 21st century. Clin. Infect.
diagnosed pericarditis or myocarditis prior to discharge. Dis. 2001; 33(6): 806–14.
4. Hospital admission is indicated for all cases of myocarditis, Trautner, B. W. and Darouiche, R. O. Tuberculous pericar-
as well as pericarditis when associated with fever, trauma, ditis: optimal diagnosis and management. Clin. Infect. Dis. 2001;
oral anticoagulants, immunosuppression, or pericardial 33(7): 954–61.
effusion >20 mm.
Additional Readings
References Brady, W. J., Ferguson, J. D., Ullman, E. A., and Perron, A. D.
Myocarditis: emergency department recognition and manage-
Acker, M. A. Mechanical circulatory support for patients with ment. Emerg. Med. Clin. North Am. 2004; 22(4): 865–85.
acute-fulminant myocarditis. Ann. Thorac. Surg. 2001; 71(3
Suppl.): S73–6. Chan, T. C., Brady, W. J., and Pollack, M. Electrocardiographic
manifestations: acute myopericarditis. J. Emerg. Med. 1999;
Adler, Y., Charron, P. Imazio, M., et al., 2015 ESC Guidelines for the
17(5); 865–72.
diagnosis and management of pericardial diseases: The Task
Force for the Diagnosis and Management of Pericardial Diseases Cooper, L. T. Myocarditis. N. Eng. J. Med. 2009; 360: 1526–38.
of the European Society of Cardiology (ESC). Endorsed by: The LeWinter, M. M. Acute pericarditis. N. Eng. J. Med. 2014; 371: 2410–16.

13
Exploring the Variety of Random
Documents with Different Content
 Afterwards, Robyn blushed to remember that the vow had been
made only in fear; but he comforted himself by thinking that “the
more deliberate consecration of himself to piety had been made
when the earth and sky had regained their equanimity, and with no
less motive than that of its own excellence.” The hour of terror had
been also the hour of realisation. This trembling child, already a
student of Nature, had begun amidst the winds and lightnings to
realise dimly the existence of Elemental Mysteries which made the
whole world tremble too. And yet, did not even these atmospheric
exacerbations flash and thunder out the command to praise Him and
magnify Him for ever? Were not the deepest, most terrible of
Elemental Mysteries but part of a Universal Benedicite?
 CHAPTER VII
THE DEBACLE
“But (as when in summer we take up our grass-horses into the stable, and give
them store of oats, it is a sign that we mean to travel them) our Philaretus, soon
after he had received this new strength, found a new weight to support.”—Robert
Boyle’s Philaretus.

