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SECOND EDITION
ii
 SECOND EDITION

Paige Bennett, MD
Associate Professor
Nuclear Medicine and Molecular Imaging
Department of Radiology
Wake Forest School of Medicine
Winston-Salem, North Carolina

Umesh D. Oza, MD
Diagnostic Radiology Residency Program Director
Baylor University Medical Center at Dallas
Clinical Associate Professor
Texas A&M Health Science Center College of Medicine
College Station, Texas

Andrew T. Trout, MD Akiva Mintz, MD, PhD, MHA, CFA

Assistant Professor of Radiology and Pediatrics Vice Chair of Finance, Department of Radiology
Department of Radiology Section Head, Nuclear Medicine and Molecular Imaging
Cincinnati Children’s Hospital Medical Center Department of Radiology and Neurosurgery
Cincinnati, Ohio Leader, Translational Imaging Program
Assistant Director, Wake Forest Clinical & Translational Science
Institute (CTSI)
Wake Forest School of Medicine
Winston-Salem, North Carolina

iii
 1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899

DIAGNOSTIC IMAGING: NUCLEAR MEDICINE, SECOND EDITION ISBN: 978-0-323-37753-9

Copyright © 2016 by Elsevier. All rights reserved.

No part of this publication may be reproduced or transmitted in any form or by any means, electronic or mechanical, including
photocopying, recording, or any information storage and retrieval system, without permission in writing from the publisher. Details on
how to seek permission, further information about the Publisher’s permissions policies and our arrangements with organizations such as
the Copyright Clearance Center and the Copyright Licensing Agency, can be found at our website: www.elsevier.com/permissions.

This book and the individual contributions contained in it are protected under copyright by the Publisher (other than as may be
noted herein).

Notices

Knowledge and best practice in this field are constantly changing. As new research and
experience broaden our understanding, changes in research methods, professional practices,
or medical treatment may become necessary.

Practitioners and researchers must always rely on their own experience and knowledge in
evaluating and using any information, methods, compounds, or experiments described
herein. In using such information or methods they should be mindful of their own safety
and the safety of others, including parties for whom they have a professional responsibility.

With respect to any drug or pharmaceutical products identified, readers are advised to check
the most current information provided (i) on procedures featured or (ii) by the manufacturer
of each product to be administered, to verify the recommended dose or formula, the
method and duration of administration, and contraindications. It is the responsibility of
practitioners, relying on their own experience and knowledge of their patients, to make
diagnoses, to determine dosages and the best treatment for each individual patient, and to
take all appropriate safety precautions.

To the fullest extent of the law, neither the Publisher nor the authors, contributors, or
editors, assume any liability for any injury and/or damage to persons or property as a matter
of products liability, negligence or otherwise, or from any use or operation of any methods,
products, instructions, or ideas contained in the material herein.

Publisher Cataloging-in-Publication Data

Diagnostic imaging. Nuclear medicine / [edited by] Paige Bennett and Umesh D. Oza.
2nd edition.
pages ; cm
Nuclear medicine
Includes bibliographical references and index.
ISBN 978-0-323-37753-9 (hardback)
1. Diagnostic imaging--Handbooks, manuals, etc. 2. Nuclear medicine--Handbooks, manuals, etc.
I. Bennett, Paige. II. Oza, Umesh D. III. Title: Nuclear medicine.
[DNLM: 1. Diagnostic Imaging--methods--Atlases. 2. Nuclear Medicine--methods--Atlases.
3. Radiopharmaceuticals--Atlases. WN 39]
RC78.7.D53 D5282 2015
616.07/57--dc23

International Standard Book Number: 978-0-323-37753-9

Cover Designer: Tom M. Olson, BA
Cover Art: Richard Coombs, MS
Printed in Canada by Friesens, Altona, Manitoba, Canada

Last digit is the print number: 9 8 7 6 5 4 3 2 1

iv
 Dedications
This book is dedicated to my family.
To Diane and Ted Bennett, who love me the most.
To Betsy, Sidney, and Lee Andrew Clark, the loves of my life.
To my extended family of friends, Dr. Kathryn Morton, Cecilia Vargas Ortega.
Nothing matters without all of you.
Thank you to everyone who works with Amirsys: Your professionalism, leadership, and vision
created the Diagnostic Imaging series, of which we are all proud to be a part.
Arthur Gelsinger and Dr. Umesh Oza: You made this endeavor fun. Double thanks.

