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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
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It was then announced that the chosen few were to muster at
Brescia to meet the officers appointed to act as censors and to
chaperon them during a tour of the Front, which was to occupy six or
seven weeks, and which would cover at least 3,000 kilometres.
From Rome to Brescia is quite a long journey, via Milan, where
one has to pass a night.
There was quite a big gathering at the reception of correspondents
in the quaint little Town Hall where we assembled, as, in spite of the
weeding-out process which had taken place in Rome, no fewer than
forty-one papers were represented—twenty-six Italian, six French,
seven English, and two Swiss.
As was to be expected, Italian journalism was widely represented.
It had no less than twenty-six correspondents, and every town of
importance in Italy appeared to have sent someone.
I cannot recall the names of all the talented fellows who had been
despatched from every corner of the Peninsula to record the doings
on the Italian Front.
First and foremost, of course, was Luigi Barzini, without whom the
assemblage would have been quite incomplete, as he is probably
the most popular of press writers in the world to-day. In Italy, in fact,
he is a sort of institution, and it is certainly no exaggeration to state
that he is as well-known by sight as the King or General Cadorna.
Then there were Benedetti, Baccio Bacci, Fraccaroli, Gino Piva,
Giovanni Miceli, and Aldo Molinari, the black and white artist and
photographer, to cite only a few names in the brilliant attroupement
of Italian journalistic talent.
The French Press had six representatives: the Temps, Jean
Carrère, one of the best known and most popular of foreign
correspondents, who speaks Italian like his mother tongue; the Petit
Parisien, Serge Basset; the Echo de Paris, Jules Rateau; the
Journal, Georges Prade; the Illustration, Robert Vaucher; and the
Petit Marseillais, Bauderesque. As genial and typically French a crew
as one could meet anywhere.
The English Press was also well to the fore. The Times, as the
most powerful of British journals on the continent, was appropriately
represented by a giant in stature, W. Kidston McClure, as amiable
and erudite a gentleman as ever stood six feet eight inches upright in
his socks, and who, by reason of his great height, raised The Times
a head and shoulders above the rest of us.
W. T. Massey was the Daily Telegraph, a good and solid
representative of the older type of modern journalism; J. M. N.
Jeffries the Daily Mail young man, a slender stripling with brains, and
bubbling over with a sort of languid interest in his work, but who, in
his immaculate grey flannels and irreproachable ties, somehow gave
the impression of just going on or coming off the river rather than
starting on a warlike expedition; Martin Donohoe, the Daily
Chronicle, the very antithesis of Jeffries, burly and energetic, and in
every way a typical representative of Radical journalism, which was
further represented by Ernest Smith of the Daily News.
Gino Calza Bedolo, one of the youngest and most talented of
rising Italian journalists was “lent” to the Morning Post for this
occasion by his paper, the Giornale d’Italia, and a very able and
spirited representative did he prove, as the readers of the Morning
Post must have found.
And lastly, the Illustrated London News, by your humble servant,
sole representative of English pictorial journalism with the Italian
Army in the Field.
There were no Americans, as with the somewhat curious
exception of the two Swiss, only the allied nations were admitted. I
may add that everyone had to wear a white band round his coat
sleeve bearing the name of the paper he represented.
We were received by General Porro, Sub-Chief of the Italian
General Staff, on behalf of the Generalissimo, and he made a cordial
speech of welcome, in which he introduced us to the officers of the
censorship and detailed the arrangements that had been made to
enable the correspondents to see as much as possible of the
operations.
Everything for our big journey had been planned out with true
Italian thoroughness, even to providing every one of us with a set of
large and reliable maps, whilst on the head of giving permission to
see all we desired there was no cause for complaint, as we were to
be allowed to go everywhere along the Front; the only reason for
disappointment being in the information that immediately after the
tour was finished we should be obliged to leave the war zone until
further orders.
It was therefore to be a modified version of the modern method of
shepherding the war-correspondents as initiated by the Japanese in
the Russo-Japanese War; however, the latitude given as to freedom
of action was very generous.
Censorships were established at important centres such as
Brescia, Verona, Vicenza, Belluno, and Udine, and visits to the
various positions along the Front within fairly easy distance of these
places were allowed.
