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To our mentors for sharing their wisdom and knowledge
To our families for providing love and support for all of our endeavors
To our patients for teaching us and to their families for trusting us
Contents
Contributors
Foreword
Preface—Inpatient Pediatrics, 2nd Edition
List of Abbreviations
1 Adolescent Medicine
Christopher B. Renjilian, MD, MBE, Krishna Wood White, MD, MPH, and Leonard J. Levine, MD
2 Allergy and Asthma
Irene Fung, MD, Solrun Melkorka Maggadottir, MD, and Terri Brown-Whitehorn, MD
3 Analgesia and Sedation
Arul M. Lingappan, MD, F. Wickham Kraemer III, MD, and Melissa Desai Patel, MD, MPH
4 Calculations
Barbara-Jo Achuff, MD, FAAP, Vanessa N. Madrigal, MD, and Donald L. Boyer, MD, MSEd, FAAP
5 Cardiology
Javier J. Lasa, MD, Chitra Ravishankar, MD, and Joseph Rossano, MD, MS, FAAP, FAAC
6 Dermatology
Leslie Castelo-Soccio, MD, PhD, and Kara N. Shah, MD, PhD
7 Emergency Medicine
Margaret Samuels-Kalow, MD, MPhil, and Angela Ellison, MD, MSc
8 Endocrinology
Christine T. Ferrara, MD, PhD, Amanda M. Ackermann, MD, PhD, and Andrew A. Palladino, MD
9 Fluids and Electrolytes
Sonal Bhatnagar, MD, and Lawrence Copelovitch, MD
10 Gastroenterology
Benjamin Sahn, MD, MS, and Petar Mamula, MD
11 Genetics
Elizabeth Bhoj, MD, PhD, Rebecca Ahrens-Nicklas, MD, PhD, and Tara L. Wenger, MD, PhD
12 Hematology
Erin Blevins, MD, MSCE, and Char Witmer, MD, MSCE
13 Human Immunodeficiency Virus Infection
Daniel H. Reirden, MD, AAHIVMS
14 Immunology
Gita Ram, MD, and Soma Jyonouchi, MD
15 Infectious Diseases
Katie Chiotos, MD, Lori Handy, MD, MSCE, Salwa Sulieman, DO, and Jeffrey S. Gerber, MD,
PhD
16 Metabolism
Rebecca Ganetzky, MD, and Can Ficicioglu, MD, PhD
17 Neonatology
Elisabeth Raab, MD, MPH, Tawia A. Apenteng, MD, Jennifer M. Brady, MD, and Mary Catherine
Harris, MD
18 Nephrology
Joann Spinale Carlson, MD, and Rebecca L. Ruebner, MD, MSCE
19 Neurology
Annapurna Poduri, MD, MPH, Renée A. Shellhaas, MD, Dennis J. Dlugos, MD, Peter H. Berman,
MD, and Gihan I. Tennekoon, MD
20 Nutrition
Jamie Merves, MD, Diane Barsky, MD, and Maria R. Mascarenhas, MBBS
21 Oncology
Jason L. Freedman, MD, Benjamin R. Oshrine, MD, and Naomi Balamuth, MD
22 Ophthalmology
Gil Binenbaum, MD, MSCE, and Stefanie L. Davidson, MD
23 Orthopedics
Christian Turner, MD, Matthew Grady, MD, and Theodore Ganley, MD
24 Otolaryngology
Pamela Mudd, MD, and John Germiller, MD, PhD
25 Procedures
Mercedes M. Blackstone, MD, Jeannine Del Pizzo, MD, and Sarah Fesnak, MD
26 Psychiatry
Rahim Rahemtulla, MD, and Amy Kim, MD
27 Pulmonology
Kelly Adams, DO, Stamatia Alexiou, MD, and Howard B. Panitch, MD
28 Rheumatology
Elaine Ramsay, MD, Alysha Taxter, MD, and Jon Burnham, MD, MSCE
29 Surgery
Jesse D. Vrecenak, MD, and Michael L. Nance, MD
30 Toxicology
Ruth Abaya, MD, MPH, and Diane Calello, MD
Appendix A
Appendix B
Index
Contributors
Ruth Abaya, MD, MPH, Attending Physician, Division of Emergency Medicine, The Children’s
Hospital of Philadelphia; and Assistant Professor of Pediatrics, Perelman School of Medicine at the
University of Pennsylvania, Philadelphia, Pennsylvania
Barbara-Jo Achuff, MD, FAAP, Assistant Professor, Department of Pediatrics, Cardiac Critical Care
Baylor College of Medicine, Texas Children’s Hospital, Houston, Texas
Amanda M. Ackermann, MD, PhD, Clinical Fellow in Pediatric Endocrinology and Diabetes, Division
of Endocrinology and Diabetes, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Kelly Adams, DO, Fellow, Pediatric Pulmonology, The Children’s Hospital of Philadelphia,
Philadelphia, Pennsylvania
Rebecca Ahrens-Nicklas, MD, PhD, Resident, The Children’s Hospital of Philadelphia, Philadelphia,
Pennsylvania
Stamatia Alexiou, MD, Fellow, Pediatric Pulmonology, The Children’s Hospital of Philadelphia,
Tawia A. Apenteng, MD, Attending Neonatologist, The Children’s Hospital of Philadelphia Newborn
Care at Pennsylvania Hospital, Philadelphia, Pennsylvania
Naomi Balamuth, MD, Attending Physician, Division of Oncology, Children’s Hospital of Philadelphia;
and Assistant Professor of Pediatrics, Perelman School of Medicine at the University of Pennsylvania,
Diane Barsky, MD, Attending Physician, Medical Director, Home Parenteral Nutrition Service, Division
of Gastroenterology, Hepatology and Nutrition, The Children’s Hospital of Philadelphia, Instructor of
Pediatrics, Clinical Assistant Professor of Pediatrics, Perelman School of Medicine at the University of
Pennsylvania, Philadelphia, Pennsylvania
Peter H. Berman, MD, Senior neurologist, The Children’s Hospital of Philadelphia; and Professor
Emeritus, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
Sonal Bhatnagar, MD, Assistant Professor of Pediatrics, Division of Pediatric Nephrology and
Hypertension, The University of Texas Health Science Center at Houston, Houston, Texas
Elizabeth Bhoj, MD, PhD, Fellow, Division of Human Genetics and Molecular Biology, The Children’s
Hospital of Philadelphia, Philadelphia, Pennsylvania
Gil Binenbaum, MD, MSCE, Attending Surgeon, Division of Pediatric Ophthalmology, The Children’s
Mercedes M. Blackstone, MD, Attending Physician, Pediatric Emergency Medicine, The Children’s
Hospital of Philadelphia, Associate Professor of Clinical Pediatrics, Perelman School of Medicine at the
Erin Blevins, MD, Attending Physician, Department of Pediatrics, Hematology and Oncology, Naval
Medical Center San Diego, San Diego, California
Donald L. Boyer, MD, MSEd, FAAP, Attending Physician, Pediatric Critical Care Medicine, The
Children’s Hospital of Philadelphia, Assistant Professor, Department of Anesthesiology & Critical Care
Medicine, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
Jennifer M. Brady, MD, Assistant Professor of Pediatrics, Division of Neonatology, Cincinnati

Children’s Hospital Medical Center, Cincinnati, Ohio
Terri Brown-Whitehorn, MD, Associate Professor of Clinical Pediatrics, Perelman School of Medicine
at the University of Pennsylvania, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Jon Burnham, MD, MSCE, Attending Physician, Division of Rheumatology, The Children’s Hospital of
Philadelphia; Associate Professor of Pediatrics, Perelman School of Medicine at the University of
Diane Calello, MD, Robert Wood Johnson University Hospital, New Brunswick, New Jersey
Leslie Castelo-Soccio, MD, PhD, Section of Dermatology, The Children’s Hospital of Philadelphia,
Assistant Professor of Pediatrics and Dermatology, Perelman School of Medicine at the University of
Marina Catallozzi, MD, MSCE, Assistant Professor of Pediatrics and Population and Family Health at
Columbia University Medical Center, New York, New York
Katie Chiotos, MD, Fellow, Divisions of Infectious Diseases and Critical Care Medicine, The
Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Lawrence Copelovitch, MD, Assistant Professor of Pediatrics, Division of Nephrology, The Children’s
Hospital of Philadelphia, Perelman School of Medicine at the University of Pennsylvania, Philadelphia,
Pennsylvania
Stefanie L. Davidson, MD, Attending Surgeon, Division of Pediatric Ophthalmology, The Children’s
Jeannine Del Pizzo, MD, Attending Physician, Division of Emergency Medicine, The Children’s
Hospital of Philadelphia; and Assistant Professor of Clinical Pediatrics, Perelman School of Medicine at
the University of Pennsylvania, Philadelphia, Pennsylvania
Dennis J. Dlugos, MD, Professor of Neurology, Perelman School of Medicine at the University of
Pennsylvania, and Attending Physician, Division of Neurology, The Children’s Hospital of Philadelphia,
Angela Ellison, MD, MSc, Assistant Professor of Pediatrics, Division of Emergency Medicine, The
Children’s Hospital of Philadelphia, Perelman School of Medicine, University of Pennsylvania,
Christine T. Ferrara, MD, PhD, Clinical Fellow in Pediatric Endocrinology and Diabetes, Division of
Endocrinology and Diabetes, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Sarah Fesnak, MD, Fellow, Division of Emergency Medicine, The Children’s Hospital of Philadelphia,
Can Ficicioglu, MD, PhD, Associate Professor of Pediatrics, Perelman School of Medicine at the
University of Pennsylvania; Attending Physician, Division of Metabolism, Director of the Newborn
Metabolic Screening Program, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Jason L. Freedman, MD, Clinical Instructor, Division of Oncology, The Children’s Hospital of
Philadelphia, Philadelphia, Pennsylvania
Irene Fung, MD, Fellow, Division of Allergy and Immunology, The Children’s Hospital of Philadelphia,
Rebecca Ganetzky, MD, Fellow, Division of Metabolism, The Children’s Hospital of Philadelphia,
Theodore Ganley, MD, Director of Sports Medicine, The Children’s Hospital of Philadelphia,
Associate Professor of Orthopaedic Surgery, Perelman School of Medicine at the University of
Jeffrey S. Gerber, MD, PhD, Assistant Professor of Pediatrics, Perelman School of Medicine at the
University of Pennsylvania, Division of Infectious Diseases, The Children’s Hospital of Philadelphia,
John Germiller, MD, PhD, Attending Surgeon, Division of Pediatric Otolaryngology, The Children’s
Hospital of Philadelphia; and Associate Professor of Clinical Otorhinolaryngology/Head and Neck
Surgery, Perelman School of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
Matthew Grady, MD, Fellowship Director, Primary Care Sports Medicine, The Children’s Hospital of
Philadelphia, Assistant Professor of Clinical Pediatrics, Perelman School of Medicine at the University
of Pennsylvania, Philadelphia, Pennsylvania
Lori Handy, MD, MSCE, Attending Physician, Division of Pediatric Infectious Diseases,
Nemours/Alfred I. duPont Hospital for Children, Wilmington, Delaware
Mary Catherine Harris, MD, Professor of Pediatrics, Division of Neonatology, The Children’s Hospital
of Philadelphia, Perelman School of Medicine at the University of Pennsylvania, Philadelphia,
Pennsylvania
Soma Jyonouchi, MD, The Children’s Hospital of Philadelphia, Assistant Professor, Division of Allergy
and Immunology, Philadelphia, Pennsylvania
Amy Kim, MD, Assistant Professor of Clinical Psychiatry, Perelman School of Medicine at the
University of Pennsylvania; Attending Physician, Department of Child and Adolescent Psychiatry and
Behavioral Sciences, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
F. Wickham Kraemer III, MD, Assistant Professor of Anesthesiology and Critical Care, Section Chief,
Acute and Chronic Pain Management, The Children’s Hospital of Philadelphia, Perelman School of
Medicine at the University of Pennsylvania, Department of Anesthesiology and Critical Care,
Javier J. Lasa, MD, Attending Physician, Divisions of Critical Care and Cardiology, Texas Children’s
Hospital, Assistant Professor of Pediatrics, Baylor College of Medicine, Houston, Texas
Leonard J. Levine, MD, Associate Professor of Pediatrics, Drexel University College of Medicine,
Attending Physician, Division of Adolescent Medicine, St. Christopher’s Hospital for Children,
Arul M. Lingappan, MD, Pediatric Anesthesiology Attending, The Children’s Hospital of Philadelphia,
Perelman School of Medicine at the University of Pennsylvania, Department of Anesthesiology and
Critical Care, Philadelphia, Pennsylvania
Vanessa N. Madrigal, MD, Attending Physician, Pediatric Critical Care Medicine, Children’s National
Medical Center, Assistant Professor, Department of Pediatrics, George Washington University,
Washington, Washington DC
Solrun Melkorka Maggadottir, MD, Allergy/Immunology Fellow, The Children’s Hospital of