PB

While we have laboriously poured heart, soul, and spirit into this textbook to impart the leading
edge of nuclear medical knowledge to the next generation, there has been an equally and
painstaking devotion paid to us by loved ones and mentors that have dedicated time, wisdom,
guidance, and advice that cannot, and should not, go unrecognized. To my beautiful wife,
Komel, thank you for your strength, guidance, and unwavering resolve. To my children, Quaid
and Willa, you are my driving force. I want for you what you have given me — courage to strive
for better, enjoy life to the absolute fullest, and run with wild abandon. To my loving parents,
                
single-minded focus raising three successful children. To Rishi and Veena, thank you for your
               
many underrecognized people. I extend my deepest gratitude to all of you — thank you!

UDO

v
 Contributing Authors

Angela P. Bruner, PhD, DABR Christopher T. Whitlow, MD, PhD, MHA

            . %
         "  
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Pushpender Gupta, MBBS Todd Michael Danziger, MD

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John M. Holbert, MD, FACR # $  %
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vi
Colin Segovis, MD, PhD Tejaswini Vasamsetty, MD
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vii
 Preface

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ix
x
Acknowledgements
Text Editors
Nina I. Bennett, BA
Sarah J. Connor, BA
Tricia L. Cannon, BA
Terry W. Ferrell, MS
Lisa A. Gervais, BS
Karen E. Concannon, MA, PhD