The Correspondents were expected to have their own motor cars,
and, of course, pay all expenses, but the Government supplied
horses or mules for the mountaineering work whenever necessary. It
had been made known in Rome that we should have to provide our
own transport, so there had been a general clubbing together with a
view to sharing cars and thus dividing up the expenses which were
bound to be heavy. Little coteries were thus formed, and, as might
have been anticipated, the three nationalities were segregated.
When I had got to Rome I found the car-parties were already
formed, and there was no room for me amongst the English, but I
was lucky enough to be introduced to two very nice young fellows,
Italians, Gino Calza Bedolo, of the Giornale d’Italia, and Aldo
Molinari, of the Illustrazion Italiana, who gladly let me take a share in
their car, as they both spoke French and were very keen on going
everywhere and seeing all there was to see. I felt I had really fallen
on my feet and was going to have an interesting time, and so it
turned out, as will be seen.
The array of correspondents’ cars was quite imposing, and as
most of them were packed full up with baggage and decorated with
the national flag of the occupants the effect may be imagined. It was
certainly a memorable occasion for Brescia, and a crowd assembled
outside the Town Hall to watch the strange scene.
The utmost cordiality sprang up immediately, not only amongst the
Correspondents but with the Censors also, who were all officers
selected for their thorough knowledge of French and English, and as,
of course, it was also necessary that they spoke these languages
fluently, this in itself helped not a little to establish at once a friendly
relationship between us all.
The good fellowship shown by the Italian journalists towards their
French and English confrères was quite remarkable from the very
start. On the evening of the day of the reception at Brescia they
invited us to a banquet to celebrate the occasion, and gave us a
delightful accueil and a splendid dinner. Belcredi, Vice-President of
the Italian Association of Journalists, was in the chair, and made a
great speech, in which he expressed the pleasure of himself and his
confrères at meeting us at Brescia, and emphasizing the sincerity of
the friendship between Italy and the Allies.
Jean Carrère, of the Temps, and McClure, of The Times,
responded eloquently in Italian on behalf of the French and English
correspondents, after which all formality ceased and the utmost
camaraderie ensued, although we had only known each other a few
hours it was also already like a gathering of old friends. It was an
evening to be remembered and of the happiest augury, as will be
seen.
CHAPTER VII
Brescia—Rough sketch of arrangements—A printed itinerary of tour

—Military passes—Rendezvous on certain dates—The “off-days”—
Much latitude allowed—We make a start—Matutinal hour—First
experience of freedom of action—Like schoolboys let loose—In the
valley of Guidicaria—First impression of trenches on mountains—A
gigantic furrow—Encampments of thousands of soldiers—Like the
great wall of China—Preconceived notions of warfare upset—
Trenches on summits of mountains—A vast military colony—Pride of
officers and men in their work—Men on “special” work—“Grousing”
unknown in Italian Army—Territorials—Middle-aged men—“Full of
beans”—Territorials in first line trenches—Modern warfare for three-
year-olds only—Hardy old mountaineers—Heart strain—The road
along Lake Garda—Military preparations everywhere—War on the
Lake—The flotilla of gun-boats—The Perils of the Lake—A trip on
the “Mincio” gun-boat—I make a sketch of Riva—A miniature
Gibraltar—Desenzano—Nocturnal activity of mosquitoes—Return to
Brescia—Something wrong with the car—Jules Rateau of the Echo
de Paris—Arrange excursion to Stelvio Pass—A wonderful motor trip
—The Valley of Valtellino—The corkscrew road—Bormio—The Staff
Colonel receives us—Permits our visiting positions—Village not
evacuated—Hotel open—Officers’ table d’hôte—We create a mild
surprise—Spend the night at hotel.
CHAPTER VII
One was not long realizing that it would have been impossible to
have obtained a real conception of the terrific character of the
mountain warfare and the indefatigable work of the soldiers if one
had not been enabled to see it for oneself at close quarters.
A better starting point than Brescia for an extended tour of the
whole of the Front would have been difficult to find, as it commands
comparatively easy access to the principal positions in this sector.
With a reliable car and no “speed limit” the radius you could cover in
a day was remarkable as we soon discovered.