Petar Mamula, MD, Division of GI, Hepatology & Nutrition, The Children’s Hospital of Philadelphia,
Professor of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, Philadelphia,
Pennsylvania
Maria R. Mascarenhas, MBBS, Section Chief, Nutrition, Division of Gastroenterology, Hepatology and
Nutrition, The Children’s Hospital of Philadelphia, Associate Professor of Pediatrics, Perelman School
of Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
Jamie Merves, MD, Attending Physician, Division of Gastroenterology, Hepatology and Nutrition, The
Children’s Hospital of Philadelphia, Assistant Professor of Clinical Pediatrics, Perelman School of
Medicine at the University of Pennsylvania, Philadelphia, Pennsylvania
Pamela Mudd, MD, Division of Pediatric Otolaryngology, The Children’s Hospital of Philadelphia,
Department of Otorhinolaryngology, Perelman School of Medicine at the University of Pennsylvania,
Michael L. Nance, MD, Professor of Surgery, Perelman School of Medicine at the University of
Pennsylvania, Josephine J. and John M. Templeton, Jr. Chair in Pediatric Trauma, Director of the
Pediatric Trauma Program, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Benjamin R. Oshrine, MD, Division of GI, Hepatology & Nutrition, The Children’s Hospital of
Andrew A. Palladino, MD, Division of Endocrinology and Diabetes, The Children’s Hospital of
Howard B. Panitch, MD, Professor of Pediatrics, Perelman School of Medicine at the University of
Pennsylvania, Director of Clinical Programs, Division of Pulmonary Medicine, The Children’s Hospital
of Philadelphia, Philadelphia, Pennsylvania
Melissa Desai Patel, MD, MPH, Assistant Professor of Pediatrics, Perelman School of Medicine at the
University of Pennsylvania, Medical Director of Sedation Services, Attending Physician, Division of
General Pediatrics, The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania
Annapurna Poduri, MD, MPH, Director, Epilepsy Genetics Program, and Associate in Neurology,
Boston Children’s Hospital; and Associate Professor of Neurology, Harvard Medical School, Cambridge,
Massachusetts
Elisabeth Raab, MD, MPH, Attending Neonatologist, Pediatrix Medical Group, Huntington Memorial
Hospital, Pasadena, California
Rahim Rahemtulla, MD, Clinical Assistant Professor, Department of Child and Adolescent Psychiatry,
New York University School of Medicine; Attending Physician, Lincoln Hospital and Mental Health
Center, Department of Psychiatry, New York, New York
Gita Ram, MD, Assistant Physician, Division of Allergy and Immunology, The Children’s Hospital of
Elaine Ramsay, MD, Rheumatology Fellow, Division of Rheumatology, The Children’s Hospital of
Chitra Ravishankar, MD, Associate Professor of Pediatrics, Division of Cardiology, The Children’s
Hospital of Philadelphia, Perelman School of Medicine at the University of Pennsylvania, Philadelphia,
Pennsylvania
Daniel H. Reirden, MD, AAHIVMS, Associate Professor of Pediatrics and Internal Medicine,
Adolescent Medicine and Infectious Disease; Director of Internal Medicine-Pediatric Residency; and
Medical Director, CHIP Youth Clinic, University of Colorado School of Medicine and Children’s
Hospital Colorado, Denver, Colorado
Christopher B. Renjilian, MD, MBE, Fellow, The Craig-Dalsimer Division of Adolescent Medicine,
The Children’s Hospital of Philadelphia, Philadelphia, Pennsylvania Resident, Pediatrics, The Children’s
Joseph Rossano, MD, MS, FAAP, FAAC, Attending Cardiologist, Cardiac Center and the Cardiac
Intensive Care Unit (CICU), Medical Director, Pediatric Heart Transplant and Heart Failure, Assistant
Professor of Pediatrics, Perelman School of Medicine at the University of Pennsylvania, The Children’s
Hospital of Philadelphia, Division of Cardiology, Philadelphia, Pennsylvania
Rebecca L. Ruebner, MD, MSCE, Attending Physician, Division of Nephrology, The Children’s
Hospital of Philadelphia; Assistant Professor of Pediatrics, Perelman School of Medicine at the
Benjamin Sahn, MD, MS, Assistant Professor of Pediatrics, Hofstra North Shore-LIJ School of
Medicine Division of Pediatric Gastroenterology & Nutrition Steven & Alexandra Cohen Children’s
Medical Center of New York North Shore - Long Island Jewish Health System New Hyde Park, New
York, New York
Margaret Samuels-Kalow, MD, MPhil, Instructor, Division of Emergency, Medicine, Department of

Pediatrics, The Children’s Hospital of Philadelphia, Perelman School of Medicine at the University of
Kara N. Shah, MD, PhD, Director, Division of Dermatology, Cincinnati Children’s Hospital, Associate
Professor of Pediatrics and Dermatology, University of Cincinnati College of Medicine, Cincinnati, Ohio
Renée A. Shellhaas, MD, Assistant Professor, Pediatrics, C.S. Mott Children’s Hospital, University of
Michigan Health System, Ann Arbor, Michigan
Joann Spinale Carlson, MD, Division of Pediatric Nephrology and Hypertension, Rutgers/Robert Wood
Johnson Medical School, New Brunswick, New Jersey
Salwa Sulieman, DO, Assistant Professor of Pediatrics, University of Missouri-Kansas City, Division of
Infectious Diseases, Children’s Mercy Hospital, Kansas City, Missouri
Alysha Taxter, MD, Rheumatology Fellow, Division of Rheumatology, The Children’s Hospital of
Gihan I. Tennekoon, MD, Attending Physician, Division of Neurology, The Children’s Hospital of
Philadelphia; and Professor of Neurology, Perelman School of Medicine at the University of
Christian Turner, MD, Primary Care Sports Medicine Fellow, The Children’s Hospital of Philadelphia,
Jesse D. Vrecenak, MD, Fellow, Division of General and Thoracic Surgery, Department of Surgery, The
Children’s Hospital of Philadelphia, Perelman School of Medicine at the University of Pennsylvania,
Nicole Washington, MD, Pediatric Chief Resident, 2014–2015, The Children’s Hospital of Philadelphia,
Tara L. Wenger, MD, PhD, Assistant Professor, Division of Craniofacial Medicine, Department of
Pediatrics, Seattle Children’s Hospital, Seattle, Washington
Krishna Wood White, MD, MPH, Director, Adolescent Medicine Program, Clinical Assistant Professor
of Pediatrics, Thomas Jefferson University, Nemours/A.I. DuPont Hospital for Children, Wilmington,
Delaware
Char Witmer, MD, MSCE, Attending Physician, Division of Hematology, The Children’s Hospital of
Philadelphia; and Assistant Professor of Pediatrics, Perelman School of Medicine at the University of
Foreword
Having started my training in pediatrics at The Children’s Hospital of Philadelphia, and then continuing
my training and practice at other major academic medical centers, I came to appreciate the premier care
that patients receive when knowledge and dedication come together. When I was a young trainee at
CHOP, a welcomed resource to inpatient care was a series of resident handouts. These were prepared by
senior residents and passed along from one year to the next, each senior class updating and improving on
the work of their predecessors. Twenty-five years after leaving CHOP, I had the privilege to return in a
leadership role for the Department of Pediatrics. Among the many welcomed surprises since my return, I
was delighted to see the valued handouts that had served me so well as a trainee have been developed
into The Philadelphia Guide: Inpatient Pediatrics. The practical information that guided me back then is
now available in this concise and well-organized book. It provides effective management of the lion’s
share of patients admitted to the hospital and is a reliable source for efficient and fact-filled teaching on
rounds.
Increasingly, patient care is evidence-based, often operationalized through clinical pathways. These
pathways may be informed by national committees with broad representation and multidisciplinary input,
or from similar local efforts, institutional experience, and application of the literature. It is in this spirit
that this book was created. The authors and editors have assembled the second edition of The
Philadelphia Guide: Inpatient Pediatrics to carry on the tradition of learning, improving, and then
sharing knowledge that I first encountered as a resident at CHOP. I am especially proud that the authors,
from all across the country, all share a connection to CHOP. They are trainees, young faculty, and more
senior leaders in their fields who enjoy carrying on the practice of life-long learning and advancement of
knowledge. I am confident that this book will serve as an important guide to diagnostic and therapeutic
decisions in the pediatric inpatient setting and a valuable tool for all of us involved in delivering care to
children and adolescents.
Joseph W. St. Geme, III, MD
Physician-In-Chief
The Children’s Hospital of Philadelphia
Chairman, Department of Pediatrics
Perelman School of Medicine, University of Pennsylvania
Preface—Inpatient Pediatrics, 2nd Edition
Care of the hospitalized child has evolved dramatically since publication of the first edition of The
Philadelphia Guide: Inpatient Pediatrics. Conditions that previously required prolonged hospitalization
are now often treated exclusively in the outpatient setting or with only a brief hospitalization. Advances in
medical technology have improved the survival rate of premature infants and those with chronic medical
conditions. Further, changes in healthcare delivery have placed renewed emphasis on value, with an
expectation of better outcomes at lower cost. As a result, the type of physician caring for these patients
has also changed. At many institutions, hospital-based specialists, or “hospitalists,” now provide care for
the majority of patients admitted to general pediatric wards, leading to the evolution of pediatric hospital
medicine as a new specialty.
As we prepared the second edition, Hospital Medicine remained our core focus. We believe that
Inpatient Pediatrics should provide clinicians with the vital information necessary to make management
decisions in the care of hospitalized children. Once again, we were fortunate that over 75 leading experts
in pediatric hospital medicine and pediatric subspecialty care, many with roots at The Children’s
Hospital of Philadelphia, share their collective wisdom by contributing to this book.
Designed to be an invaluable resource on the hospital wards, Inpatient Pediatrics features:
• Practical diagnostic strategies
• Extensive differential diagnosis suggestions
• Up-to-date treatment and management guidelines
• Alphabetical organization within chapters for rapid access
• Structured format with consistent headings throughout
• Bulleted format for efficient and effective presentation of relevant information
• Print and electronic versions to maximize portability and ensure access to information whenever and
wherever necessary
Appendices cover normal vital signs, neonatal codes, and PALS algorithms as well as rapid access to
pediatric dosages for emergency, airway, and rapid sequence intubation medications, and cardioversion.
A formulary was omitted with the understanding that pediatric dosing information is now accessible
through most institutional formularies and widely available mobile apps.
As many clinicians are involved in the care of children, this book is ideal for practitioners of all
levels, from students to attending physicians, physician assistants, advanced practice nurses, pediatric
nurses, and health practitioners from all disciplines involved in the care of the hospitalized child.
The goal of this book is to provide a single reference with sufficient detail to guide diagnostic and
therapeutic decisions for a wide range of conditions. We believe that the consistent format, detailed focus
on diagnosis and management, and comprehensive coverage of topics have accomplished that goal,
enabling you to give the best possible care to your patients. We hope you think so, too.
Samir S. Shah
Lisa B. Zaoutis
Marina Catallozzi
Gary Frank
November 2015
List of Abbreviations
AIN: acute interstitial nephritis