Image Editors
Y@ Y5  $ 
Lisa A. M. Steadman, BS

Medical Editors
Philippe A. Tirman, MD
Whitney J. Morgan, MD

Illustrations
Richard Coombs, MS
Lane R. Bennion, MS
Laura C. Sesto, MA

Art Direction and Design

Tom M. Olson, BA
Laura C. Sesto, MA

Lead Editor
Arthur G. Gelsinger, MA

Production Coordinators
Angela M. G. Terry, BA
Rebecca L. Hutchinson, BA

xi
xii
 Sections

SECTION 1: Cardiac

SECTION 2: Central Nervous System

SECTION 3: Gastrointestinal

SECTION 4: Lymphatic and Vascular

SECTION 5: Musculoskeletal

SECTION 6: Thyroid and Parathyroid

SECTION 7: Thoracic

SECTION 8: Urinary Tract

SECTION 9: Pediatrics

SECTION 10: Miscellaneous

SECTION 11: Oncology

SECTION 12: Nuclear Medicine Therapy

SECTION 13: Physics

SECTION 14: Safety

xiii
 TABLE OF CONTENTS

SECTION 1: CARDIAC MOVEMENT DISORDERS

INTRODUCTION 56 Parkinson Disease
Akiva Mintz, MD, PhD, MHA, CFA
4 Approach to Cardiac Imaging
Paige Bennett, MD VASCULAR
FUNCTION AND CORONARY ARTERY 60 Brain Death
DISEASE Akiva Mintz, MD, PhD, MHA, CFA and Tejaswini
Vasamsetty, MD
6 Left Ventricular Function 64 Cerebrovascular Ischemia
Paige Bennett, MD Akiva Mintz, MD, PhD, MHA, CFA and Colin Segovis, MD,
10 Myocardial Infarction and Ischemia PhD
Paige Bennett, MD
16 Myocardial Viability SECTION 3: GASTROINTESTINAL
Paige Bennett, MD
20 Right-to-Left Shunt INTRODUCTION
Christopher R. McAdams, MD and Hollins Clark, MD 68 Approach to Gastrointestinal Imaging
Paige Bennett, MD
SECTION 2: CENTRAL NERVOUS SYSTEM
INTRODUCTION HEPATOBILIARY
70 Acute Cholecystitis and Biliary Obstruction
24 Approach to Central Nervous System Imaging
Paula Vergara-Wentland, MD and Paige Bennett, MD
Akiva Mintz, MD, PhD, MHA, CFA
78 Biliary Leak
CEREBROSPINAL FLUID Paula Vergara-Wentland, MD and Paige Bennett, MD
82 Functional Hepatobiliary Disease
26 CSF Leak Evaluation Paula Vergara-Wentland, MD and Paige Bennett, MD
Akiva Mintz, MD, PhD, MHA, CFA and Tejaswini 86 Benign Solid Liver Lesions
Vasamsetty, MD Paula Vergara-Wentland, MD and Paige Bennett, MD
30 CSF Shunt Patency
Akiva Mintz, MD, PhD, MHA, CFA and Tejaswini GASTROINTESTINAL
Vasamsetty, MD
90 Gastrointestinal Bleed Localization
34 Normal Pressure Hydrocephalus
Paula Vergara-Wentland, MD and Paige Bennett, MD
Valerie E. Stine, MD and Paige Bennett, MD
96 Gastric Emptying
DEMENTIA Paula Vergara-Wentland, MD and Paige Bennett, MD

38 Alzheimer Disease INFECTION AND INFLAMMATION

Akiva Mintz, MD, PhD, MHA, CFA and Bryan J. Neth, BS
100 Abdominal Infection and Inflammatory Disease
44 Frontotemporal Dementia
Paula Vergara-Wentland, MD and Paige Bennett, MD
Akiva Mintz, MD, PhD, MHA, CFA and Bryan J. Neth, BS
48 Lewy Body Disease SPLEEN
Akiva Mintz, MD, PhD, MHA, CFA and Bryan J. Neth, BS
52 Multi-Infarct Dementia 106 Spleen Localization
Akiva Mintz, MD, PhD, MHA, CFA and Bryan J. Neth, BS Paige Bennett, MD and Paula Vergara-Wentland, MD
and Christopher T. Whitlow, MD, PhD, MHA
SECTION 4: LYMPHATIC AND VASCULAR
INFECTION AND INFLAMMATION INTRODUCTION
54 Brain Abscess and Encephalitis
110 Approach to Lymphatic and Vascular Imaging
Akiva Mintz, MD, PhD, MHA, CFA and Paige Bennett, MD
Paige Bennett, MD