It may possibly be of interest at this juncture to give a rough sketch
of the “arrangements” that we found had been made for us by the
Headquarters Staff. A printed itinerary was given to each
correspondent, from which he could gather at a glance the
programme, subject only to occasional modifications as events might
warrant, for every day of the tour.
The first impression, of course, was that we were to be on a sort of
“personally conducted tour,” and no little disappointment ensued, but
it was soon found that, although you had to adhere to it in its main
points, there was really not any irksome restriction, as will be seen.
The scheme briefly was that the whole party should assemble at
certain dates in the towns where Press Censorship Headquarters
were established, and then officers were detailed to accompany the
different parties to the positions along the Front nearest to these
centres in order to explain the nature of the operations going on, and
to give any other information required.
Salvo condotti, i.e., military passes, were issued to everyone;
these passes were for use on the road and in the positions, and had
to be renewed at each censorship, otherwise they were valueless.
Although therefore it was obligatory to present yourself at all these
points de repère at certain dates, you could choose your own road to
get to them and halt where you pleased en route.
The “off-days,” when you were not officially visiting the positions,
were to give you the opportunity of writing your articles and
submitting them to the Censor, as obviously nothing could be posted
without the official visé, though, of course, this did not prevent you
from getting off as soon as you were through with him and had
received your fresh permit and making for the next stopping place.
The latitude the arrangement gave to each car was demonstrated
at once. We were booked to remain in Brescia for eight days, during
which period there were to be no “official” excursions anywhere. Our
passes were handed us, and we were free to go where we pleased
so long as we turned up on time at Verona, the next stopping place.
The reason for this pleasing relaxation at the very commencement
of the tour did not transpire; perhaps it was an oversight when the
programme was drawn up; anyhow, my companions suggested our
taking advantage of it and getting away from Brescia as soon as
possible and making for the nearest positions. So we started off the
next morning at the matutinal hour of 5 o’clock.
We had somehow thought our idea was quite original, but we
found that several of our confrères had gone off even earlier than us,
but in another direction; we therefore had the road we had chosen all
to ourselves.
As there was no particular reason for us to return that day, we
decided to put up somewhere for the night, and took our handbags
with us. The zone of operations we were going to is a popular region
for tourists in peace time, so there was no fear of not finding lodgings
somewhere.
It was a glorious summer morning, and as we sped along in the
invigorating air through sleepy, picturesque villages and wide tracts
of tranquil country, covered with vines and maize-fields, towards the
distant mountains, it was difficult to realize that we were not on a
holiday jaunt but on our way to scenes of war.
To me especially the feeling of entire freedom of action was
particularly delightful after the anxious weeks I had spent in Udine
and on the Isonzo front, when the mere sight of a carabinieri would
make me tremble in my boots for fear I was going to be arrested.
Now, with my salvo condotto safe in my pocket and my
correspondent’s “brassard” on my coat sleeve, I could look
carabinieri and all such despots in the face without misgivings of
unpleasant happenings.
There must have been some subtle tonic effect in the atmosphere
that morning, for my companions were equally elated, and we were
positively like three schoolboys let loose: even the chauffeur was
infected by our boisterous spirits, and for the first few miles he
pushed the car along at its top speed with reckless impetuosity.
The firing line we were making for was in the sector comprised
between the Stelvio Pass and the Lake of Garda. In the valley of
Guidicaria we reached the trenches, and had our first impression of
the magnitude of the operations the Italians are undertaking.
What had been accomplished here during the three months since
the war started was en évidence before our eyes. I was fully
prepared from what I had seen on the Udine front for something
equally astonishing in this sector, but I must confess the scenes
before me, now that we were in touch with the troops, filled me with
amazement. The achievements on the middle Isonzo were great, but
here they were little short of the miraculous.
It was almost unbelievable that what we saw was only the work of
three short months. Trenches and gun emplacements confronted
you on all sides.
A sort of gigantic furrow wound through the valley and climbed the
mountain like some prehistoric serpent, till lost to view away up on
the summits more than two thousand metres above; and round
about this fantastic thing were numberless little quaint grey shapes
dotted here and there on the rocks, and often in positions so steep of
access that you wondered how they got up there at all, and for what
purpose.