In the spring of 1641, some months after the thunderstorm

episode, Marcombes bought horses, and they set out on a three
weeks’ tour in the neighbouring country. The Earl had not yet given
his permission for the Italian tour, and Francis and Robert had been
sixteen months at their lessons, and were beginning to long for a
holiday. Riding and walking, they visited Chambéry, Aix, and
Grenoble, and then found their way into “the wild mountains where
the first and chiefest of the Carthusian Abbies does stand seated.”
Robyn’s “conversion” by the thunderstorm appears to have been
quite unknown to Frank and Marcombes: they had no conception of
the thoughts that were churning in the boy’s head.
It was the Devil, so Robert Boyle says in his Philaretus, who,
taking advantage of the deep raving melancholy of the place, and
the pictures and stories to be found in the Monastery of Bruno,[88]
the Father of the Order, tempted him with “such hideous thoughts
and such distracting doubts of some of the fundamentals of
Christianity, that, though his looks did little betray his thoughts,
nothing but the forbiddenness of self-dispatch hindered his acting it.”
It was more probably an acute attack of home-sickness, following
on a prolonged diet of “yᵉ catechisme of Calvin”; but it was
remembered, by this sensitive boy, as a very real temptation. He
wrote to his father when they returned to Geneva, mentioning the
little tour only as one “wherein we have had some pleasure mingled
with some paines.” It was a sad little letter: “Your Lordship seems,”
says Robyn, “to be angry with my brother and I.” They had not
written often, or fully enough; and letters that are all beginnings and
endings do not tell much. Marcombes, on the other hand, wrote
ebulliently to the Earl. He never forgot to sing the praises of his
pupils—Robyn, especially, was semper idem, and “Capable of all
good things”; while the nature and disposition of both boys were “as
good and sweete as any in the worlde.”
On their return to Geneva, they had found letters from the Earl,
giving them leave to travel into Italy; and during the summer of 1641
the boys were “fincing”, and “dansing”, and learning Italian, and
holding their heads well and their bodies straight, and Mr. Francis
was now taller than my Lord Dungarvan, while as for Mr. Robert, he
was “an Eale”, tall for his age, and big proportionably. They rose
betimes, loved to ride abroad, and always came home with “a very
good stomacke.” And as Marcombes assured the Earl that they went
regularly to church, and in private also “sarved God very religiously”,
it may be supposed that the months of “tedious perplexity”, of which
Robert Boyle speaks in his Philaretus and of which Marcombes and
Frank knew nothing, were drawing to a close. There came a day,
indeed, when Robyn no longer excused himself from receiving the
Sacrament by reason of his “yonge age.” It pleased God, he says,
one day that he had taken the Sacrament to restore to him “the
withdrawn sense of his favour.”
Although the Earl of Cork had given his permission, he was very
dubious about the wisdom of the Italian journey.
“For,” wrote the Earl in London to Marcombes in Geneva, “we
have lately had a popish priest hanged, drawn and quartered; and a
many moe in prison which I think wilbe brought to the like cloudy
end, for that they did not depart the Kingdome by the prefixed date
lymited by the late statute.”
The Earl’s friends in London, “suspecting revenge,” had advised
him against the Italian journey, and drawn horrible pictures of an
Inquisition worse than death. But the old man was anxious to satisfy
the boys’ desires, and really wanted them to learn Italian, and to see
“all those brave Universities, States, Cities, Churches, and other
remarkeable things”[89] which only Italy could show them. And so
they were to go; but Marcombes was to take great care of them, and
to remember that the Earl was entrusting “these my Jewells” to him
in a strange country.
In preparation for Italy, Madame Marcombes was making for them
all kinds of new linen; and Marcombes bought for them three suits of
clothes apiece, and they were to have more when they reached
Florence—“where I doe intend to keep them a coach, God willing.”
Marcombes was anxious that the Earl should obtain for them a
letter (in Latin) from the King, “to all Kings, Princes, Magistrates,”
etc., in which Marcombes himself should be named “by name and
surname.” And they ought also, he said, to have a special licence
from the King to allow them to travel in Rome, “least your Lordship or
your sons should be questioned hereafter.” The Genevan household
were up in arms against Tom Killigrew, who had gone home and
reported, most untruly, that Marcombes was keeping the boys short
of clothes and pocket money.
In July 1641 Robyn wrote again to his father. The Earl seems to
have been still angry with “my brother and I”:—“My most honoured
Lord and father, I desire with passion and without any question to go
into Italy, but I protest unto your Lordship that I doe not desire it half
so much as to heare from your Lp; for the three moneths (or
Thereabouts) that we have been deprived of that sweet
communication seem to me 3 long Ages, and would to god that the
interruption of that pleasing commerce may proceede from your
private and publique employments.”
Marcombes also had written to the Earl of Cork. He dared not be
so bold, he said, as to beg for some news of “yᵉ affaires of yᵉ Island.”
They, in Geneva, had heard of Strafford’s death, “yᵉ catastrophe of
yᵉ last Deputy of Ireland”; but they did not know who was his
successor,[90] or what had become of the Archbishop of Canterbury,
and of “yᵉ armys both of England and Scotland.” In Geneva, by the
grace of God, they were enjoying a profound peace: “yᵉ storme
having been driving another way.”
 It was September 1641 when the boys and their governour, all
“well horsed”, bade good-bye to Madame and the children, and set
off on their long-talked-of Italian journey. Once more they crossed
the “hideous mountains”; they saw the source of the Rhine “but a
brook,” and came down in the valley of Valtollina, a little earthly
paradise abounding “with all that Ceres and Bacchus are able to
present.”
Robert Boyle always remembered standing on the spot where the
little town of Piur, “once esteemed for its deliciousness,” had about a
quarter of a century before been suddenly submerged and buried so
deep that “no after search by digging has ever prevailed to reach it.”
And still among the Alps, but surrounded by higher mountains,
“where store of crystal is digged,” and which “like perpetual penitents
do all the year wear white,” the boy found himself, for the first time in
his life, above the clouds. He never forgot how, as they descended la
Montagna di Morbegno, he looked down on the clouds that darkened
the middle of the mountain below them, while he and his
companions were above, in “clear serenity.”
From the Grisons they passed into Venetian territory and the vast
and delicious plains of Lombardy, through Bergamo, Brescia,
Verona, Vincenza and Padua, to Venice, Bologna, Ferrara and
Florence. They were very young; and their “peregrination” must not
be compared in the matter of sightseeing and adventure with John
Evelyn’s tour taken over much the same ground—only the reverse
way—a year or two later. At Florence they sold their horses, and
settled down for the winter of 1641-2; and there they resumed their
lessons, Italian chiefly and “modern history”; and Robyn read the
Lives of the Old Philosophers, and became so enamoured of the