AKI: acute kidney injury
ALCL: anaplastic large cell lymphoma
ALK: anaplastic lymphoma kinase
ALL: acute lymphoblastic leukemia
Alph1-AT: alpha-1 antitrypsin
AMKL: acute megakaryocytic leukemia
AML: acute myeloid leukemia
ANA: antinuclear antibody
ANC: absolute neutrophil count
ANCA: anti-neutrophil cytoplasmic antibody
Anti-SMA: anti-smooth muscle antibody
APGAR: appearance, pulse, grimace, activity, respiration
APML: acute promyelocytic leukemia
ASCA: anti-Saccharomyces cerevisiae antibody
ASD: atrial septal defect
ATN: acute tubular necrosis
ATRA: all-trans retinoic acid
BP: blood pressure
BWS: Beckwith–Wiedemann syndrome
CBD: common bile duct
CCK: cholecystokinin
CD: Crohn’s disease
CGD: chronic granulomatous disease
CHD: congenital heart disease
CHF: congestive heart failure
CINV: chemotherapy-induced nausea vomiting
CML: chronic myelogenous leukemia
CMV: cytomegalovirus
CNS: central nervous system
CRT: cardiac resynchronization therapy
CXR: chest x-ray
DBP: diastolic blood pressure
DISIDA scan: diisopropyl iminodiacetic acid labeled with 99m-technetium
DVT: deep venous thrombosis
EBV: Epstein–Barr virus
ECG: electrocardiogram
ECMO: extracorporeal membrane oxygenation
EPS: extrapyramidal symptoms
ETT: via endotracheal tube
FENa: fractional excretion of sodium
FISH: fluorescence in situ hybridization
GAS: group A streptococcus
GER: gastroesophageal reflux
GERD: gastroesophageal reflux disease
GFR: glomerular filtration rate
GI: gastrointestinal
GN: glomerulonephritis
GNR: gram negative rods
GVHD: graft-versus-host disease
HELLP: hemolysis, elevated liver enzymes, low platelets
HHV6: human herpesvirus 6
HLA: human leukocyte antigen
HLH: hemophagocytic lymphohistiocytosis
HLHS: hypoplastic left heart syndrome
HOCM: hypertrophic obstructive cardiomyopathy
HSCT: hematopoietic stem cell transplantation
HSP: Henoch–Schönlein purpura
HSV: herpes simplex virus
HUS: hemolytic uremic syndrome
IBD: inflammatory bowel disease
IBS: irritable bowel syndrome
IC: indeterminate colitis
ICU: intensive care unit
IM: intramuscular
IN: intranasal
IV: intravenous
JDM: juvenile dermatomyositis
JIA: juvenile idiopathic arthritis
JMML: juvenile myelomonocytic leukemia
LA: left atrium
LDH: lactate dehydrogenase
LES: lower esophageal sphincter
LGBTQ: lesbian, gay, bisexual, transgender, and questioning
LKM: liver-kidney-microsomal
LLSB: left lower sternal border
LSD: D-lysergic acid diethylamide
LV: left ventricle
LVAD: left ventricular assist device
LVNC: left ventricular noncompaction
MAS: Macrophage activation syndrome
MDS: myelodysplastic syndrome
MLL: mixed lineage leukemia
MPGN: membranoproliferative glomerulonephritis
MRS: magnetic resonance spectroscopy
a primary immunodeficiency syndrome caused by genetic mutations in the X-linked
NEMO:
NEMO gene
NHL: non-Hodgkin Lymphoma
NMDA: N-methyl-D-aspartate
NPO: nothing by mouth
NS: nephrotic syndrome
NSAIDs: nonsteroidal anti-inflammatory drugs
PAC: premature atrial contraction
PCA: patient controlled analgesia
PCP: phencyclidine
PDA: patent ductus arteriosus
PDD: pervasive developmental delay
PG: prostaglandin
Pi: protease inhibitor
PICC: peripherally inserted central catheters
PMBCL: primary mediastinal B-cell lymphoma
PNET: peripheral neuroectodermal issue
PO: by mouth
PPI: proton pump inhibitor
PR: per rectum
PRSA: post-streptococcal reactive arthritis
PTLD: post-transplant lymphoproliferative disease
PUCAI: pediatric ulcerative colitis activity index
PUD: peptic ulcer disease
PVC: premature ventricular contraction
PVR: pulmonary vascular resistance
RA: right atrium
RCM: restrictive cardiomyopathy
RTA: renal tubular acidosis
RUQ: right upper quadrant
RV: right ventricle
SaO2: oxygen saturation
SBP: systolic blood pressure
SC: subcutaneous
SCID: severe combined immunodeficiency
SCT: stem cell transplantation
SI: suicidal ideation
SIRS: systemic inflammatory response syndrome
SLA: soluble liver antigen
SLE: systemic lupus erythematosus
SMS: superior mediastinal syndrome
STEC: Shiga toxin-producing Escherichia coli
SVCS: superior vena cava syndrome
SVR: systemic vascular resistance
SVT: supraventricular tachycardia
TAPVR: total anomalous pulmonary venous return
TD: tardive dyskinesia
TGA: transposition of the great arteries
TMD: transient myeloproliferative disorder
TPN: total parenteral nutrition
TTP: thrombotic thrombocytopenic purpura
UAG: urine anion gap
UC: ulcerative colitis
URI: upper respiratory infection
UTI: urinary tract infection
VADs: ventricular assist devices
VIP: vasoactive intestinal peptide
VOD: veno-occlusive disease
VSD: ventricular septal defect
VT: ventricular tachycardia
VZV: varicella zoster virus
WAS: Wiskott–Aldrich syndrome
WBC: white blood cell
WPW: Wolff–Parkinson–White syndrome
XRT: radiotherapy
CHAPTER 1 Adolescent Medicine
Christopher B. Renjilian, MD, MBE

Krishna Wood White, MD, MPH
Leonard J. Levine, MD
ANOREXIA NERVOSA
DSM-V CRITERIA* FOR ANOREXIA NERVOSA ARE SUMMARIZED BELOW
• Restriction of calories compared to requirements which leads to significantly low weight
• Intense fear of gaining weight
• Disturbance in the way in which one’s body weight or shape is experienced
• Restricting type: During the prior 3 months with anorexia nervosa, the person has not achieved weight
loss through being regularly engaged in binge eating or purging behavior (self-induced vomiting, use of
laxatives/diuretics/enemas) but through dieting and excessive exercise
• Binge eating/Purging type: During the prior 3 months with anorexia nervosa, the person has regularly
engaged in binge eating or purging behavior (self-induced vomiting, use of laxatives/diuretics/enemas)
*Note: DSM-V no longer sets a specific percent of ideal body weight but states that “significantly low
weight” is less than is minimally normal or normally expected (for children and adolescents). DSM-V
removes amenorrhea as a criterion for anorexia as it did not apply to males, females on contraceptives, or
pre-menarchal females. Also, patients that meet all of the criteria except amenorrhea have the same
clinical course as those who meet all four criteria.
EPIDEMIOLOGY
• 1% of adolescent females; female:male = 20:1
• Age at presentation ranges from 10 to 25 years
• Increasing incidence in adolescent males, nonwhite populations, and lower socioeconomic groups; more
common among individuals involved in sports or activities where size and body shape impact their
success
• Bimodal age of onset at 14 and 18 years corresponding with life transitions (i.e., puberty, moving from
high school to college or work)
• Mortality rates range from 1.8% to 5.9% (usually because of cardiac complications or suicide)
ETIOLOGY
• Genetic: Increased risk in first-degree relatives with an eating disorder
• Neurotransmitters: Serotonin and its relationship to hunger and satiety
• Psychologic: Theories range from perfectionism, identity conflicts, history of abuse, negative comments
from others about weight or appearance, enmeshed families, and sociocultural influences
CLINICAL MANIFESTATIONS
• Menstrual disorders are the most common presentation
• Frequently, patients do not have complaints, but family members are concerned about significant weight
loss, secondary amenorrhea, dizziness, lack of energy, gastrointestinal complaints (e.g., constipation),
and/or pale skin
• Depending on amount of weight loss, clinical findings can range from normal to findings of orthostasis,
bradycardia, hypothermia, hypotension, dry skin, lanugo hair, thinning hair, brittle nails, peripheral
edema, acrocyanosis, and findings suggestive of purging such as eroded tooth enamel, scars on knuckles,
or parotid enlargement
• External evidence of self-harm, such as scars from cutting on the extremities
DIAGNOSTICS
• Must consider the differential diagnosis for weight loss and exclude malabsorption and catabolic states
• Clinical information is vital. Questions should focus on disordered thinking and behavior. Screening
questions (e.g., SCOFF questionnaire) can be helpful:
Do you make yourself sick because you feel uncomfortably full?
Do you worry you have lost control over how much you eat?
Have you recently lost more than one stone (6.3 kg [14 lb]) in a 3-month period?
Do you believe yourself to be fat when others say you are too thin?
Would you say that food dominates your life?
Give one point for every yes; scores of 2 or more indicate anorexia nervosa or bulimia
• Laboratory studies are not diagnostic of anorexia nervosa. Table 1-1 suggests tests to obtain in the
initial assessment of a patient suspected of having anorexia nervosa. Further tests should be ordered
based on clinical suspicion for other diseases
TABLE 1-1 Laboratory Studies in Anorexia Nervosa

• ECG: Indicated for bradycardia less than 50 bpm to rule out prolonged QTc or dysrhythmias. Low
voltage, ST segment depression, or conduction abnormalities may also be seen
• DEXA: Evaluate bone density in patients who are amenorrheic greater than 6 months
• Imaging: Chest x-ray, brain magnetic resonance imaging, barium enema, and upper gastrointestinal
series with small bowel follow-through should be considered based on clinical concern for other
conditions as an explanation for symptoms
MANAGEMENT
• Indications for inpatient treatment are listed in Table 1-2
TABLE 1-2 Criteria for Hospital Admission for Children, Adolescents, and Young Adults with Anorexia Nervosa
• Interdisciplinary team: Comprised of a physician, dietician, and mental health professional should
generate a coordinated consistent plan of care and be available for team meetings with patient and
family; recent studies highlight importance of family-based therapy
• Fluids/Electrolytes/Nutrition:
Correction of dehydration
Blind weights with the patient wearing only a gown at same time and on the same scale each day are
best. Expected rate of weight gain is 0.9–1.4 kg (2–3 lb) per week
• Refeeding syndrome: Constellation of cardiac, neurologic, and hematologic complications as phosphate
shifts from extracellular to intracellular compartments in patients with total body phosphate depletion
secondary to malnutrition
Pathophysiology: Catabolic→anabolic state→energy used as adenosine triphosphate
(ATP)→phosphorus→erythrocyte 2,3 diphosphoglycerate (2,3 DPG)→tissue hypoxia
Risk factors: Moderate to severe anorexia (less than 10% below ideal body weight)
Prevention: Slow refeeding with or without phosphorous supplementation (in patients with normal
renal function)
Monitoring: Telemetry, frequent vital signs, and electrolytes especially phosphorus, potassium, and
magnesium
Clinical manifestations: Cardiac arrest, delirium, congestive heart failure
• Cardiovascular: Telemetry for patients with significant bradycardia, dysrhythmias, and electrolyte
abnormalities until resolution of conditions
• Gastrointestinal: Control of constipation with stool softeners (avoid laxatives). Metoclopramide may
be helpful with bloating and constipation secondary to delayed gastric emptying
• Endocrinology:
Osteopenia: Weight gain is best therapy; a multivitamin with 400 IU of vitamin D and 1200–1500
mg/day of elemental calcium is recommended. Estrogen or estrogen/progestin replacement therapy
should be considered
Amenorrhea: Menses will resume with adequate weight gain and improved nutritional status; no
hormonal therapy required
• Psychiatry:
Safety and compliance: 1:1 observation by qualified staff with experience with eating disorders is
required, especially in the beginning of treatment
Mental status abnormalities improve with correction of malnourished state. Most interventions should
begin after patient is medically stable
Psychotherapy: Cognitive behavioral therapy is the most effective form of therapy
Pharmacotherapy: Indicated only for treatment of comorbid disorders (i.e., depression, obsessive
compulsive disorder). There is no FDA-approved drug for treatment of anorexia nervosa
ABNORMAL UTERINE BLEEDING