These were the encampments of the thousands of Italian soldiers
who have accomplished all this marvel of mountain warfare, and in
the teeth of the Austrians and of nature as it were as well, and have
carried the line of entrenchments across wooded hills, meadows,
torrents and snow-clad slopes.
It is safe to assert that, with the exception perhaps of the great
wall of China, never before in the history of warfare have operations
of such magnitude been undertaken. In many places the trenches
had to be actually blasted out of the rock, and were reinforced with
concrete or anything that military science or nature could offer to
render them still more invulnerable.
As we advanced further into this impressive zone of military
activity you realized that all your preconceived notions of mountain
warfare were upset.
Along the big military highway constructed by Napoleon (see page 45)
To face page 74
Instead of the fighting taking place in the valleys and passes as

one would have expected, the positions and even the trenches were
frequently on the very summits of what one would have taken to be
almost inaccessible peaks and crags, and in some places actually
above the snow-line.
The whole region was positively alive with warlike energy, and
what was only a few months previously a desolate and uninhabited
area, had been transformed into a vast military colony, so to speak.
I was much struck with the pride of both officers and men in their
work, and the evident pleasure it gave them to shew us everything,
though, of course, our salvo condotti acted as open sesame
everywhere. Visitors, still less pressmen, are not always welcome,
especially when they turn up unexpectedly as we did.
Not the least astonishing feature of all these operations to my
mind was the fact that men of branches of the service one does not
usually associate with “special” work were working at it as though to
the manner born.
The Bersaglieri, for instance, who are men from the plains, were
doing sappers’ jobs amongst the rocks, or stationed high up on the
mountains where you would have only expected to find Alpini; but
they were all, I was told, gradually getting accustomed to their
unaccustomed work, and often developing undreamed of
capabilities, while their cheerfulness under the circumstances was
always astounding, even to their own officers.
“Grousing” appears to be an unknown quantity in the Italian Army.
I had a little chat with a sergeant of a Territorial regiment. He spoke
French fluently, and told me he had lived several years in Paris. He
was now in charge of a small detachment in a particularly exposed
spot.
To my surprise I learned that the greater part of his regiment was
composed of men well on in years, as one understands soldier life,
most of them being close on forty, and that in his particular
detachment he had several who were nearer fifty, though they did
not look it. Yet they were as cheery and “full of beans” as the
youngsters, he told me.
The reason for putting men of “territorial” age in first line trenches I
could not manage to ascertain, for however good physically they
may be for their age, one would have thought that their place was in
the rear and that younger men would always have been found in the
van.
It is indisputable that modern warfare is not for “veterans,” but, as
our friend, Rudyard Kipling, would put it, for “three-year olds only,”
for only youth can stand for any length of time the terrific physical
and moral strain it entails.
I learned that there are a few hardy old mountaineers fighting
shoulder to shoulder with the youngsters up on the peaks; but these,
of course, are exceptions such as one will find anywhere, for the
capability of endurance is no longer the same as it was when on the
right side of thirty, and the strain on the heart at these altitudes
especially is enormously increased. But to revert to our excursion.
Our road for some distance skirted the shore of Lake Garda, which
is intersected by the Austrian frontier at its northern end, where the
important fortified town of Riva is situated.
Here again the extraordinary preparedness of Italy was
demonstrated. There were military works everywhere—barricades of
barbed wire and trenches right down to the edge of the water—with
men behind them watching and in readiness for any emergency.
The war had even been carried on to the Lake itself, in the form of
a flotilla of serviceable gun-boats which had made its appearance,
almost miraculously, so it is said, within a few hours of the opening of
hostilities, and practically bottling up the Austrians in their end of the
lake.
This “fleet” was continually out patrolling—night and day and in all
weather. What this means will be realized by anyone who knows
Lake Garda, for there is probably no expanse of water in the world
where navigation is more exposed to sudden peril than here. It bears
the evil reputation of being the most treacherous of Italy’s inland
seas. Owing to its peculiar configuration and entourage of
mountains, tempests arise so unexpectedly that unless a vessel is
handled by an experienced skipper it has but little chance to reach
its port safely if it is caught in one of these Lake Garda hurricanes.