Stoics that he insisted on “enduring a long fit of the toothache with
great unconcernedness.”[91] In all his journeys, he had carried his
pet books with him. Frank laughed at his younger brother’s
inveterate habit of reading as he walked—“if they were upon the
road, and walking down a hill, or in a rough way, he would read all
the way; and when they came at night to their inn, he would still be
studying till supper, and frequently propose such difficulties as he
met with, to his governour.”[92]
 While they were wintering at Florence, Galileo died “within a
league of it.” They never saw him; but they read and heard a great
deal about the “paradoxes of the great Star Gazer”; and Robert
carried away with him from Italy an undying memory of the attitude of
the Romish Church to scientific discovery. Galileo’s paradoxes had
been “confuted” by a decree from Rome, “perhaps because they
could not be so otherwise”; and the Pope had shown himself “loth to
have the stability of that earth questioned, in which he had
established his kingdom.” It was in Florence that Robert Boyle heard
the story told of the friars who reproached Galileo with his blindness,
telling him it was “a just punishment of heaven”, and of the sightless
astronomer’s memorable answer: “He had the satisfaction of not
being blind till he had seen in heaven what never mortal eyes beheld
before.” In Florence, Marcombes and his pupils lodged in the same
house with some “Jewish Rabbins,” from whom Robyn learned a
great deal about pre-Christian “arguments and tenets.” Frank,
perhaps, was more interested in the carnaval, and the ducal tilts, and
the gentlemen’s balls, to which both the brothers were invited. And
Marcombes took good care of the Earl’s “jewells”, though they were
allowed to look open-eyed upon all the vice, as well as the
splendour, of seventeenth-century Italy: “the impudent nakedness of
vice” Robert called it then and afterwards. He had never found, he
used to say, “any such sermons against the things he then saw as
they were against themselves.”[93]
In March 1642 they were in Rome, where it was thought safest for
Robert to pass for a Frenchman. English Protestants were at the
moment especially unpopular, and Master Robyn was less willing
than his brother Frank to “do at Rome as the Romans do.” Rome
itself indeed seems to have disappointed the young Puritan. After all
his studies in Latin history and literature, it was a disappointment to
find Rome dominated, not by victorious legions, but by what he
called “present superstition.” He found Modern Popes where the
Ancient Cæsars should have been, and “Barberine bees flying as
high as did the Roman Eagle.” It was a come-down, certainly; but the
little party did a good deal of sightseeing of the simple kind; and they
saw the Pope and his Cardinals in chapel, and Robyn’s observant
eyes watched a young churchman after the service “upon his knees
carefully with his feet sweep into his handkerchief” the dust that had
been consecrated by his Holiness’s feet. Robert Boyle did not gather
up any dust; but he obtained and read the Latin and Tuscan poems
written by this same Pope. “A poet he was,” was Robyn’s verdict of
Pope Urban VIII; a poet—and some other things besides.
To escape the heat of Rome they returned to Florence, by Perugia
and Pistoia, and thence by the river Arno to Pisa and Livorno. From
Livorno they coasted in a felucca, drawing up their boat on shore
every night and sleeping in some Mediterranean townlet, to Genoa;
and so, travelling by slow degrees, by Monaco, Mentone, Nice and
Antibes, they reached Marseilles in May 1642.
At Marseilles, they expected to find letters from the Earl of Cork,
and bills of exchange to carry them on to Paris. Hitherto, though
difficulties of transit had now and then arisen, their quarterly
allowance had been punctually sent. The Earl had allowed them
£500 a year in Geneva, and £1000 a year while they were in Italy;
and the money had always come to hand, thanks to the combined
activities of Mr. Perkins the tailor, Mr. Philip Burlamachy, a certain Mr.
Castell, “merchant stranger,” who travelled between England and
Geneva, and, last but not least, Mr. Diodato Diodati, the Genevan
banker. Once or twice while they were in Italy letters had come from
home, and they knew vaguely that sinister things had been
happening there. And Frank and Betty wrote to each other: Betty
was begging Frank to come back to her, and even threatening to
come to him; and so terror-struck was Marcombes at the bare
suggestion that he was looking “very narrowly” after poor Frank. He
had of late been keeping Frank very short of money, lest he might do
“I doe not kgnow what.”
And then at Marseilles, even while they were idly waiting for their
bills of exchange and watching the French King’s galleys put to sea
with about two thousand slaves tugging at the oars, there came to
Francis and Robyn, and to Marcombes too, for that matter, a rude
awakening.
 “Ye affaires of ye Island” had been going from bad to worse.
Wentworth’s tragic end was almost an old story in May 1642, so
quickly had events been hurrying on. He had got his earldom at last,
in January 1640. For one little year he was indeed Earl of Strafford
and Lord Lieutenant of Ireland; he had headed the loan to King
Charles for the expenses of the second “Bishops’” War. Strafford
was in the King’s Cabinet, and the Earl of Cork had been made a
Privy Councillor. On April 13, 1640, the “Short Parliament” had met,
and it had been dissolved on May 5—“the doleful Tuesday, when the
Parliament was dissolved before any Act was passed.”[94] The Earl
and his family were back at Stalbridge in July; and now it was
Broghill’s turn to raise “a Hundred Horse for Scotland,” and
Kynalmeaky and Barrymore and George Goring were all bound for
the North in the second “Bishops’ War”. But by November the war
was over, and the Parliament (that was to be the Long Parliament)
had met. On November 11, Strafford was impeached and called to
the Bar of the House on his knees (“I sitting in my place covered,”
wrote the Earl of Cork in his diary); and on November 25 Strafford
was in the Tower. All through the London winter of 1640, and right on
into the spring of 1641, Strafford and Strafford’s trial filled the minds
of all men, not in London only, but throughout England, Scotland and
Ireland. During those fateful months, the diary gives one or two vivid
glimpses of the Earl’s old enemy. There is no description of the
scenes in the Houses, or the trial itself in Westminster Hall; the grim
pageant of Lords and Commons; the plates of meat and bottles of
drink being handed from mouth to mouth; the royalties in their little
trellissed rooms; the King apart, “anxiously taking notes”; the ladies
also, moved by pity, with paper, pens and ink before them,
“discoursing upon the grounds of law and state”[95]. None of these
things finds a place in the diary. The Earl’s old eyes were fixed upon
Strafford, and Strafford only: Strafford on his knees before the Bar,
with his six attendant lawyers; Strafford bringing his answer—his “18
skins of parchment, close-written”—into the House of Peers;
Strafford attempting, in his own defence, to “blemish” the Earl of
Cork with “accusations....”[96]
 It was a grim time. And yet, such is human life, while Strafford was
in the Tower and the Committee of the Commons preparing his
indictment, all London was talking of my Lord Broghill’s brilliant
marriage with the Lady Margaret Howard, daughter of the late Earl of
Suffolk, in “the Lord Daubigne’s house in Queenes street covent
garden.”[97]