Bleeding from the uterine endometrium unrelated to an anatomic lesion. Abnormal bleeding can be
identified as menstrual cycles that occur less than 21 or more than 45 days apart, bleeding lasting
more than 8 days, or blood loss greater than 80 mL/cycle.
ETIOLOGY
• Anovulatory cycles (over 75% of cases)
Commonly occurs in first few years after menarche
Hypothalamic-pituitary-ovarian axis not fully mature→ovarian estrogen production doesn’t
consistently reach level needed to trigger luteinizing hormone (LH) surge→failure to ovulate each
month
No ovulation→estrogen unopposed because no corpus luteum or progesterone
secretion→continuously stimulated endometrium without stromal support→lining outgrows blood
supply→endometrium breaks down with variable shedding, necrosis, and irregular bleeding
DIFFERENTIAL DIAGNOSIS
• Anovulatory cycles: Immaturity of hypothalamic-pituitary-ovarian (HPO) axis
• Pregnancy: Ectopic, threatened or incomplete abortion, placenta previa, hydatidiform mole
• Sexually transmitted infection (STI): vaginitis (e.g., Trichomonas), cervicitis (e.g., gonorrhea,
Chlamydia), pelvic inflammatory disease (i.e., endometritis)
• Endocrinopathy causing anovulation: Thyroid disease (hypothyroidism, hyperthyroidism),
hyperprolactinemia (e.g., prolactinoma, dopamine antagonists), adrenal disorders (e.g., Addison
disease, Cushing disease), polycystic ovary syndrome (PCOS), or other disorder of androgen excess
• Systemic disease causing anovulation: Chronic renal failure, systemic lupus erythematosus
• Hematologic disorder: Thrombocytopenia (e.g., idiopathic thrombocytopenic purpura, leukemia),
defects in platelet function (e.g., von Willebrand disease), coagulation disorders
• Medications: Direct effect on hemostasis (e.g., warfarin, chemotherapeutic agents), indirect effect by
altering hormone levels (e.g., breakthrough bleeding with hormonal contraception)
• Trauma: Laceration to vaginal mucosa or cervix
• Foreign body: Retained tampon or condom
• Endometriosis
• Structural abnormalities (rare): Uterine polyps, myoma, cervical hemangioma, arteriovenous
malformation, neoplasm
• Bleeding pattern can help guide evaluation
Consider hematologic disorder if normal cyclic intervals with increased bleeding during each cycle,
especially if occurs since menarche
Normal intervals with bleeding between cycles may suggest infection pregnancy, or foreign body
Endocrinopathy, anovulatory cycles, and medication effects are suggested by lack of any cycle
regularity
• Physical exam may be unremarkable, especially if due to anovulatory cycles
• May have evidence of anemia (e.g., pallor, lethargy) or hypovolemia, depending on amount of blood
loss
• Signs and symptoms will reflect underlying etiology. For example:
Prolactinoma: Headaches, visual changes, nipple discharge
Thyroid disease: Diarrhea or constipation, palpitations, skin changes, heat or cold intolerance
Bleeding disorder: Epistaxis and gingival bleeding, easy bruising
Sexually transmitted infection: Fever, abdominal pain, vaginal discharge, dysuria
Retained foreign body: Foul smelling odor and discharge
PCOS: Acne, hirsutism, acanthosis nigricans
DIAGNOSTICS
Clinical Assessment
• Obtain menstrual history: Age of menarche, interval between menses, duration of flow, frequency of
tampon/pad changes, with or without cramping (cramping often is a marker for ovulatory cycles due to
progesterone secretion), last menstrual period
• Obtain sexual history in confidential manner
• Ask about symptoms of anemia (e.g., dizziness or lightheadedness)
• Assess hemodynamic stability
• Special attention to: nutritional status, visual fields (i.e., pituitary lesions), thyroid size, breast exam
(for galactorrhea), evidence of androgen excess (hirsutism, acne), ecchymoses or petechiae, Sexual
Maturity Rating
• Pelvic exam if ever been sexually active (including bimanual exam) or to visualize source of bleeding
Studies
• Pregnancy test: On every adolescent female presenting with vaginal bleeding
• Complete blood count with differential
• STI testing: Wet prep for white blood cells or Trichomonas, nucleic acid amplification testing for N.
gonorrhea and C. trachomatis (urine or cervical swabs)
• PT/PTT
• Depending on history, may also consider von Willebrand studies, thyroid-stimulating hormone, prolactin
level, LH, follicle-stimulating hormone, serum androgens (e.g., free testosterone,
dehydroepiandrosterone-S, androstenedione)
• Pelvic ultrasound (if mass palpated on bimanual exam or if concerned for structural abnormalities)
MANAGEMENT
• Depends on severity of bleeding and degree of anemia
• Hormonal therapy is the mainstay of treatment: Usually oral contraceptive pill (OCP) used to provide
hemostasis (estrogen) and to stabilize the endometrium (progesterone). Note: Must ask about
contraindications to estrogen use specified in the Center for Disease Control’s Medical Eligibility
Criteria for Contraceptive Use (2012) and if category 3 or 4 use progesterone only
(http://www.cdc.gov/reproductivehealth/UnintendedPregnancy/USMEC.htm)
• Address underlying pathology (e.g., infection, endocrinopathy)
• Adjunct management: Menstrual diaries, iron supplementation, NSAIDs
• Mild dysfunctional uterine bleeding (DUB) (hemoglobin greater than 12 g/dL, no active bleeding)
Prolonged menses or shortened cycles
Reassurance and observation
• Moderate DUB (hemoglobin 10–12 WITHOUT active bleeding): Combined OCP with 30–35 μg
ethinyl estradiol (EE) plus progestin
One pill daily for 6 months, then reevaluate
If estrogen contraindicated, use oral progesterone only: Medroxyprogesterone acetate 10 mg orally for
10 days, repeat monthly
• Moderate DUB (hemoglobin 10–12 WITH active bleeding)
Combined OCP with 30–35 μg EE plus progestin
One pill twice a day until bleeding stops, then once daily
• Severe DUB (hemoglobin less than 10 WITH active bleeding)
Combined OCP with higher dose of estrogen (50 μg EE (preferred) or 35 μg EE if not available)
One pill four times daily for 4 days, then three times daily for 3 days, then twice daily for 2 days, then
once daily
If not tolerating oral medications or if hemodynamically unstable, can use high-dose conjugated
estrogen (Premarin) given intravenously every 4 hours up to 24 hours to control bleeding, then add
oral progesterone or switch to OCP as soon as possible to avoid heavy estrogen withdrawal bleed
Give antiemetics when estrogen given in multiple doses per day. Table 1-2 lists antiemetics
Blood transfusions are rarely necessary in the management of AUB
May require hospitalization if actively bleeding; requires close outpatient follow-up once stabilized
EMERGENCY CONTRACEPTION
Emergency contraception is a method of contraception where a drug or intrauterine device is used
after unprotected intercourse.
INDICATIONS
• Pregnancy prevention following unprotected vaginal intercourse, contraceptive failure (e.g., broken
condom, missed or late doses of hormonal contraceptives), sexual assault
• Most effective within 72 hours or less since aforementioned event; additional data supports
effectiveness within 120 hours
OPTIONS
• Three general classes of hormonal emergency contraception (EC) are currently approved for use in the
United States (see Table 1-3):
TABLE 1-3 Emergency Contraception Regimens *
Progestin-only oral regimens including levonorgestrel (e.g., Plan B, Next Choice)

Novel progestin receptor agonist/antagonist oral regimens including ulipristal (Ella)
Combination estrogen and progestin oral regimens using alternative dosing of combination OCPs, also
known as the Yuzpe method
• Nonhormonal methods of EC are currently limited to insertion of the copper intrauterine device (IUD).
Copper IUD is currently the most effective method of EC
CONTRAINDICATIONS
• All regimens: Pregnancy; hypersensitivity to drug components; undiagnosed vaginal bleeding
• Method-specific contraindications
Progestin-only oral regimens: No contraindications
Progestin receptor agonist/antagonist: Unclear if can be used safely in pregnancy
Combination OCPs: Same as above, but also include contraindications to estrogen exposure (e.g.,
history of thrombophilia, thromboembolic disease, migraine with aura or neurologic changes; refer to
Center for Disease Control’s Medical Eligibility Criteria for Contraceptive Use [2012])
Copper IUD: Abnormal genital tract anatomy, infection at the time of insertion
MECHANISM OF ACTION
• Inhibit or delay ovulation
• Disrupt follicular development
• Impairment of corpus luteum
• Create unfavorable environment for sperm function
• Copper IUD also alters endometrium, likely interfering with implantation; unclear if such alteration also
occurs with hormonal emergency contraception
ADVERSE EFFECTS
• Occur mostly with combined EC (containing estrogen): Nausea/vomiting; dizziness; fatigue; breast
tenderness, altered menstrual cycle
• Copper IUD may cause cramping or increased menstrual flow; also low risk of uterine perforation upon
insertion
SAFETY
• Short course of therapy leads to few complications
ANTICIPATORY GUIDANCE
• Nausea/vomiting: Common in combined regimen; can be reduced by pretreatment with oral anti-emetic
(e.g., metoclopramide 10 mg or meclizine 25–50 mg) given 1 hour before EC
• Effect on menstrual cycle: Next menses may be early or late but should come within 21 days
• Effect on pregnancy: Levonorgestrel and combined OCP regimens do not affect established pregnancy
or lead to birth anomalies; data on progestin receptor agonist/antagonist and pregnancy still unclear
• Follow-up: Not required but recommended for contraceptive counseling and/or pregnancy testing if no
menses in 21 days
PELVIC INFLAMMATORY DISEASE