A gale from the North-East will raise waves equal to anything the
open sea can produce. Italy’s inland Navy is therefore exposed to
other perils than the guns of the Austrian batteries.
I was lucky enough to get a trip on the gun-boat “Mincio,” and saw
much of great interest on board. Everything was carried out on
strictly naval lines, so much in fact that one might have imagined
oneself out at sea, this illusion being heightened by the strong wind
blowing at the time and the unpleasantly lumpy seas which kept
breaking over us.
The officers and crews of these boats are all picked men from the
Royal Navy, and I was told that they have taken to their novel duties
with the greatest enthusiasm. The “Mincio” which was of about 150
tons, carried a very useful-looking Nordenfeldt quick-firer, mounted
on the fore-deck, and also a big searchlight apparatus.
There are other boats of the same class, and the little “fleet” had
already given good account of itself, whilst curiously enough, so far it
had escaped entirely scot free from mishap, in spite of the
endeavours of the Austrian gunners.
We steamed up the Lake till we were as near as prudence would
permit to the fortifications which protects Riva, for me to make a
sketch of it, but we did not remain stationary long as may be
imagined.
Seen from the Lake, the fortress of Monte Brioni reminds one
singularly of the Rock of Gibraltar in miniature, and it is said to be so
honeycombed with gun embrasures as to be equally impregnable,
and it is known that this impregnability is further guaranteed by
mining the Lake in its vicinity.
I rejoined my companions in the car at a harbour some distance
down the Lake, and we then made for Desenzano, where we thought
we would spend the night as it was already late. It is a quaint little
town on the lake shore, and we had no difficulty in getting rooms. To
our surprise a very good hotel was open, as every place at first sight
appeared to be shut up since there were no tourists to cater for.
There was no sign of military activity here, as it is many miles from
the Front, but whatever was wanting in this respect was made up for
by the nocturnal activity of the mosquitoes. I don’t think I ever
experienced anything to equal their ferocity anywhere. I have since
been told that Desenzano is notorious, if only by reason of its annual
plague of these pests of the night, and that they are a particular tribe
indigeneous to the place.
We returned to Brescia the following day. Our excursion had been
very pleasant and instructive in every respect, but what we had seen
only whetted one’s appetite for more. Life here in this provincial town
seemed very tame when you remembered what was going on so
comparatively short a distance away.
I should, therefore, have liked to get off again at once into the
mountains, but it was not so easy, and for a reason that admitted of
no argument. Something had gone wrong with the car, so our
chauffeur told us, and it could not be put right for a few days. This
was only what all motorists have continually to put up with, so there
was nothing for it but to grin and bear it.
At this juncture one of my French confrères, Jules Rateau, of the
Echo de Paris, a very jovial fellow, with whom I had become very
friendly, and to whom I had confided my troubles, invited me to go for
a trip with him in his car, his own companion having had to go to
Milan for a few days. I gladly accepted, and we arranged to attempt
to get as far as the positions on the Stelvio Pass. This meant again
staying away a night, as we learned it was far too arduous a journey
to be done in a single day.
Our intention was to make Bormio our first stage, sleep there and
push on to the Stelvio the following day.
It would be impossible to conceive a more wonderful motor trip.
For scenery it is probably unsurpassed in the world. I have never
seen anything to equal it. Our route part of the way went along that
most romantic of lakes Idro. The road, which is magnificent, follows
all the sinuosities of the shore on the very edge of the water, winding
in and out, and in many places passing through tunnels in the cliff-
like rocks.
You somehow had the feeling that one ought not to be on a
warlike expedition in such glorious surroundings, for the grandeur of
it all overwhelmed you.
Further on we passed through the valley of Valtellino, famous for
its grape vines, and for several miles we were driving past the
curious terrace-like vineyards in the mountain side, looking so
peaceful in the glorious sunshine. Then, as we gradually ascended,
the scenery changed, and we were in amongst gaunt, forbidding
mountains, towering above the road on either side.
All trace of cultivation disappeared by degrees; nature here no
longer smiled, grim pine forests made black patches against the
rugged slopes; there were traces of early snow on the high peaks,
and the air was becoming chilly. The contrast with the tender beauty
of the lower part of the valley was impressive in the extreme.