“At Charing Cross hard by the way

Where we (thou knowst) do sell our hay,
There is a house with stairs....”

There is no description of Broghill’s wedding from the Earl of

Cork’s pen; but Sir John Suckling has left a very graphic account of it
in his “Ballad upon a Wedding,” which, it is said, was hawked about
the London streets at the time.[98]
The bridegroom, “pestilent fine,” walked on before all the rest:—
London had not forgotten the duel with Mr. Thomas Howard.

“But wot you what? the youth was going

To make an end of all his wooing.”

And the bride was a beautiful creature: the blush on her cheek
was like a Catharine pear—“the side that’s next the sun”; while her
red underlip looked as if “some bee had stung it newly.”

“Her finger was so small the ring,

Would not stay on which they did bring,
...
Her feet beneath her petticoat,
Like little mice, stole in and out
As if they feared the light.”

This was the bride for whom Broghill had forgotten Mrs. Harrison
and the duel in which nobody was hurt. This was the beautiful “Lady
Pegg,” who was to prove herself a woman “beautiful in her person,
very moderate in her expences, and plain in her garb; serious and
decent in her behaviour, careful in her family, and tender of her
lord”[99]—nay, more, in Broghill’s after-life it is easy to see that he
had not only a brave helpmeet, but a clever one. Robert Boyle
himself has called her the “great support, ornament, and comfort of
her Family.”[100]
The old Earl was in his place when, after many long debates and
“sevral heerings”, Strafford was sentenced to death—only eleven
voices of all the Lords declaring “not content”; and on May 12
Strafford—to whom the King had pledged his word that not a hair of
his head should be touched—was beheaded on Tower Hill. “As he
well deserved” is the brief comment in the Earl of Cork’s diary.
And what had the Earl’s young daughter, the “unrewly Mary,” been
doing? She and Frank’s wife, Betty, having spent the summer at
Stalbridge with the Earl and his customary house-party, were now
back in town, staying with Lady Dungarvan in her house in Long
Acre. Betty had taken the measles, and Mary had promptly followed
suit; and they had both been packed off to another house in Holborn.
Charles Rich had shown such anxiety about Mary that the family’s
suspicions were at last aroused; and Betty’s mamma, very much
afraid of the Earl of Cork, had threatened to tell everything, “and in a
great heat and passion did that very night do it.”[101] Betty in the
meantime contrived to give the lovers one more chance. Charles
Rich went down on his knees before the convalescent Mary, and
remained in that attitude for two hours, while Betty kept guard at the
door; and “so handsome did he express his passion” that Mary at
last said “yes.” The very next day Broghill—himself a married man—
carried his little sister off in disgrace to a very small house near
Hampton Court which belonged to Betty’s sister, Mrs. Katharine
Killigrew; and there for weeks Mary lived in exile, Charles Rich riding
down daily to see her. His father, the Earl of Warwick, and Lord
Goring interceded with the old autocrat, and at last their combined
influence carried the day The Earl saw, “and was civil to,” Mr.
Charles Rich, and Mary’s portion was to be £7000. It was now Mary
who went down on her knees before her father, begging for his
pardon. The old man upbraided her, shed some tears, and told her to
marry Charles Rich as soon as she liked.
 It might be supposed that this was enough, but no;—Mary Boyle at
sixteen had been “always a great enemy to a public marriage.” She
much preferred running away. Charles Rich was quite willing, and
the young people were privately married on July 21, 1641, in the little
parish church of Shepperton, near Hampton Court. And a few days
later, Mary’s elder sister, the Lady Katharine Jones, too kind and too
wise to be angry with so rare a thing as a love-match, especially
when the wedding was over, accompanied the young couple in her
carriage to the Earl of Warwick’s house of Leeze in Essex, and
handed them over to the care of that patriarchal family.[102]
Some of the Cork family,—the Barrymores, and Kynalmeaky,
without his wife,—seem to have been already in Ireland in the
autumn of 1641; and the Earl of Cork was making his own
preparations to return to Lismore. He had been buying six black
horses and harnesses for his new light travelling coach, a sedan
chair lined with carnation velvet, and a “horslytter,” with two black
stone coach-horses. August is a hot month for “feasting” in any case,
and the summer of 1641 had been particularly hot, and the plague
and smallpox were rife in London; but in August the old Earl had
entertained at his Cousin Croone’s at the Nag’s Head Tavern in
Cheapside all the Lords, Knights, and Gentlemen of the Committees
of both Houses of Parliament for Ireland; and a few days later,