Clinical condition referring to infection and inflammation involving the female upper genital tract
including endometritis, salpingitis, tubo-ovarian abscess, and pelvic peritonitis. Pelvic inflammatory
disease (PID) is a common and morbid complication of some sexually transmitted infections (STIs),
in particular Chlamydia trachomatis (most commonly) and Neisseria gonorrhoeae.
EPIDEMIOLOGY
• Affects 8% of US women during reproductive years
• Approximately 1 million US women are diagnosed with PID each year. The true incidence of PID and
its complications have been difficult to ascertain because no national surveillance or reporting
requirements exist, national estimates are limited by insensitive clinical diagnosis criteria, and
definitive diagnosis can be challenging
• Major cause of other reproductive health problems including infertility, ectopic pregnancy, abscess
formation, and chronic pelvic pain
• Risk factors for PID include adolescence, history of PID, current or past infection with gonorrhea or
chlamydia, male partner with gonorrhea or chlamydia, multiple partners or partner with multiple
partners, douching, IUD insertion with previous 3 weeks, bacterial vaginosis, low socioeconomic status
(may be surrogate marker for decreased access to care)
• Sexually active women younger than 25 years old are most at risk because the immature cervix (i.e.,
cervical ectopy) is more likely to be infected with an STI
ETIOLOGY
• Microorganisms ascend from the lower genital tract (cervix) to infect the upper genital tract (uterus,
fallopian tubes, etc.)
• Most cases of PID are considered to be polymicrobial
• C. trachomatis and N. gonorrhoeae are the most commonly implicated organisms
• Several microorganisms that comprise the vaginal flora (anaerobes, Gardnerella vaginalis,
Haemophilus influenzae, Streptococcus agalactiae, enteric gram-negative organisms) and other
pathogens (genital mycoplasmas, cytomegalovirus, and Ureaplasma urealyticum) have also been
associated with PID
• Pathogenesis is a complicated and poorly understood process involving interactions between genetics,
immunology, and bacterial virulence factors
• Symptoms can range from none to severe
• Lower abdominal pain is the most common presentation
• Other symptoms may include fever, abnormal vaginal discharge, dyspareunia, dysuria, DUB, right upper
quadrant pain (consistent with perihepatitis or Fitz–Hugh–Curtis syndrome secondary to capsular
inflammation)
DIAGNOSTICS
• The clinical diagnosis of acute PID is imprecise. The most common clinical presentations (e.g., lower
abdominal pain) are nonspecific, but the use of diagnostic criteria to increase specificity has a
significant impact on sensitivity. Because of the high risk of adverse outcomes with untreated PID, it is
recommended that health care providers maintain a low threshold for the diagnosis of PID and err on the
side of overtreatment
• Minimum criteria in women with lower abdominal pain: Uterine tenderness, adnexal tenderness, or
cervical motion tenderness on bimanual examination
• Additional criteria to increase specificity: WBCs on vaginal wet preparation, abnormal cervical or
vaginal mucopurulent discharge, temperature (oral) greater than 38.3°C, elevated erythrocyte
sedimentation rate or C-reactive protein, laboratory documentation of infection with C. trachomatis or
N. gonorrhoeae
• PID is less likely if no WBCs are found on the wet preparation of the vaginal secretions
• Most specific criteria for the diagnosis of PID include: Endometrial biopsy with evidence of
endometritis, transvaginal ultrasound or MRI demonstrating thickened fallopian tubes or tubo-ovarian
complex/abscess, and laparoscopic abnormalities consistent with PID
• Laparoscopy is the gold standard, but is not frequently warranted
MANAGEMENT
• Regardless of laboratory results, treatment for PID must include coverage of C. trachomatis, N.
gonorrhoeae, anaerobes, gram-negative organisms, and streptococci
• Because early treatment is an important part of the strategy to prevent adverse outcomes from PID, many
clinical situations may warrant empiric therapy even while an evaluation for other causes of the
presenting illness is still underway
• Criteria for hospitalization: Pregnancy; poor clinical response to oral therapy; failure to follow or
tolerate outpatient oral therapy; severe illness evidenced by nausea, vomiting, or high fever; tubo-
ovarian abscess (TOA); inability to rule out a surgical abdomen (e.g., appendicitis). Note that
adolescence is no longer a criterion for hospitalization
• Parenteral regimens (adapted from the CDC STD treatment guidelines):
Regimen A: Cefotetan 2 g IV every 12 hours OR cefoxitin 2 g IV every 6 hours PLUS doxycycline 100
mg orally (preferable because of pain with infusion and same bioavailability) or IV every 12 hours;
discontinue IV therapy 24 hours after clinical improvement and complete total of 14 days of
doxycycline; for TOA, can add clindamycin or metronidazole for increased anaerobic coverage
Regimen B: Clindamycin 900 mg IV every 8 hours PLUS gentamycin loading dose IV or IM (2 mg/kg
of body weight) followed by a maintenance dose (1.5 mg/kg) every 8 hours; discontinue IV therapy 24
hours after clinical improvement and complete total of 14 days of doxycycline 100 mg orally twice a
day or clindamycin 450 mg orally four times a day (clindamycin has better anaerobic coverage for a
TOA)
Alternative parenteral regimens exist but have not been as well studied
• Outpatient regimens (adapted from the CDC STD treatment guidelines):
Ceftriaxone 250 mg IM in a single dose OR cefoxitin 2 g IM in a single dose (given with probenecid 1
g orally) OR other parenteral third-generation cephalosporin (ceftizoxime or cefotaxime) PLUS
doxycycline 100 mg orally twice a day for 14 days
Additional anaerobic coverage may be provided by adding metronidazole 500 mg orally twice a day
for 14 days to the above regimen
Alternative oral regimens using fluoroquinolones are no longer recommended due to changing
resistance patterns for N. gonorrhoeae. However, if parenteral cephalosporin therapy is not feasible,
use of fluoroquinolones (levofloxacin 500 mg orally once daily or ofloxacin 400 mg twice daily for
14 days) can be considered low community prevalence and individual risk for gonorrhea
Expect clinical improvement within 3 days of initiating outpatient treatment; if no improvement,
patient may require hospitalization, additional testing, or surgical intervention
• Partners who have had sexual contact with the patient during the 60 days before symptoms occurred
should be treated empirically for C. trachomatis and N. gonorrhoeae
• Instruct patients to abstain from sexual intercourse until patient and current partner have both completed
treatment regimen and are free from symptoms
• All women diagnosed with PID should be offered HIV testing at the time of diagnosis
• Repeat screening of all women who have been diagnosed with chlamydia or gonorrhea is recommended
3–6 months after treatment
• Prevent PID by screening high-risk women, treating any suspected PID, avoiding douching, treating
bacterial vaginosis (because of the association with PID), and promoting condom use
CHAPTER 2 Allergy and Asthma
Irene Fung, MD
Solrun Melkorka Maggadottir, MD
Terri Brown-Whitehorn, MD
ANAPHYLAXIS
Anaphylaxis is an acute, potentially life-threatening systemic allergic reaction. It is most commonly
triggered by interaction of an allergen with specific IgE antibody bound to mast cells and basophils
leading to cell activation and mediator release. Non-IgE-mediated direct mast cell degranulation
results in mediator release.
EPIDEMIOLOGY
• Lifetime prevalence for all triggers is 0.05–2%
• Food is the most common cause of anaphylaxis, affecting up to 8% of young children and 3–4% of adults
• Drugs are the second most common cause of anaphylaxis
• Anaphylaxis leads to 500–1000 deaths per year in the United States
ETIOLOGY
• Major causes are food (milk, egg, soy, wheat, peanut, tree nut, fish, and shellfish); medications
(antibiotics, aspirin, nonsteroidal anti-inflammatory drugs (NSAIDs), biologics, chemotherapeutics,
muscle relaxants, blood products, radiocontrast media); latex; insect stings (especially bees and
wasps); and allergy immunotherapy
• Rare causes include exercise-induced and idiopathic forms
• Other causes of shock (hypovolemic, cardiogenic, and septic), myocardial infarction, pulmonary
embolism, status asthmaticus, pneumothorax, vasovagal reaction, serum sickness, hereditary
angioedema, scombroid poisoning, carcinoid syndrome, pheochromocytoma, and underlying systemic
mastocytosis (which increases risk of anaphylaxis)
PATHOPHYSIOLOGY
• Previous exposure to an allergen (antigen) leads to allergen-specific IgE antibody production. IgE binds
to the surface of mast cells and basophils. Upon subsequent exposure, the antigen binds cell-bound IgE,
triggering cell activation and degranulation. At times, there is no known prior allergen exposure and
reaction occurs on first known exposure
• Mediators involved include histamine, arachidonic acid derivatives (prostaglandins and leukotrienes),
tryptase, bradykinin, and platelet-activating factor. These mediators cause smooth muscle spasm
(bronchi, coronary arteries, and GI tract), increased vascular permeability, vasodilation, and
complement activation. Patients therefore develop urticaria, angioedema, wheezing, emesis, diarrhea,
and hypotension
• Nonimmunologic (previously known as anaphylactoid) reactions result from non-IgE-mediated
degranulation of mast cells and basophils. This can occur with radiocontrast media, NSAIDs, opiates,
and other agents
HISTORY
• Exposure to a known allergen and/or prior history of anaphylaxis is helpful but not always present
• Onset is typically within 30 minutes from exposure to allergens. Symptoms typically progress very
rapidly. At times, reactions may occur up to 2 hours post exposure
• When treated, symptoms usually resolve within a few hours. However, biphasic responses can occur in
up to 20% of cases with recurrence of symptoms 8–10 hours later
• Cutaneous (80–90% of patients): Urticaria, pruritus, flushing, and angioedema. Patients with severe
manifestation of anaphylaxis do not always present with skin findings
• Respiratory (60% of patients): Lower airway symptoms include wheezing, cough, stridor, chest
tightness, and dyspnea. Upper airway symptoms include: sneezing, congestion/rhinorrhea, dysphonia,
laryngeal edema (drooling), and hoarseness
• Gastrointestinal (45% of patients): Nausea, vomiting, abdominal pain, diarrhea
• Cardiovascular (45% of patients): Chest pain, palpitations, tachycardia or bradycardia, dysrhythmia,
hypotension, shock, cardiac arrest
• CNS (15% of patients): Feeling of “impending doom,” anxiety, headache, confusion, and/or behavior
changes. In younger children, this may manifest as irritability, fatigue, or cessation of play
• Anaphylaxis can progress within minutes to shock, arrhythmia, and cardiac arrest. Death is most often
from upper and/or lower airway obstruction or cardiovascular collapse
DIAGNOSTIC TESTING
• Diagnosis is clinical and early intervention is life-saving. Treatment should never be withheld while
awaiting laboratory/imaging results
• Plasma tryptase level is elevated if obtained <4 hours of start of symptoms. Tryptase is often normal in
food-induced anaphylaxis
• ECG may show dysrhythmia, ischemic changes, or signs of myocardial infarction and cardiac enzymes
can be elevated
MANAGEMENT
First Line
• ABCs, airway management as needed, supplemental oxygen
• Epinephrine 1:1000, 0.01 mL/kg IM per dose (maximum 0.5 mL per dose) or epinephrine auto-injector;
repeat in 5–15 minutes as needed. Auto-injectors are recommended to decrease risk of error. Administer
epinephrine IM as soon as anaphylaxis is recognized
• Isotonic intravenous fluid resuscitation for hypotension, progressing to volume expanders and/or
vasoactive infusions if inadequate response to epinephrine IM
• Trendelenburg position
Second Line
• Diphenhydramine liquid (H1-antihistamine) 1 mg/kg IV/PO (maximum 50 mg per dose); every 6 hours
(maximum 300 mg/day) OR Cetirizine liquid (H2-antihistamine) daily
• Nebulized albuterol (β-adrenergic agonist) 2.5–5 mg/3 mL for wheezing/chest tightness if not resolved
after epinephrine administration
• Ranitidine (H2-antihistamine) 1 mg/kg IV/PO (maximum 50 mg per dose); every 6 hours (maximum 300
mg/day)
• Hydrocortisone 2 mg/kg IV (maximum 60 mg) once, then 1 mg/kg IV every 6 hours. Alternatives:
methylprednisolone 1–2 mg/kg IV, then 1 mg/kg/dose every 6 hours; or oral prednisone 2 mg/kg once
then 1 mg/kg/dose (maximum 60 mg). There is no evidence to support glucocorticoid treatment beyond
the acute setting
• If patient is taking a β-agonist medication and symptoms not responsive to epinephrine IM consider
giving glucagon
• There is no definitive length of time for therapy. If a patient is being discharged from the hospital, 24
hours of antihistamines and oral steroids should be sufficient. However, if a patient is admitted to the
hospital to manage a severe reaction, it is reasonable to continue therapy at least until symptoms have
completely resolved
HOSPITAL ADMISSIONS
• Admissions to the hospital for observation should include patients with one or more of the following:
Current severe reaction with hypotension or need for >1 dose of epinephrine
History of severe reaction or biphasic reaction
History of severe asthma or in a current asthma exacerbation
FOLLOW UP
• Patients that do not require hospitalization should be observed at least 8 hours
• Upon discharge
Prescribe an epinephrine auto-injector and train patient/caregivers in its proper use
Develop an anaphylaxis action plan and review with patient/caregivers
Educate patient/family around allergen avoidance if an allergen has been identified
List identified allergen in the medical record
Recommend a medical alert bracelet/necklace
Make a referral for an allergy follow-up appointment
ANGIOEDEMA AND URTICARIA

Urticaria refers to transient, raised, pruritic, erythematous, blanching skin lesions. Angioedema is a
transient, often asymmetric swelling in the deep dermis and subcutaneous or submucosal tissues
with little or no pruritus. Angioedema and urticaria often occur together. A hereditary form of
isolated angioedema also exists.
EPIDEMIOLOGY
• Acute urticaria/angioedema, lasting <6 weeks, is seen in up to 20% of the population
• Chronic urticaria/angioedema, lasting >6 weeks, is seen in 0.5% of the population
ETIOLOGY
Acute Urticaria/Angioedema
• Causes of acute urticaria/angioedema include infections (most often viral, but has been associated with
parasites and certain bacteria), foods, contact reaction, environmental allergen exposure (dog, rolling in
grass), medications (NSAID, aspirin, angiotensin converting enzyme [ACE] inhibitors), insect stings,
activities which increase body temperature (cholinergic), and physical triggers (cold, heat, water,
vibration, and sunlight)
Chronic Urticaria and Angioedema
• A specific cause of chronic urticaria and angioedema is rarely found, especially in pediatrics. Rare
causes include underlying autoimmune urticaria, malignancy, or mast cell disease, such as urticaria
pigmentosa or systemic mastocytosis
PATHOPHYSIOLOGY
• IgE-mediated: Previous allergen (antigen) exposure leads to production of allergen-specific IgE
antibody. IgE binds to surface of mast cells and basophils. Upon subsequent exposure, the antigen binds
cell-bound IgE, leading to cell activation and degranulation, resulting in urticaria and/or angioedema
• Non-IgE-mediated: Nonspecific activation and degranulation of mast cells and/or basophils. Triggers
are physical stimuli (e.g., cold, heat, pressure, vibration, water, sunlight), complement factors (e.g., C3a,
C4a, and C5a), and some medications (e.g., NSAIDs, opiates)
• Autoimmune urticaria: Chronic idiopathic urticaria is a diagnosis of exclusion. In 30–40% of cases an
auto-antibody against the IgE receptor on mast cells and basophils is identified. Rarely, anti-IgE
antibodies are demonstrated. Thyroid auto-antibodies can be seen but only have value in the context of
abnormal thyroid hormone levels
• Viral exanthem, contact dermatitis, papule urticaria, erythema multiforme, urticarial vasculitis, and
systemic lupus erythematosus (SLE)
CLINICAL MANIFESTATION
• Individual urticarial lesions are transient lasting <2–3 hours, resolve, and reappear in another area.
Each individual lesion does not last >24 hours. Dermatographism may be seen when stroking of skin
leads to linear wheals (occurs in 2–5% of population)
DIAGNOSTICS
• Diagnosis is clinical
• Allergy testing for acute urticaria is useful if a specific food or environmental trigger is suspected based
on history. If hives last longer than 24 hours, a “hidden” food allergy is unlikely
• Extensive studies to determine infectious etiology are not often recommended as they do not typically
change management
• Consider a skin biopsy and dermatology referral when individual urticarial lesions persist >24 hours or
are atypical in appearance
• Laboratory workup should be considered for chronic urticaria if there are additional concerning
symptoms (e.g., joint pain/swelling, fatigue, fever, weight loss) that may be suggestive of autoimmune,
myeloproliferative, oncologic, endocrine or vasculitis disorder or a family history of angioedema
MANAGEMENT
• If a trigger is identified, avoidance is advised
• Acute cases usually self-resolve. Treatment is aimed at decreasing pruritus and providing comfort.
First- or second-generation (non-sedating) antihistamines (e.g., cetirizine, fexofenadine) are used for
primary management. First-generation antihistamines may cause sedation and do not last as long. If
symptoms are not well controlled, high-dose non-sedating antihistamines are used in combination with
H2 antihistamines (e.g., ranitidine). If symptoms recur after antihistamine administration, scheduled
dosing of antihistamines for 2-5 days may be considered
• In chronic urticaria additional medications may be considered, including leukotriene-receptor
antagonists (e.g., montelukast), biologics (e.g., omalizumab), alternative anti-inflammatory medications
(e.g., sulfasalazine, dapsone), or immunosuppressive medications (e.g., cyclosporine, tacrolimus)
• Glucocorticoids can reduce symptoms; however, they are not recommended long term as acute
worsening of symptoms may occur when stopped
• Cyproheptadine is useful in cold-induced urticaria
• Initial acute urticaria may progress to anaphylaxis and epinephrine would be warranted. Observation for
a few hours may be indicated in select cases
ANGIOEDEMA—HEREDITARY FORMS
EPIDEMIOLOGY
• Hereditary angioedema (HAE) is a rare disease, accounting for about 2% of angioedema cases. Its
prevalence is about 1/10,000–1/50,000
• Autosomal dominant inheritance. However, family history can be negative
ETIOLOGY
• Type I (85%): Low or absent the protein C1-inhibitor (INH)
• Type II (15%): Normal/high levels of C1-INH but the protein is nonfunctioning
• Type III: Rare, more severe, and more common in women. Underlying mediator remains unidentified,
but has been associated with estrogen and coagulation factor XII mutations. Level and function of C1-
INH may be normal
PATHOPHYSIOLOGY
• Without proper levels or function of C1-INH, there is unopposed activation of the first component of the
classical complement pathway. Angioedema occurs due to formation of bradykinin and complement
factors
• Acquired forms exist where a lymphoproliferative disorder leads to production of a monoclonal
antibody that neutralizes existing C1-INH
• Allergic reactions, malignancy, allergic urticaria/angioedema, rheumatologic disease, ACE-inhibitor-
induced angioedema
• Angioedema, without urticaria, lasting 1–4 days
• A prodromal reticular rash may present prior to onset
• Affected areas include the skin and mucous membranes, larynx, and bowel wall
• Episodes are often spontaneous but known triggers include trauma, surgery (including dental work),
emotional stress, infection, exogenous estrogen, and menstruation
DIAGNOSTICS
• Serum C4 level is the best screening test and is low due to consumption. The sample should be placed
on ice, otherwise complement levels can be falsely low
• C1-INH level and function can also be measured and can differentiate among the forms of HAE
MANAGEMENT
Acute Treatment
• Plasma-derived C1-INH (Berinert®)
• Recombinant kallikrein inhibitor (Ecallintide®), for patients >16 years of age
• Recombinant bradykinin-2 receptor inhibitor (Icatibant®), for patients >18 years of age
• If the above are not available, consider fresh frozen plasma (FFP) as it contains C1-INH
• Aminocaproic acid and tranexamic acid can be useful but take hours to exert an effect
• Intravenous fluids and pain medications (perhaps avoid opiates, which can cause nonimmune-mediated
mast cell degranulation)
Chronic/Prophylactic Treatment
• Androgens (danazol or stanozolol); increase hepatic C1-INH synthesis
• Plasma-derived C1-INH (Cinryze®) infusions every 3–4 days
Short-Term Prophylaxis Prior to Surgery/Trauma
• Fresh frozen plasma (FFP) the night prior to or on the day of surgery
• Plasma-derived C1-INH on the day of surgery
• Androgen medication started 3–4 days prior to surgery
DRUG ALLERGY
CLASSIFICATION
• Modified Gel-Coombs Classification of Hypersensitivity reactions (Table 2-1)
TABLE 2-1 Classification of Hypersensitivity Reactions