We were now approaching the area of military operations, and
occasionally we heard in the far distance the dull boom of guns. The
ascent became steeper, and at length the road left the valley and
began to climb up through the mountains by a series of corkscrew
turns that are so familiar in mountainous districts, but here the
acclivity was so steep that the turns were correspondingly numerous,
and it was a veritable nightmare of a road.
Our car, a Daimler of an old model, with a big, heavy tonneau,
soon began to feel the test and commenced to grunt and hesitate in
a manner that was not at all pleasant, considering that we were on
the edge of a precipice and there was no parapet.
The way the chauffeur had to literally coax the panting engine at
each turn makes me shudder even now to think of—every time I fully
expected it would fail to negotiate it, and we should go backwards
and be over the edge before he could put the break on, so little
space was there to spare. The only thing to do was to sit tight and
trust to luck. However, we reached the top safely, and at length
arrived at Bormio.
We had been advised that the first thing to do was to ascertain the
whereabouts of the commanding officer of the division and get his
permission to visit the positions, as it lay entirely within his discretion.
Our Salvo Condotti being subject to such restrictions as might be
deemed necessary at any place.
There was no difficulty in discovering the Headquarter Staff
building; it was a short distance from the town, in a big, new hotel
and hydropathic establishment, with fine park-like grounds. In peace
time it must have been a delightful place to stay in.
The General was away, but we were received by a Staff Colonel,
who spoke French. On seeing our papers he made no objection to
giving us permits to visit any position in this sector, and even went so
far as to suggest that we should go the following day up to the fort on
the Forcola close to the Stelvio Pass, and that an Alpino could
accompany us as guide. It was probable that we should be under fire
a good part of the way, he added, but what we should see would be
sufficiently interesting to compensate for the risk.
We gladly accepted his suggestion, so it was arranged we should
start early the next day as we had a stiff climb before us. We then
went back to the village.
It was getting towards nightfall, and the narrow main street
recalled vaguely Chamonix. It was crowded with Alpine soldiers, and
in the dusk they conveyed some impression of mountaineering
tourists, the illusion being heightened by the clank of their hobnailed
boots on the cobbles and the alpenstoks they all carried.
The village had not been evacuated as most of them are near the
Front, so there were women and children about. The principal hotel
was open, and we got two good rooms for the night, and what was
more to the point, for we were both famished after our long drive,
one of the best dinners I have had anywhere in Italy, the big cities
included. It was a table d’hôte for the officers, but we were informed
there was “probably no objection” to our dining at it.
Our appearance in the dining room created no little surprise, as we
were the only civilians present, our Press badges especially exciting
much comment, as this was the first time that correspondents had
been here.
Following the lead of my colleague, I bowed first to the Colonel,
who was at the head of the table, then to the rest of the officers
present, and we sat down at a small table by ourselves, amidst the
somewhat embarrassing attention we were attracting. This soon
wore off, however, as Italian officers are gentlemen not Huns, and it
was evidently realised that we had permission to come to Bormio or
we should not have ventured to be there.
CHAPTER VIII
On the summit of the Forcola—We start off in “military” time—Our

guide—Hard climbing—Realize we are no longer youthful—Under
fire—Necessary precautions—Our goal in sight—An awful bit of
track—Vertigo—A terrifying predicament—In the Forcola position—A
gigantic ant-heap—Unique position of the Forcola—A glorious
panorama—The Austrian Tyrol—The three frontiers—Shown round
position—Self-contained arsenal—Lunch in the mess-room—
Interesting chat—The “observation post”—The goniometre—Return
to Bormio—Decide to pass another night there—An invitation from
the sergeants—Amusing incident.
CHAPTER VIII
The summit of the Forcola is only nine kilometres as the crow flies
from Bormio, but we were told that it meant covering at least three
times that distance to reach our destination, and the hard climb
would make it appear much more.
We therefore got off in military time in the morning, and went a bit
of the way in the car till we came to a sort of wayside châlet, quite
Swiss in appearance, where a detachment of Alpini was stationed.
On presenting our letter from the Colonel at Headquarters, the
Officer in command ordered one of his men to accompany us, so
leaving the car here to await our return, we started off without delay.