xiv
 TABLE OF CONTENTS
190 Complex Regional Pain Syndrome
LYMPHATIC Umesh D. Oza, MD
112 Lymphedema 194 Sickle Cell Disease
Christopher R. McAdams, MD and Paige Bennett, MD Umesh D. Oza, MD
116 Sentinel Lymph Node Mapping
Christopher R. McAdams, MD and Paige Bennett, MD SECTION 6: THYROID AND
PARATHYROID
VASCULAR
120 Large Vessel Vasculitis
INTRODUCTION
James Patrick Davidson, MD and Paige Bennett, MD 200 Approach to Thyroid and Parathyroid Imaging
122 Vascular Graft Infection Paige Bennett, MD
James Patrick Davidson, MD and Paige Bennett, MD
THYROID
SECTION 5: MUSCULOSKELETAL 202 Graves Disease
Paige Bennett, MD
INTRODUCTION 206 Nodular Thyroid Disease
128 Approach to Musculoskeletal Imaging Paige Bennett, MD
Umesh D. Oza, MD
PARATHYROID
BONE TUMORS 210 Parathyroid Adenoma
130 Bone Neoplasms Paige Bennett, MD and T. Alex McKnight, MD
Umesh D. Oza, MD and Daniel G. Hampton, MD
136 Metastatic Bone Tumors SECTION 7: THORACIC
Pushpender Gupta, MBBS
INTRODUCTION
BONE DYSPLASIAS 216 Approach to Thoracic Imaging
142 Fibrous Dysplasia Paige Bennett, MD
Umesh D. Oza, MD
146 Paget Disease INFECTION AND INFLAMMATION
Umesh D. Oza, MD 218 Atypical Infectious Diseases
Todd Michael Danziger, MD and Hollins Clark, MD
BONE MINERAL DENSITY 222 Granulomatous Disease
150 Osteopenia and Osteoporosis Todd Michael Danziger, MD and Hollins Clark, MD
Umesh D. Oza, MD
LUNG PERFUSION AND VENTILATION
INFECTION AND INFLAMMATION 226 Pulmonary Embolism
156 Arthroplasty Complication Paige Bennett, MD and G. Lance White, MD
Umesh D. Oza, MD 230 Quantitative Lung Perfusion
160 Inflammatory Arthritis John M. Holbert, MD, FACR and Brad Perry, MD
Umesh D. Oza, MD and Brad Perry, MD
164 Osteomyelitis and Septic Arthritis SECTION 8: URINARY TRACT
Umesh D. Oza, MD and Brad Perry, MD
INTRODUCTION
METABOLIC DISEASE 234 Approach to Urinary Tract Imaging
170 Metabolic Bone Disease Andrew T. Trout, MD
Umesh D. Oza, MD and Daniel G. Hampton, MD
INFECTION AND INFLAMMATION
TRAUMA 236 Renal Scar and Pyelonephritis
174 Heterotopic Ossification Christopher R. McAdams, MD and Paige Bennett, MD
Umesh D. Oza, MD
178 Occult Fracture RENAL FUNCTION
Umesh D. Oza, MD and Charlotte Myers, MD 240 Hydronephrosis
182 Stress and Insufficiency Fracture Amie M. McPherson, MD and Paige Bennett, MD
Umesh D. Oza, MD 244 Vesicoureteral Reflux
Amie M. McPherson, MD and Paige Bennett, MD
VASCULAR 248 Renal Transplant Evaluation
186 Avascular Necrosis Matthew Bennett, MD and Paige Bennett, MD
Umesh D. Oza, MD

xv
 TABLE OF CONTENTS
252 Renovascular Hypertension 316 Primary Breast Cancer
Matthew Bennett, MD and Paige Bennett, MD Umesh D. Oza, MD and Kelli Y. Ha, MD
320 Breast Cancer Staging
SECTION 9: PEDIATRICS Umesh D. Oza, MD and Kelli Y. Ha, MD
INTRODUCTION CENTRAL NERVOUS SYSTEM
258 Approach to Pediatric Imaging 326 Brain Metastases
Andrew T. Trout, MD Paige Bennett, MD
328 Post-Radiation CNS Evaluation
CENTRAL NERVOUS SYSTEM Paige Bennett, MD and Aidan Burke, MD
260 Seizure
Andrew T. Trout, MD CUTANEOUS
330 Melanoma
THYROID Paige Bennett, MD and Katarina Kesty, MD, MBA
264 Congenital Hypothyroidism
Andrew T. Trout, MD GASTROINTESTINAL TRACT
334 Esophageal Cancer
GASTROINTESTINAL Paula Vergara-Wentland, MD and Paige Bennett, MD
268 Gastric Motility 338 Gastric Cancer and Gastrointestinal Stromal Tumor
Andrew T. Trout, MD Paula Vergara-Wentland, MD and Paige Bennett, MD
272 Meckel Diverticulum 342 Colorectal and Anal Cancer
Andrew T. Trout, MD Paige Bennett, MD and Charlotte Myers, MD