• Nonimmunologic-mediated (pseudoallergic) reactions: Due to nonimmune degranulation of mast cells
and basophils (e.g., vancomycin, radiocontrast dye, opiates, NSAID-induced urticaria)
HISTORY
• Hives, angioedema, and anaphylaxis-type symptoms occurring within minutes to hours suggest Type I
hypersensitivity
• Cough within 10 days of drug administration (e.g., nitrofurantoin) with peripheral eosinophilia and
migratory infiltrates suggests pulmonary drug hypersensitivity
• Maculopapular exanthem days after drug administration (e.g., amoxicillin) suggests a T-cell-mediated
reaction
• Skin reaction always occurring in the same area suggests a fixed drug eruption
• Lichenification/eczema occurring 1–3 days after drug administration (e.g., hydrochlorothiazide) suggests
photo-allergic reaction
• Fine pustules, fever, and neutrophilia occurring after days of drug administration suggest acute
generalized exanthematous pustulosis (AGEP)
• Rash and fever with lymphadenopathy, arthralgia, gastrointestinal symptoms, and proteinuria occurring
after 1–3 weeks after drug administration suggest serum sickness or serum sickness-like reaction
• Rash and fever with eosinophilia, facial edema, and organ involvement (e.g., liver, kidney, lymph
nodes) 2–8 weeks after drug administration suggest drug reaction with eosinophilia and systemic
symptoms (DRESS)
• Mucosal erosion, target lesions, epidermal necrosis, and multi-organ involvement occurring days to
weeks after drug administration suggest Stevens–Johnson Syndrome/Toxic Epidermal Necrolysis
(SJS/TEN)
RISK FACTORS FOR DRUG ALLERGY
• Host factors include patient’s genetics, history of prior allergic reaction, underlying concomitant
diseases (e.g., HIV, cystic fibrosis), and female sex
• Drug factors include high dose, repetitive courses, large molecular weight of drug, and intravenous
administration
DIAGNOSTICS
• Serum tryptase
High positive predictive value (PPV) but low negative predictive value (NPV) in peri-operative
anaphylaxis
• Skin-prick testing and specific IgE testing:
For patients who have reaction to penicillin, skin testing is available
Skin testing to other drugs is not validated but may be helpful
Neither skin nor specific IgE tests are diagnostic for cytotoxic, immune-complex, or cell-mediated
drug-induced allergic reactions
MANAGEMENT
• Stop the medication. If anaphylaxis occurs, follow treatment as outlined in Anaphylaxis section
• Drug avoidance
• Drug desensitization is used when there is history of immediate reaction, there are no alternative drugs,
and the drug is medically necessary. This is best performed by an allergist in a critical care setting as
the patient may develop anaphylaxis
COMMONLY IMPLICATED DRUGS

• Antibiotics
Penicillin can cause all types of reactions, from Type I to Type IV
Sulfa antibiotics
The majority of reactions are cytotoxic, although 30% of reactions are Type I
Patients with HIV have a higher risk of reacting to sulfonamides
• Chemotherapeutics
Type I reactions are reported for almost all commonly used agents, and range from mild skin reactions
to severe anaphylaxis
Paclitaxel and docetaxel produce non-IgE-mediated (anaphylactoid) reactions in up to 42% of patients
on first administration, but rarely with subsequent cycles
Platinum compounds (cisplatin, carboplatin) can produce Type I reactions
• Asparaginase can produce Type I and pseudo-allergic reactions
• Local anesthetics
Allergy testing is available
• Muscle relaxants
Can cause an IgE or pseudo-allergic reaction
• Natural Rubber Latex (NRL)
High-risk groups include those with history of multiple surgeries (especially genitourinary and
abdominal surgery), and those with occupations where latex gloves are frequently used
Positive skin-prick test to a reliable crude NRL extract is more sensitive than specific IgE to latex to
confirm diagnosis
• Nonsteroidal anti-inflammatory drugs (NSAIDs) and aspirin
For patients with history of urticaria or angioedema to NSAIDs, avoidance is recommended. If
required, graded challenge protocol may be used
Aspirin exacerbated respiratory disease (AERD) is characterized by aspirin- or NSAID-induced
respiratory reaction in patients with underlying asthma
• Radiocontrast media
Can cause a non-IgE-mediated reaction that is unpredictable. If there is a history of prior reaction,
pretreatment protocols may prevent reaction: a corticosteroid (e.g., prednisone) given at 13, 7, and 1
hour prior to procedure and an antihistamine (e.g., diphenhydramine) given1 hour prior. Reaction is
not related to underlying shellfish allergy
NON-IgE-MEDIATED FOOD ALLERGY

A food allergy is an abnormal reaction to a food or food additive. Reactions can be divided into IgE-
and non-IgE-mediated. IgE-mediated reactions have been described earlier in this chapter. This
section focuses on non-IgE-mediated reactions seen in the inpatient setting including food protein-
induced colitis, food protein-induced enterocolitis (or food protein-induced enterocolitis syndrome
[FPIES]), and eosinophilic esophagitis.
FOOD PROTEIN-INDUCED COLITIS

Clinical Manifestations
• Healthy appearing infants who present with streaks of blood or mucous in stools without fissure or
identifiable cause. Unlike those with food protein-induced enterocolitis, these babies are well and are
often managed as outpatients
Epidemiology
• Food protein-induced colitis is thought to occur in 2–6% of infants in developed countries.
Approximately 60% are breast fed. The most common foods triggers are milk and soy
Diagnostics
• Diagnosis of food protein-induced colitis is made by history
• Elimination of food from diet (maternal and/or infant) resolves symptoms
Treatment/Prognosis
• Stop offending food(s)—most often milk and/or soy
• Consider reintroduction of food around 12 months of age, as typical natural history is resolution by this
time
FOOD PROTEIN-INDUCED ENTEROCOLITIS (FPIES)

Clinical Manifestations
Another random document with
no related content on Scribd:
but the description given of the field in which the tournament was
held, corresponds, in a most minute manner, with the “Tournament
Field,” still so called, at the neighbouring village of Smisby, and has
for ages been identified with that famous “Passage of Arms.” Eight
miles south-east of Repton this very interesting “habitation among
the ash trees” is situated.
The first authentic mention we have of it is about the year 1066,
when William the Conqueror granted the Manor to Hugh de
Grentemaisnel, one of his most valiant captains at the battle of
Hastings. In Domesday Book we read of its having a priest and
church. Soon afterwards it fell into the hands of Robert de Beaumeis,
another Norman, whose successor, Philip, granted “the church of St.
Helen of Ashby, with the church of Blackfordby,” &c., &c., to the
Abbey of Lilleshall, Salop. Philip de Beaumeis, having no son to
succeed him, left his estates to his daughter Adeliza, who married
Alan la Zouche, a descendant of the Earls of Brittany. Alan settled at
Ashby, and added the family name to it, to distinguish it from the
other towns of that name. Alan was succeeded by his son Roger,
who was succeeded by his son Alan, the last of the real Zouches, in
the male line, who held the Manor of Ashby, he granted it to Sir
William Mortimer, a distant relative, who assumed the name, and
passed it on to his son Alan, who fought at the battle of Creçy, 1346,
and died in that year, he was succeeded by his son Hugh, who died
in 1399, leaving no heir, with him the name, finally, became extinct.
Plate 16.
Ashby Castle. (Page 92.)
Staunton Harold. (Page 135.)

The property was held by Sir Hugh Burnett for about twenty years,
when James Butler, Earl of Ormond (a Lancastrian noble), by some
means or other, obtained possession of the land, he was executed at
Newcastle after the battle of Towton Moor in 1461. In that year
Edward, Duke of York, became King, and rewarded his partisans
with titles and grants of land. Among them was Sir William Hastings,
whom he created Baron Hastings of Ashby, &c., Steward of
Leicester, and ambassador, with the Earl of Warwick, to treat for
peace with Louis XI., King of France, who gave him a pension of
2000 crowns per annum. The first payment was made in gold, which
Lord Hastings is said to have received with these words, “Put it here
into my sleeve; for other testimonial (receipt) you shall get none: no
man shall say that King Edward’s Lord Chamberlain hath been
pensioner to the French King.” This may be the origin of the crest of
the Hastings’ family, a maunch or sleeve. King Edward also gave
him “licence to enclose and impark 3000 acres of land and wood at
Ashby-de-la-Zouch,” and to erect and fortify houses, &c., there and
elsewhere. In the year 1474 he built Ashby Castle, nine years later
the Protector (Richard, Duke of Gloucester) accused him of high
treason, and, without trial, had him beheaded on a log of wood on
Tower Green. His remains were interred in Windsor Castle, where a
splendid monument was erected to his memory.
As we are not writing a history of the Hastings family, we must
confine ourselves to those members of that family connected with
the history of the place, which for two centuries centred round its
castle and church. Ashby Castle was, as we have seen, built by the
first Lord Hastings in 1474. It stands on the south side of the town.
Judging by its ruins, it must have been indeed a stately pile. Entering
from the west we see the remains of the kitchen, with its fire-places,
&c.; it had a groined roof, over which were rooms, with another
storey over them, access to these was obtained by a spiral staircase
in the north-east corner of the kitchen. The west front of this block
has been destroyed, so nothing can be written about its chief
entrance, its height is about seventy feet, the dimensions of the
kitchen are fifty feet long, by twenty-seven broad, and thirty-seven
feet high.
In the kitchen are two doorways leading into the “servants hall,”
from this two doorways lead into the Great Hall, and from this
admission was obtained to a “drawing room.” At the end of this room,
a little to the south, is the chapel, lit by four windows, on either side,
and an east window. At the west end, over the west door, is a gallery,
to which a spiral staircase leads. Adjoining the east end, to the south
of it, were rooms for the chaplain. On the south is a courtyard formed
by the chapel, chaplain’s rooms, a thick wall, and the Great Tower.
This tower must have been an imposing building of, at least, four
storeys, with cellar, kitchen, dining hall, drawing room, and sleeping
apartments. Its southern half is destroyed, but what is left on the
north side—turrets, windows, fire-place, armorial bearings, &c.,
prove how richly the fabric was sculptured over. Very probably there
was a wall from the Great Tower on its west side, like that on its east
side, which met a wall built out from the kitchen. The ground plan of
the Castle would form a parallelogram with kitchen, servants’ hall,
great hall, drawing room, and chapel on the north side, chaplain’s
room at the east end, Great Tower, with walls on the south side, and
a wall and kitchen at the west end. A subterraneous passage
connects the kitchen with the Great Tower.
The chief historical events connected with the Castle are the visit
of Mary, Queen of Scots, in November of the year 1569. She was on
her way from Tutbury to Coventry. Anne, wife of James I., and Prince
Henry were entertained at the Castle in June, 1603, and King James
himself paid the Earl a visit in the year 1617. The expenses of this
visit were so great, the Earl’s income became seriously diminished,
as one of his descendants, Lady Flora, daughter of the 1st Marquis
of Hastings wrote, a propos of the visit,
The bells did ring,