Our guide, a brawny and typical young Italian mountaineer, leading
the way at a pace that soon compelled us to ask him to slow down a
bit.
We had been advised, as we were unaccustomed to climbing, not
to “rush” it at first, as we had at least two hours of strenuous
plodding to reach the fort, and it was a very hot day, which would
make us feel the strain the more.
To our athletic cicerone this was evidently but an ordinary walk in
the day’s work; in fact, so light did he make of it that he obligingly
insisted on carrying our overcoats and other paraphernalia in spite of
his being encumbered with his rifle, ammunition belt and heavy
cape.
We were not long in discovering that the stiffness of the climb we
were undertaking had not been exaggerated, and also that we were
neither of us as young as we had been. This latter point in particular
I recollect was irritatingly brought home to me at one time when we
were really making splendid progress as we thought. Some Alpini, in
full marching order, caught us up and passed us as easily as if we
had been standing still. However, it was no good being discouraged
because we were no longer youthful, and we continued to make our
way slowly but surely up the winding rocky track.
We had got about half way, and so far there had been nothing in
the nature of an incident, and no indication whatever that we were
actually right up at the Front and within range of the Austrian
batteries, for a dead silence had reigned in the mountains all the
morning.
Suddenly, as we were crossing a comparatively level bit of
boulder-strewn ground, the report of a big gun resounded in the still
air, and in a few seconds we heard a wailing sort of shriek
approaching, and an instant after the loud crash of a shell bursting a
short distance away.
We stopped and looked at each other, uncertain what to do as
there was no cover anywhere near. Our guide settled it for us without
a moment’s hesitation.
“The Austrians have seen us, that’s why they have commenced
firing in this direction; they probably think we may be part of a
detachment of troops going up to the fort—we must hurry on, and
with intervals of a couple of hundred yards or so between us.”
There was no time to lose, for whilst he was speaking another
shell burst nearer than the previous one.
So off we went again with the Alpino leading the way. Rateau was
in the centre, and I brought up the rear. Two hundred yards are not
much on the level, but on a steep mountain track the distances are
difficult to estimate, so the soldier was quite out of sight at times from
where I was.
The firing still continued in a desultory manner, shells dropping
aimlessly here and there, with no particular object so far as one
could judge, but probably with the idea of hampering any movements
of troops on the mountain. Meanwhile there was no response
whatever from the Italian batteries. They were letting the Austrians
waste their ammunition since they were so minded.
Our goal at last came into view high above on the summit of a
cyclopean wall of rock and seemingly an inaccessible point to reach.
It looked an awful place to climb up to and only to be tackled by
mountaineers, yet somewhere on that precipitous height there was
surely a means of ascent indistinguishable from below; and so it
proved.
The track now became more and more steep and zig-zag, till at
length the windings terminated, and there appeared a long straight
stretch, going without a break along the face of the bluff, up to the
summit at an angle of at least 60 degrees. Even now when I recall it,
it makes me shudder.
It was certainly not more than a couple of feet in width, and
overhung an abyss hundreds of feet deep. The mere aspect of it
almost gave me vertigo.
Hesitation, however, was out of the question after coming so far;
moreover, I was now quite alone, as my companions had already
reached our destination; I had to go on.
Within a few yards of the top I happened unconsciously to look
down. The effect produced by the sight of the yawning gulf beneath
me was terrifying: a giddiness came over me, my knees began to
tremble, and had I not managed to turn and clutch frantically at a
projecting piece of rock I should have lost my balance and fallen
over.
I shut my eyes and held on for a few minutes, not daring to stir;
then, with a strong effort of will, I pulled myself together sufficiently to
edge along with my face to the rock and grasp hold of some barbed
wire outside the opening leading into the fort; then, of course, I was
safe.
Almost needless to add that when I got inside I did not relate my
perilous experience. You are not supposed to be subject to vertigo
when you tackle mountain climbing; it might prove awkward for your
comrades.
A wonderful spectacle confronted me as I looked round. The
Forcola is nearly 10,000 feet high, and here, right on the summit,

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The Philadelphia Guide: Inpatient

Pediatrics 2nd Edition Samir Shah

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