Cousin Croone, at the Nag’s Head, had “feasted” his great kinsman
the Earl of Cork.
During those last months also the Earl had been busy settling his
affairs: there was the purchase of Marston Bigot in Somersetshire for
Broghill and his wife, and the purchase of the smaller Devonshire
estate of Annarye, and the settling of Stalbridge on Robert, his
Benjamin. There was the paying of debts and bonds and jointure
moneys, and the packing, locking, sealing and lettering of “yron
chestes” and “lyttle trunckes” and “lyttle boxes,” to be left behind in
the care of various trusted friends. Among them were boxes of
deeds and writings for Frank, to be left with Betty’s stepfather, Sir
Thomas Stafford; and at least two other boxes, “fast sealed”, for
Robert, one of them to be left with the Earl’s friend, Lord Edward
Howard of Escrick, and the other, containing duplicates, with the
Earl’s own cousin, Peter Naylor, the lawyer, of New Inn. Stalbridge
was to belong to Robert after the Earl’s death, besides the Irish
lands already settled on him, and a house specially built for him at
Fermoy. And the old man had set his match-making old heart on a
splendid marriage for Robyn—with the Lady Ann Howard, the very
young daughter of Lord Edward Howard of Escrick, first cousin of
“Lady Pegg.” One of the Earl’s last rides in England was with his son
Dungarvan to Hatfield to take leave of the Salisbury family; and there
also he saw “my Robyn’s yonge Mrs.,” to whom on this occasion the
Earl presented “a small gold ring with a diamond.”
The last visit of all was to Leeze in Essex—carried there in
Charles Rich’s own coach—to bid good-bye to the beloved “unrewly
Mary”. The last of the Earl’s many gifts in England appears to have
been to an “infirme cozyn” of his own—a welcome gift from one old
man to another—“a pott of Sir Walter Raleigh’s tobackoe.”[103]
There were a good many leavetakings with English friends and
kinsfolk between London and Stalbridge, and an almost royal
progress from Stalbridge by Marston Bigot—where he held a
“Court”—to the coast. Lady Kynalmeaky had been persuaded to
accompany her father-in-law to Ireland, and Broghill and his wife
crossed with them. The Dungarvans were, apparently, to follow
shortly after. Youghal was reached on October 17, and a day or two
later the Earl and his family were at the House of Lismore again.
The old biographers give a picturesque account of a great banquet
at Castle Lyons in honour of the Earl’s home-coming. They tell how,
while Lord Barrymore was feasting his guests, the old Earl was
called out of the banqueting hall to see a messenger, who, in a few
breathless, horror-stricken words, brought him tidings of the bloody
outbreak of rebellion in Munster. A week or two later Lord Barrymore
—the only one of the old Irish nobility to remain absolutely loyal to
the Protestant cause—was buying ordnance for the defence of
Castle Lyons. Lismore was being strengthened and stored with
ordnance, carbynes, muskets, Gascoigne wines and aqua vitæ.
Gunpowder and match were being bought in large quantities, money
was being paid out on every hand—the Earl was “maintaining”
everything and everybody—and money was getting ominously
scarce. In December, Lady Kynalmeaky left Ireland for the Hague,
and Kynalmeaky took over the charge of Bandonbridge, with a troop
of horse and 500 foot, “all English Protestants.” In January 1642,
Broghill was defending Lismore with a troop of horse and 200 “good
shot.” He was a dependable son: “My lord,” he wrote to his father,
“fear nothing for Lismore, for if it be lost it shall be with the life of him
that begs your lordship’s blessing, and stiles him, my lord, your
lordship’s most humble, most obliged, and most dutiful son and
servant, Broghill.” The old Earl himself had undertaken to hold
Youghal, to keep the command of that harbour, and to “preserve that
towne”; and he was never to leave it. The sheet-lead on the “tarras”
of the old college was to be torn up to make “case-shott” for his
ordnance. Pikes, muskets, halberds and “brownbills”—everything in
the shape of a weapon—were collected from Devonshire and
Dorsetshire and everywhere else, and the “Mortall Sowe” was to play
a great part in the defence of Bandonbridge and Lismore.
Dungarvan, at the head of 1200 foot, was with the Lord President.
[104] The Protestant ladies had left, or were leaving, for England or
the Hague; but Dungarvan’s wife and Broghill’s wife stayed as long
as possible on the spot.[105]
It was from Lismore—just before the Earl was sent to defend
Youghal—that he negotiated the bills of exchange to be sent through
Perkins, the London tailor, to Marcombes: the quarterly allowance of
£250 for the three months from March 1 to June 1, 1642. And it was
from Youghal, on March 9, that he sent the letter—one of the finest
and saddest appeals ever written by a father to his children—that
was to greet Marcombes and the boys on their arrival at Marseilles.
[106]