The gracious King
Enjoyed his visit much;
And we’ve been poor
Ere since that hour
At Ashby-de-la-Zouch.
Again in May, 1645, another Stuart was a guest at Ashby. Charles
I., flushed with the success of his army at Leicester, spent a short
time at the Castle. Fifteen days later, June 14th, he came again, this
time a fugitive from the fatal and final battle of Naseby Field. The
Royalist garrison yielded Leicester, and marched out, the Governor
Hastings (Lord Loughborough) to Ashby, the officers and men to
Lichfield. For months the Parliamentary army, under Sir Thomas
Fairfax, beseiged the town and castle, which held out bravely for the
Royal cause. On the 28th February, 1646, articles of agreement
were drawn up, and signed by Lord Loughborough, and Colonel
Needham. The articles consisted of eleven “items.” The officers and
soldiers were “to march away to Bridgenorth or Worcester, with their
horses, arms, and ammunition, bag, and baggage, trumpets
sounding, drums beating, colours flying,” &c., or they might “lay
down their arms, and have protection to live at home if they please,”
“and the works and fortifications of the town and garrison should be
sleighted,” “after which the sequestrations of Colonel General
Hastings, the Earl of Huntingdon, should be taken off,” or “the
Colonel General, with the said gentlemen, could go to Hull or Bristol
to have a ship provided to transport them to France or Holland,
whither they please.” In 1648 the “sleighting” of the Castle was
performed, only too well, by one William Bainbrigg, of Lockington, in
the county of Leicester. On the north side of the Castle was a green,
on the south a garden, a wall, still existing, surrounded it with towers
of brick, with stone facings, used as summer-houses, or “look outs.”
On the east of the Castle is a triangular tower, triangular in shape,
called the “Mount House,” it is said to be connected with the kitchen
by a subterraneous passage. The “Manor House” on the north-east
side, occupies the site of a suite of apartments made to
accommodate King James I. in the year 1617.
Ashby Church, dedicated to St. Helen, occupies the site of an
earlier building, probably Norman. During the fourteenth and fifteenth
centuries it was rebuilt, and consisted of chancel, nave, north and
south aisles, with tower at the west end. During the last twenty-three
years nearly £16,000. have been spent in enlarging and restoring it.
Now it consists of nave with two aisles on its north and south sides,
all the galleries have been removed, and the old pews have been
replaced by well-designed oak seats. The choir stalls are placed at
the east end of the nave, leaving the chancel unoccupied. Over the
altar there is a fine reredos of oak, ascribed to Grinling Gibbons. On
the south side of the chancel is the mortuary chapel of the
Huntingdon family. A most magnificent tomb of Francis, 2nd Earl of
Huntingdon, and his wife Katherine, occupies the centre of it. Every
detail of it is well worth a very close inspection. There are also many
mural tablets in the chapel.
Within a sculptured recess in the north wall of the church is a finely
executed figure of a pilgrim. Lying on his back, the head rests on a
cushion, just above the right shoulder a portion of a pilgrim’s hat with
scallop-shell is seen. Round the shoulders, and over the breast, is
the collar of SS. The figure is clothed with a long cloak, the feet,
which rest on a dog, are shod with laced boots with pointed toes.
Across the body is a pilgrim’s staff, clasped by the left fore-arm, the
hands meet over the breast, pressed together in the attitude of
prayer, his scrip, ornamented with scallop-shells, is suspended,
diagonally, from his right shoulder. The statue is supposed to be a
Hastings, at least the family claim it, and have had their badge—the
maunch—sculptured on the wall of the recess. Among other
monuments in the church are those to Robert Mundy and his two
wives, a very curious one to Mrs. Margery Wright with high-crowned
hat, ruffles and ermine muff! and many modern ones. The most
curious relic of mediæval days is an old finger pillory, formerly used
for the punishment of disorderly-behaved persons in church. It is in
front of the screen which separates the nave from the tower. The
windows of the church are nearly all of stained glass, and illustrate
scenes in the life of our Lord.
The town of Ashby is well known for its baths. In the year 1822
they were opened, but the great expectations of converting the town
into a fashionable health resort have not been realized. The water is
not found at Ashby, but is pumped from deep coal pits at Moira,
some three miles distant, and conveyed to the baths in tanks
specially constructed for that purpose.
Ashby received quite an unusual class of visitors in the year 1804.
During the prolonged wars between England and France many
thousands of prisoners were landed on our shores. According to Sir
Archibald Alison there were no less than 50,000 French prisoners in
Great Britain. For the accommodation of “the rank and file” such
places as Dartmoor prison were erected, but the officers were
quartered in different towns. On Friday, September 26th, 1804, the
first detachment, consisting of forty-two officers, arrived in Ashby,
other detachments followed, till about two hundred found lodgings
there, among them were officers of the army and navy, and about
thirty others described as merchants. They lived on excellent terms
with the good people of Ashby for ten years, they were allowed
liberty to walk a mile in any direction out of the town. Some escaped,
and some were exchanged for English officers imprisoned in France.
Canon Denton, Vicar of Ashby-de-la-Zouch, has written a most
interesting account of its castle, and this French occupation in
“Bygone Leicestershire.” He obtained the information about the
latter, from the lips of one of his parishioners (Mrs. Whyman), who
lived at the time, and saw them. He also had access to a diary kept
by an Ashby physician (Dr. Kirkland). The church registers contain
entries of marriages contracted between the officers and residents,
also entries of baptisms and burials, which, as the Canon writes,
“show, among other things, that the prisoners of war, who were
quartered at Ashby, did not allow national prejudices to prevent them
forming the closest ties with the inhabitants of the place of their
captivity.”
Little more remains to be written about this interesting town. Its
Grammar School, founded in 1567 by the Earl of Huntingdon and
others, augmented about thirty years after its foundation, by an
inhabitant who is said to have lost his way, and was guided to his
home by the sound of the church bell. In gratitude for this he
conveyed to the trustees of the school certain property on condition
that the bells “should be rung for a quarter of an hour at four o’clock
in the morning.” This custom was kept up till 1807, when it was
discontinued. The property is still known as the “Day Bell Houses.”
One of the Headmasters was Dr. Samuel Shaw, son of Thomas
Shaw, of Brook End, Repton, blacksmith, and was at Repton School
under Dr. Ullock. At the age of 15 Samuel Shaw was admitted as a
sizar at St. John’s College, Cambridge. In 1658 he was Rector of
Long Whatton, ejected in 1661, and was elected Headmaster of
Ashby Grammar School in 1668.
Plate 17.
Barrow-on-Trent Church. (Page 99.)

Swarkeston House. (Page 101.)
On Thursday, July 24th, 1879, a memorial cross, in design like

Queen Eleanor’s cross at Northampton, was unveiled. It bears the
following inscription, written by the late Earl of Beaconsfield: “In
memory of Edith Maud Countess of Loudoun in her own right,
Baroness Botreux, Hungerford, De Moleyns and Hastings, who
sprung from an illustrious ancestry herself possessed their noblest
qualities, the people of Ashby-de-la-Zouch and the neighbourhood
have raised this cross as a tribute of admiration and of love.” The
cross was designed by the late Sir Gilbert Scott, R.A., and executed
by Messrs. Farmer and Brindley at a cost of £4,500.
BARROW, SWARKESTON, AND STANTON-BY-

BRIDGE.
One of our pleasantest walks from Repton is to Barrow, down
Brook End, up Monsel Lane, past the (Canons’) Meadow Farm, and,
by a field path to the left, to the river Trent, over which there is a
ferry, to Twyford village. After passing through Twyford, turn to the
right along the road, or by a field path, and the picturesque old
village of Barrow will soon be reached. Barrow, most probably,
derived its name from a barrow within the parish, which parish
includes the villages of Arleston, Sinfin, Stenson and Twyford. Of
these villages little can be written, Arleston has some ancient
buildings and ruins which belonged to the preceptory of the Knights
Templars or Hospitallers. Sinfin is noted only for its moor, on which
the Derby races were formerly run. In the year 1804, it was enclosed
by Act of Parliament, and divided among the adjoining townships.
Stenson and Twyford were manors belonging to the Ferrars at the
time of the Domesday Survey, later on they passed to the Curzons,
Findernes, and Harpurs.
The church at Twyford, dedicated to St. Andrew, is a chapelry of,
and held by, the Vicars of Barrow. A Norman arch divides the nave
from the chancel, the rest of the church is of the Decorated period. It
has a tower terminated by an octagonal spire. There are three bells,
and a few mural monuments to the Harpur, Vernon, and Bristowe
families.
Barrow-on-Trent, as it is usually called, dates back to Norman
days, when it had a priest and a church. One portion of the manor
formed part of the endowment of the bishopric of Carlisle, the other,
and proper manor, including the church, belonged to the ancient
family of Bakepuz, one of whom, Robert de Bakepuz, gave the
church to the Priory of St. John of Jerusalem, Knights Templars, or
Hospitallers, who had a preceptory, as we have seen, at Arleston in
the parish of Barrow. For a full and interesting account of the
connection between Barrow and the Knights, see “Cox’s Churches of
Derbyshire,” Vol. IV., pp. 11-19.
When the Order was dissolved in the reign of Henry VIII., the
manor and advowson of the vicarage were granted to the family of
Beaumont, and remained with them till 1638, since that time the
advowson has very frequently changed hands, by sale, or otherwise.
In 1638 Daniel Shelmerdine (an O.R.) was chosen and elected by
the parishioners, and held the living till he was ejected in 1662. The
church, dedicated to St. Wilfred, consists of nave, chancel, north and
south aisles, south porch, and tower at the west end. There are now
no remains of the Norman church. During the reign of Henry III.
(1216-1272), the church was probably rebuilt, and again, in the
Decorated and Perpendicular periods, alterations and additions were
made. There are monuments in memory of the Bothes, Beaumonts,
and Sales.
SWARKESTON.
At the time of the Domesday Survey, Swarkeston (Suerchestune

or Sorchestun) was divided between the King and Henry de Ferrers.
In the reign of Edward I. it belonged to John de Beke, or Beck, and
Robert de Holland. Joan, wife of John de Beck, left it to her son and
heir. In the fourteenth century the manor and advowson was
purchased by the Rollestons, of Rolleston, in Staffordshire, with
whom they remained till about the middle of the sixteenth century
when the manor passed into the family of the Finderns. Jane
Findern, daughter and heiress of George Findern, conveyed it, by
marriage, to Richard Harpur, who built a mansion at Swarkeston.
This mansion was fortified, and the bridge defended by earth-works,
for the King, by Colonel Hastings in 1642. In January, 1643, Sir John
Gell marched against it with Sir George Gresley’s troops, the house
was abandoned on their approach, but the defenders of the bridge
only yielded after a stubborn defence.
Swarkeston Bridge is the most famous one in Derbyshire, and
from end to end measures 1304 yards. The modern part of the
bridge, over the river Trent, is about 138 yards, the remainder forms
a raised causeway, about eleven or twelve feet wide, with arches,
here and there, so that the flood water can escape. The greater part
of the bridge is in the parish of Stanton-by-Bridge. There is a legend
that the old bridge was erected at the sole cost of two maiden
sisters, who lost their lovers when attempting to ford the swollen
waters, to pay a visit to their betrothed ones. It is also said that the
ladies spent the whole of their fortunes on the bridge, and lived a life
of penury ever afterwards.
The earliest mention of the bridge, discovered by the Rev. Charles
Kerry, editor of the Derbyshire Archæological Journal, is in the
Hundred Rolls, and is as follows: “Inquisition held at Derby on the
Feast of S. Hilary, in the Church of S. James, anno 3 Edward I. (Oct.
1, a.d. 1275). The jury reported that the merchants of Melbourne
passing over the bridge had for three years withheld passage money
and tolls, unjustly and without warrant, to the prejudice of our lord the
King and the borough of Derby.”
“The Patent Rolls give three pontages for Swarkeston; viz.:—2nd
Pat., 18 Ed. II., m. 31.; 1st Pat., 12 Ed. III., m. 26. This latter was
granted to the men of Swarkeston for four years; the collectors of the
bridge tolls being Hugo de Calke, and John the son of Adam. Given
at Westminster, March 1st, 1338. The 3rd will be found in 3rd Pat.,
20 Ed. III., which refers to the ruinous state of the bridge, and
appoints John the son of Adam de Melbourne, senior, and John the
son of Adam de Melbourne, junior, to receive tolls for the reparation
of the bridge for three years. Given at Reading the 28th of
December, 1347.” A long list of things to pay toll, and the amount
varying from ¼d. to 6d. is given.
Another inquisition held at Newark, Oct. 26th, 1503, refers to the
chapel on Swarkeston bridge, and a parcel of meadow land, lying
between the bridge and Ingleby, granted to the Priory of Repton for a
priest to sing mass in the Chapel, which had not been done for 20
years.
In 1745 “bonnie Prince Charlie,” the Young Pretender, marched
from Derby, with his advanced guard, as far as Swarkeston Bridge,
but on the 6th of December was compelled, most reluctantly, to
commence a retreat to Scotland, which ended in the fatal battle of
Culloden Moor.
The village, now chiefly known as a fishing resort, with its church,
and posting house, is pleasantly situated on the banks of the Trent.
The ancient church was “restored” in 1876, that is to say, it was
rebuilt, with the exception of the tower and Harpur chapel. Beneath
an arch, to the north of the altar, is a raised tomb on which is fixed a
large alabaster slab, on this is carved the effigies of a man and
woman, the front of the tomb is divided into four compartments, in
the two middle ones are figures of seven sons and seven daughters.
Round the margin of the slab is the following inscription:—
“John Rolston Esquire sūtyme lord of Swarkston dysscysyd the iii.
day of De̅ c̅ ber ye yere of our lord MCCCCLxxxij, and Susane hys
wyffe dysscysyd the 23ᵈ of De̅ c̅ ber the yere of our lord MCCCCLX
and IV on whose sowlys God have mcy.”
On the south side of the chancel is the Harpur mortuary chapel. In
it are two large raised tombs, each supporting a pair of recumbent
effigies. One tomb is that of “Richard Harpur one of the justyces of
the Comen Benche at Westminster and Jane the wife, sister and
heyre of and unto Thomas Fynderne of Fynderne Esquyer. Cogita
mori.”
The other tomb bears beautifully-carved effigies of Sir John Harpur
and his first wife. Over the tomb, on a tablet, is this inscription:—“In
piam posteritatis memoriam et spem certam futuræ resurrectionis
monumentum hoc struxit Johannes Harpur Miles Filius Richardi
Harpur armigeri justiciarii de Banco Regio. Cui uxorem ducenti
Isabellam filiam Georgii Pierpont militis, Deus amplam et fœlicem
dedit filios filiasque duodecium quorum nomina scutis infra
præponuntur, Mortem obiit septᵒ die Octobris Anno Domini 1627.” In
front of the tomb, kneeling at a double prayer desk, are the figures of
seven sons, and five daughters.
STANTON-BY-BRIDGE.
Pleasantly situated on the high ground overlooking the valley of