It is a long letter. The Earl had received their news from Florence,
and was glad to hear of their health and proficiency; but the thought
of them, and how hereafter they were to subsist, was most grievous
unto him—
“And now or never,” he wrote to Marcombes, “is the tyme for you
to give yourself honour, and to make me and them your faithfull
friends for ever hereafter. Necessitie compells me to make you and
them know the dangerous and poore estate whereunto, by God’s
providence, I am at this instant reduced.”
An account of the outbreak and course of the Rebellion follows; of
Dungarvan’s and Kynalmeaky’s and Broghill’s doings, and of the
Earl’s own position in Youghal. It was a case of about “200,000 in
armes and rebellion against a poor handful of British Protestants.”
He tells Marcombes how in January he had scraped together with
much difficulty—by selling of plate—the £250 for their quarterly
allowance, and made it over to be paid by Mr. Perkins to Mr. Castell.
So far he had punctually supplied them—“which longer to doe I am
no waies able.” The £250, when they should receive it, must be
husbanded carefully, and employed to bring both boys home again.
They must land at Dublin, Cork, or Youghal. If they cannot do this,
they must go to Holland and serve under the Prince of Orange. They
must, in any case, manage to maintain themselves: “for with inward
greefe of soul I write this truth unto you that I am no longer able to
supply them ... but as I am compelled in my age to doe, so must they
in their younger yeares com̃ end themselves....
“But if they serve God and be carefull and discreet in their
carridge, God will bless and provide for them as hitherto he hath
done for me, who began in the raising of my fortune by good
endeavours; without any assistance of parents and friends....” And
he knows Marcombes is too generous to leave the boys, “my two
yong Sonnes that are soe deere unto me,” till he can see them safely
shipped for Ireland or “well entred in the warres of Holland”—as they
may desire and Marcombes advise.
This, then, was the letter that Marcombes and the two boys
received at Marseilles. It was then May, and the letter was dated
March 9; it was already two months old. They must have looked
blankly at each other. How were they to carry out the Earl’s wishes?
How were they both, without money, to make their way home? No
bill of exchange had reached them: Mr. Perkins, the London tailor,
had played them false.
It seems to have been arranged between them that Frank, the
elder brother, who at nineteen would be of some use at his father’s
side, should, with Marcombes’s assistance, make his way as quickly
as he could to Ireland and to Youghal. There is no mention of Betty
in this moment of decision. Marcombes was evidently able to scrape
together enough money out of what they still had to carry one of the
boys home—and it was to be Frank. And Robyn? Robyn at fifteen
was an “Eale” still. Had Marcombes sometimes exaggerated, in his
letters to the Earl, Robyn’s stature and strength? The sequel will
show. Poor Carew, in the Eton days, and Marcombes himself, wrote
of Robyn as a boy of sedentary habits, and a little “thicke.” If the truth
must be told, there was not much of the soldier in Robert Boyle. He
was the student, thinker, dreamer; and he knew himself to be
unqualified, at fifteen, “to be received among the troops.” And,
without money, it was quite impossible to provide himself with the
necessary “equipage.”
Apparently they all three—Marcombes, Frank, and Robyn—went
on as far as Lyons; and there it seems likely they parted: Frank in the
saddle, his horse’s head turned towards Ireland, and Robyn and
Marcombes returning in deep melancholy to Geneva. There Robyn
was to wait for further orders—to employ his time in learning to make
“an honourable living.” It is all told in his sad little letter, written from
Lyons to the Earl at Youghal: a letter which may have been carried to
Ireland in Frank’s pocket.
“My most honoured Lord and Father, Having according to your
Lordship’s order and directions seriously pondered and considered
the present estate of our affairs, we have not thought it expedient for
divers reasons that my Brother will tell your Lordship by word of
mouth that I should goe into Holland; for besides that I am already
weary and broken with a long journey of above eight hundred miles, I
am as yet too weake to undertake so long a voyage in a strange
country, where when I arrive I know nobody and have little hope by
reason of my youth to be received among the troops....” He explains
that the money had not come; but M. Marcombes had offered to
keep him at Geneva till they should hear further from the Earl, “or till
it pleased God to change the face of the affaires”; and Robyn had
gratefully accepted this offer. He hoped to fit himself to defend his
religion, King, and country, “according to my little power....
 “... If your Lordship hath need of me in Ireland, I beseech your
Lordship to acquaint me therewith and to believe that I have never
beene taught to abandon my parents in adversity, but that there and
in all other places I will always strive to shew myself an obedient
sonne....”
Frank, he said, was ready to take horse to “goe towards Ireland, to
secoure your Lordship according to his power,” and would carry all
their news. And Robert ends his letter—
“I most humbly take my leave, commending your Lordship and him
and us all unto the protection of Almighty God, beseeching your