the Trent is the village of Stanton-by-Bridge (Swarkeston). The De
Stantons were lords of the manor for many generations. In the reign
of Edward III., John Frances of Tickenhall married Margaret,
daughter and heiress of John de Stanton, so the manor passed to
the Frances family, and remained with them till an heiress of that
house married Sir Thomas Burdett, Bart., of Bramcote,
Warwickshire. About this time the manor was divided between the
Burdetts and Harpurs, each, in turn, appointing to the living. Now it is
in the sole patronage of the Harpur-Crewe family.
The church, dedicated to St. Michael, is a small one, about 60 feet
long, and consists of nave, chancel, north aisle, south porch with a
bell turret on the west gable. The chancel arch, a plain semi-circular
one, is considered to be Saxon, and the south doorway, ornamented
with chevron, or zizag, and billet mouldings, is of the Norman period,
not later than Stephen’s reign. There are several remains of incised
sepulchral slabs, and also slabs of alabaster bearing incised effigies
of the Sacheverell and Francis families. During a restoration in 1865,
some of the older slabs were discovered, and were placed as they
are now.
About a mile south of Stanton is a farmhouse called St. Bride’s,
supposed to be once a grange chapel of Burton Abbey. Built into its
walls are many remains of Norman work, and in the yard are stone
coffins, and other fragments of worked stone.
BRETBY AND HARTSHORN.
Three miles south of Repton is the village of Bretby. Like most of
the land round, it used to belong to the Earls of Chester, from them it
passed into the hands of the Segraves, who possessed, among
other manors and estates, Coton-in-the-Elms, Rosliston, Linton, and
Repton.
In 1300 John de Segrave received a license to castellate his
mansion at Bretby. Soon after it passed, with the manor, into the
families of the Mowbrays, Dukes of Norfolk, and, through one of the
co-heiresses of that family, to the Berkeleys, who, in 1585, sold it to
Sir Thomas Stanhope, grandfather of Philip, 1st Earl of Chesterfield,
and now, by descent, it belongs to the Earl of Carnarvon.
Plate 18.
Anchor Church. (Page 123.)
Bretby Hall. (Page 104.)

It is not known when the castle was pulled down, but most
probably in the days of Philip, 1st Earl of Chesterfield (1585-1656),
who built a mansion on the present site, within the park. The old
castle stood on the land to the south-west of the church, the grass
covered mounds indicate the foundations of a very strong fortress,
consisting of two courts.
The stones of the castle were probably used in the building of the
mansion in the park, which must have been a grand place, built “in
the midst of a large park, well wooded, and stored with several kinds
of deer, and exotic beasts; several fine avenues of trees leading to
the house, which is of stone, though not of modern architecture, very
regular, convenient, and noble, with a very curious chapel, (designed
in the Grecian (Ionic) style, by Inigo Jones), very good outbuildings.
The gardens, after the plan of Versailles, in the old grand style, with
terraces, leaden images of wild beasts, fountains, labyrinths, groves,
greenhouses, grottoes, aviaries, &c., &c.,” the park, with its chain of
fishponds, and fine timber, must have presented a scene of
unsurpassed natural beauty. Amidst such surroundings, an open-air
masque, written by Sir Aston Cokayne, was “presented at Bretbie in
Derbyshire on Twelfth Night, 1639,” before the Earl and Countess
and a great company. The masque is printed in “Glover’s History of
Derbyshire,” Vol. II., part I., p 184.
In November, 1642, during the Civil War, the house, which had
been fortified by the Earl, witnessed another scene. Four hundred
foot, with a party of dragoons and two sacres, under the command of
Major Molanus, were sent to Bretby by Sir John Gell. They
compelled the Earl, and his garrison of 40 musketeers and 60 horse,
to abandon the house, and fly towards Lichfield. “Then the Countess
was asked by the victorious officers to give 2s. 6d. to each soldier, to
save the house from plunder, but she said she had not so much in
the house; they proposed 40 marks as a composition, to which she
returned the same answer; they then offered to advance it to her, but
she declared she would not give them a penny; then the soldiers
plundered the house, but the officers saved her own chamber, with
all her goods.” (Sir John Gell’s M.S. Narrative).
In the year 1780, the young Earl “was persuaded ‘by an artful
steward,’ to pull down this splendid mansion and chapel, as being in
a dangerous state of decay, though it was afterwards proved to have
been very substantial.” The gardens also suffered a like fate.
Fortunately the fine cedar of Lebanon, planted in February 1676-7,
on the east side of the house, escaped destruction. It is considered
to be the oldest in the kingdom, and still flourishes, braced together
by iron chains, and is the chief object of admiration to visitors to
Bretby and its park. The present house was begun by the 5th Earl,
who died in 1815, when the building operations ceased. The
architect was Sir Geoffrey Wyatville, assisted by Mr. Martin, the
Earl’s architect. A ground plan of the house is printed on page 187 of
“Glover’s History of Derbyshire,” Vol. II., signed by W. Martin,
architect and builder, September, 1828. When completed it will form
a four-sided building, with a courtyard within it.
The church of Bretby, or rather the chapel, for it is one of the
seven chapelries of Repton, was rebuilt in the year 1877, in the
place of a very old building, built in the thirteenth century. It occupies
the old site with the addition of an aisle, which forms a large pew for
the noble owners, and a vestry, both on the north side. The village
consists of a few scattered houses. To the east of the park is Bretby
mill, on a small stream; which, rising in the Pistern hills, runs in a
northerly direction, through Repton, till it joins the river Trent.
HARTSHORN.
About four miles south of Repton is the ancient village of

Hartshorn, which at the time of the Domesday Survey belonged to
Henry de Ferrers. Later on the Priory of Repton had lands, a moiety
of a park, and the important right of free warren over the manor.
According to the list of patrons of the living, various families
succeeded to the manor, among whom are mentioned the de la
Wards, Meynells, Dethicks, the Earls of Shrewsbury, and the Earls of
Chesterfield. One of the rectors was Stebbing-Shawe, jun., (an
O.R.,) editor of the Topographer, and historian of Staffordshire. The
church, which is well placed on the higher part, with the rectory on
the east side of it, forms a very pleasing object from a distance, a
closer inspection reveals the fact that, at the restoration of 1835,
when the nave of the church was rebuilt, cast iron windows, imitating
Perpendicular tracery, were inserted! The east window of the
chancel, of two lights, belongs to the Decorated period. The
embattled tower is a fair specimen of the Perpendicular period, and
contains a ring of five bells. Three of them were placed there during
the time of Stebbing-Shawe, sen. The other two are of pre-
Reformation date, and bear well lettered inscriptions: “Hec Campana
Beata Trinitate Sancta Fiat,” and “Ave Maria Gracia Plena Dominus
Tecum.”
Under an arch in the north wall of the chancel is an altar tomb, on
which lie alabaster effigies of Humphrey Dethick, and his wife Eliza,
of Newhall. In front of the tomb are representations of their six
children, three sons and three daughters. The father and one son
are clothed in plate armour. Above the tomb is a shield bearing the
quartered arms of Dethick, Allestree and Meynell; at the east and
west ends are shields quartering Longford with Hathersaye,
Deincourt and Solney; Dethick impaling Longford, and Meynell
impaling Longford.
Many other ancient monuments used to be in the church, but they
have been “made away with.” There is a fine old parish chest, seven
feet long, in the vestry.
In Vol. VII. of the Derbyshire Archæological Society there are
many extracts from the parish records of Hartshorn: under the date
1612, an inventory of the church goods is given, the first item
mentioned is “a Co̅ m̅ uio Cupp of Silver wᵗʰ a plate of silver having
Ihon Baptᵈ head vppon it.” This plate was photographed by Mr.
Keene, of Derby, and a copy of it, with a descriptive note by Mr. St.
John Hope, was published in Vol. VIII. of the Journal. From it we
gather the following facts.
The “plate of silver” is a paten of silver-gilt, 5¼ inches in diameter.
The rim is quite plain, with the exception of four narrow lines
engraved on the extreme edge. The centre has a circular
depression, which again contains a slightly sunk sexfoil with the
spandrils filled with a rayed leaf ornament. The central device is a
Vernicle, (i.e., the face of our Saviour, as transferred to the
handkerchief of St. Veronica, and usually called a Vernicle). The
churchwardens wrongly described it as the head of St. John the
Baptist. Round the head is a nimbus, with rays issuing from it. There
are three “hall marks,” two of which, the maker’s name, a Lombardic
B in a dotted circle, and a leopard’s head crowned, are remaining;
the third, the date letter, is obliterated, so it is impossible to say, with
certainty, when it was made, but as this type of paten prevailed
between 1450 and 1530, the opinion is that its date is about 1480.
The communion cup bears the London date mark for 1611-12, and
the inscription:
Justus fide vivet + J + R + C.
1612.
The letters J. R. C. probably stand for James Royll,

Churchwarden, 1612, who, with Denis Hashard, made the inventory
at that date.
EGGINTON, STRETTON, AND TUTBURY.

At the making of the Domesday Survey, the manor of Egginton
was held by Geoffrey Alselin, and had a priest and a church. The
Alselins’ estates passed, through an heiress, into the family of
Bardulfs. Under them the manor was held by Ralph Fitz-Germund,
whose son William Fitz-Ralph, Seneschall of Normandy, and founder
of Dale-Abbey, gave it to William de Grendon, his nephew. In
exchange for Stanley, near Dale-Abbey, William’s wife gave it, as a
marriage portion of her daughter, Margaret, to Robert Fitz-Walkelin,
one of whose daughters married Sir John Chandos. At the death of
his descendant, another Sir John Chandos, one moiety of the manor
passed to his niece Elizabeth, daughter of Sir John Lawton, and wife
of Sir Peter de la Pole, one of the Knights of the Shire in 1400, from
whom it descended to the Chandos-Poles of Radbourne. Another
daughter of Robert Walkelin, Ermentrude, married Sir William de
Stafford, whose son, Robert, left it to five co-heiresses, and so their
moiety became divided into many shares, which were re-united, by
purchase, by the family of Lathbury. A co-heiress of Lathbury
brought her moiety to Robert Leigh, of Whitfield, Cheshire. In the
reign of James I., the estate passed to Anne, daughter of Sir Henry
Leigh of Egginton, who married Simon Every, Esq., of Chard,
Somersetshire, created 1st Baronet in 1641, ancestor of the present
owner, a minor, the 11th Baronet.

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Jennifer M. Brady, MD, Assistant Professor of Pediatrics, Division of Neonatology, Cincinnati

Solrun Melkorka Maggadottir, MD, Allergy/Immunology Fellow, The Children’s Hospital of

Margaret Samuels-Kalow, MD, MPhil, Instructor, Division of Emergency, Medicine, Department of

AIN: acute interstitial nephritis

Christopher B. Renjilian, MD, MBE

TABLE 1-1 Laboratory Studies in Anorexia Nervosa

ABNORMAL UTERINE BLEEDING

Progestin-only oral regimens including levonorgestrel (e.g., Plan B, Next Choice)

PELVIC INFLAMMATORY DISEASE

ANGIOEDEMA AND URTICARIA

TABLE 2-1 Classification of Hypersensitivity Reactions

COMMONLY IMPLICATED DRUGS

NON-IgE-MEDIATED FOOD ALLERGY

FOOD PROTEIN-INDUCED COLITIS

FOOD PROTEIN-INDUCED ENTEROCOLITIS (FPIES)

Ashby Castle. (Page 92.)

Staunton Harold. (Page 135.)

The bells did ring,

Barrow-on-Trent Church. (Page 99.)

On Thursday, July 24th, 1879, a memorial cross, in design like

BARROW, SWARKESTON, AND STANTON-BY-

At the time of the Domesday Survey, Swarkeston (Suerchestune

Pleasantly situated on the high ground overlooking the valley of

Anchor Church. (Page 123.)

Bretby Hall. (Page 104.)

About four miles south of Repton is the ancient village of

Justus fide vivet + J + R + C.

The letters J. R. C. probably stand for James Royll,

EGGINTON, STRETTON, AND TUTBURY.

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