Lordship to believe that whatsoever misery or affliction it pleaseth
God to send me I will never doe the least action unworthy of the
honor that I have to be, my Lord, your Lordship’s most dutiful and
obedient son, Robert Boyle.”[107]
Dr. Grosart, in editing the Lismore papers, found the original letter
much damaged, a large piece of it having been torn away in the
breaking of the seal. The Earl had evidently torn it open hastily in his
anxiety to know what “my Robyn” was going to do. Whether or no
Frank delivered the letter into his father’s hands, Frank was certainly
quickly back in Ireland, and very much on the spot. By August 1
Robyn had received a letter from Frank, full of enthusiasm for
Kynalmeaky’s conduct at home.
For Kynalmeaky was in his element at last. “I have left Sleeping in
ye afternoone,” wrote Kynalmeaky to his old father in Youghal. The
son who had shown “all the faults a prodigall inordinate young man
can have, which if he take not up in tyme will be his ruine and the
breaking of my hart”, was redeeming himself. Kynalmeaky’s wife (the
Earl of Cork always called her “my deare deare daughter-in-law”)
had not been able to live with her husband; even the younger
brothers must long ago have known what Kynalmeaky was. And now
Frank had written to tell Robyn in Geneva that Kynalmeaky was
acting like a hero. And Robyn, so far away from home, had written
off on August 1 a little letter of tender admiration to this elder brother,
who had set them every bad example and yet had kept such a place
in their hearts. On the margin of this letter Robyn added a little
boyish postscript—only to say he could not express in words what he
was feeling, and ending with “Adieu, Dearest Lewis, idle Cosin. Bon
Anné, Bon Solé, bon Vespré. Adieue a Di vous commande.”
Did Kynalmeaky ever have this letter? It was dated from Geneva,
Aug. 1, and it was endorsed by the Earl of Cork himself, “from my
sonn Robert to his brother Kynal. Rec. 13 Oct.” Had it been sent to
the Earl, with Kynalmeaky’s papers—or had it indeed come too late?
For the battle of Liscarrol had been fought on Sept. 3. The Earl’s
loyal son-in-law, Lord Barrymore, and all the Earl’s sons except
Robert, fought in that battle.[108] And at the Battle of Liscarrol
Kynalmeaky was killed; killed on his horse, by a musket-shot through
the head. It was Frank—the “sweet-spirited Frank,” fresh from the
fencing and dancing and vaulting lessons in Geneva and Italy—who,
“carrying himself with undaunted resolution,” rescued his brother’s
body and horse, and kept troop and foot together.
The old man did not know then which of these two sons to be
proudest of. It was a grim satisfaction to the Earl, after all that had
passed, when “Kynal” had been buried in Lismore Church, to sit
down and make that entry in his diary: “Six of the rebell ensignes
were carried to his widdoe.”[109]
Robyn was to hear from his father once or twice after that. The
Earl held out brave hopes of being able to procure some “office” for
his boy “at his coming over.” And he sent his own “choice dun mare”
to Lismore, with orders that it was to be “kept and drest carefully” for
Robyn, when God should send him home again. And when Broghill’s
wife, “Lady Pegg,” was at last obliged to return to England, the old
Earl gave her a commission to buy for him a ring “besett rownd with
diamonds,” and to present it, from him, to her fair young cousin the
little Lady Ann Howard, whom he thought of always, even in those
dark days, as “my Robyn’s yonge Mrs.”
There is something Shakespearean in the mood in which this old
fighter lived his last months and drew his last breath. Shut up in
Youghal, “preserving” that town for his King, his sons away fighting,
his daughters and grandchildren scattered, Kynalmeaky and
Barrymore dead, and poor Lettice dying,[110] his lands despoiled, his
fortune vanished, he was still the great Earl of Cork, the head of a
great family, the old man of action and experience, the Elizabethan
soldier-statesman to whom the younger men, statesmen and
kinsmen alike, turned in this hour of extremity, and not in vain. There
is nothing stronger or more human of its kind, or more characteristic
of the man, than the positively last will and testament made by
himself in Youghal so late as November 1642, ten months before his
death.[111]
The end came, nobody knows exactly when, but about the very
time of the signing of the truce at Sigginstown, in the middle of
September 1643, “from infirmities incident to old age, and the want
of rest and quiet.”
He was buried in the great tomb at Youghal. All his life he had
believed in three things: in God’s Providence, his own integrity of
purpose, and the righteousness of a Cause. And in the debacle—in
his and Ireland’s darkest moment, when the clouds hung low over
his native land and the land of his adoption—his belief in these three
things remained unmoved.
Shakespeare has told us how Faith and Uncertainty go hand in
hand—
“If it be now, ’tis not to come; if it be not to come, it will be now: if it
be not now, yet it will come....”
 CHAPTER VIII
IN ENGLAND AGAIN
“And though his boiling youth did often very earnestly solicit to be employed in
those culpable delights that are useful[112] in and seem so proper for that season,
and have repentance adjourned till old age, yet did its importunities meet ever with
denials, Philaretus ever esteeming that piety was to be embraced not so much to
gain heaven, as to serve God with....”—Robert Boyle’s Philaretus.

In the summer of 1644, a slim, sunburnt, foreign-looking youth

came back into the London he had left when he was quite a little
fellow, nearly five years before. Even now, he was not yet eighteen,
and he was still an “Eale”. None of his family expected his return; he
had little or no money in his purse, and but vague ideas as to what
he was going to do next.
How things had changed! Where were the King and Queen,
whose hands Frank and he had kissed? And the gay Court that had
clustered about them? And his Father! There was no “Great Earl of
Cork” any more; no “greatest family in all London,” living
“extraordinarily high,” in the House of the Savoy; no child weddings
in the royal chapel at Whitehall. What had become of Frank’s
wedding shoes, that had been lent afterwards to poor Kynalmeaky?
There can have been little but troops, and talk of troops, on the
dusty summer roads, as Robert Boyle came towards London; and
the quick, hot jargon of names and phrases that was in all men’s
mouths—the political idiom of the moment—must have been doubly
difficult to understand by the boy who had so long been living in
studious exile, speaking “all and allwayes French,” and breathing an
atmosphere of profound peace—“the storme having been driving
another way.”
 As he neared London, Robyn’s thoughts must have been still with
the Marcombes household, till so recently his home, and the little
circle of learned and pleasant Genevan friends whom he had left
behind him. For Marcombes had more than fulfilled his trust. No
remittances had come to Robert Boyle since the old Earl wrote that
letter to Marcombes in March 1642. The boy had been running up a
big debt, of money and gratitude alike, to his governour: “As for me,”
he had written to his brother Kynalmeaky about Marcombes (the old
letter is scarcely decipherable in parts), “he hath so much obliged me
the ... despaire of ever being able to desingage myselfe of so many
and so greate ... that I have unto him.”[113]
And when at last, eight or nine months after the Earl’s death,
Robyn, chafing in his idleness and exile, made up his mind to break
from his surroundings and find his way home somehow, Marcombes
had used his own interest in Geneva to “take up” for his pupil “some
slight jewels at a reasonable rate,” by the sale of which, from place
to place, the boy might pay his way back to London.
And now he was there; and the life of the little Swiss University
town lay behind him, too recent to be forgotten: the life of a “well-
fortified city,” with the great Gothic fabric of a Cathedral in its midst,
on one of whose four cannon-mounted turrets there stood “a
continual Sentinel.” It was a Cathedral, of course, no longer. It was
there that the celebrated Dr. John Diodati, and the brilliant young
Professor Morice better known as Alexander Morus, “poet and chief
professor of the University,” discoursed eloquently after the discipline
of Calvin and Beza.[114] Dr. Diodati preached on Thursdays in Italian
to his Italian Protestant Congregation, and on Sundays in French,
with his hat on, after the “French mode.” Dr. Diodati lived at the Villa
Diodati, on the south bank of the lake, two miles out of the city: the
old Bishop’s Palace was now the prison. The University was a “faire
structure,” with its class-rooms, its hall, and its excellent library. And
Divines and Professors, in their gowns and caps and hats, flitted
about the wooden-arcaded streets. There was an “aboundance of
bookesellers”; and good screwed guns and Geneva watches, pewter
and cutlery, were to be bought; and amongst the hoary relics of
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