HEPATOBILIARY HEAD AND NECK

276 Biliary Atresia 346 Salivary Gland Tumors
Shane C. Masters, MD, PhD Amanda Jo Lott Marcellino, MD and Paige Bennett, MD
350 Squamous Cell Carcinoma
INFECTION AND INFLAMMATION Paige Bennett, MD and Aidan Burke, MD
280 Fever of Unknown Origin
Andrew T. Trout, MD
HEPATOBILIARY
282 Osteomyelitis and Septic Joint 356 Hepatobiliary Malignancy
Andrew T. Trout, MD Paula Vergara-Wentland, MD and Paige Bennett, MD

MUSCULOSKELETAL LYMPHOMA
286 Avascular Necrosis 360 Hodgkin Lymphoma
Bimal Vyas, MD, MS and Andrew T. Trout, MD Virginia Barnes Planz, MD and Hollins Clark, MD
292 Pediatric Lower Back Pain 364 Non-Hodgkin Lymphoma
Bimal Vyas, MD, MS and Andrew T. Trout, MD Virginia Barnes Planz, MD and Hollins Clark, MD
296 Nonaccidental Trauma
Bimal Vyas, MD, MS and Andrew T. Trout, MD MUSCULOSKELETAL
368 Multiple Myeloma
SECTION 10: MISCELLANEOUS Pushpender Gupta, MBBS
302 Lacrimal Complex Dysfunction
Paige Bennett, MD and Zachary Allen Lindsey, MD NEUROENDOCRINE
306 Salivary Gland Scintigraphy 372 Carcinoid Tumor
Paige Bennett, MD John M. Holbert, MD, FACR
376 Pancreatic Neuroendocrine Tumors
SECTION 11: ONCOLOGY Umesh D. Oza, MD
380 Pheochromocytoma and Paraganglioma
INTRODUCTION Paige Bennett, MD and Charlotte Myers, MD
310 Approach to Oncologic Imaging 384 Medullary Thyroid Carcinoma
Paige Bennett, MD Ashley C. Mays, MD and Paige Bennett, MD

BREAST PANCREAS
312 Benign Breast Disease 388 Pancreatic Adenocarcinoma
Kelli Y. Ha, MD and Umesh D. Oza, MD Paula Vergara-Wentland, MD and Paige Bennett, MD

xvi
 TABLE OF CONTENTS
478 Hepatic Metastases Therapy
REPRODUCTIVE ORGANS Trevor Downing, MD and Paige Bennett, MD and Brian
392 Uterine and Endometrial Cancers Kouri, MD
Paige Bennett, MD and Brad Perry, MD and Charlotte 482 Metastatic Bone Tumor Therapy
Myers, MD Pushpender Gupta, MBBS
396 Ovarian Cancer
Paige Bennett, MD and Brad Perry, MD and Charlotte SECTION 13: PHYSICS
Myers, MD 488 Basic Physics and Radionuclides
400 Cervical Cancer Angela P. Bruner, PhD, DABR and John Bailey, MD and
Paige Bennett, MD and Brad Perry, MD and Charlotte Umesh D. Oza, MD
Myers, MD 492 Nonimaging Detectors
404 Vulvar and Vaginal Cancer Angela P. Bruner, PhD, DABR and John Bailey, MD
Paige Bennett, MD and Brad Perry, MD 494 Gamma Camera Imaging
408 Prostate Cancer Angela P. Bruner, PhD, DABR and John Bailey, MD
Paige Bennett, MD and Brad Perry, MD 498 SPECT
412 Testicular Cancer Angela P. Bruner, PhD, DABR and John Bailey, MD
Paige Bennett, MD and Brad Perry, MD 502 PET
Angela P. Bruner, PhD, DABR and John Bailey, MD
THORACIC
506 Radiation Biology and Dose
416 Malignant Pleural Mesothelioma Angela P. Bruner, PhD, DABR and John Bailey, MD and
John M. Holbert, MD, FACR and Brad Perry, MD Umesh D. Oza, MD
420 Non-Small Cell Lung Cancer
Anita Thomas, MD and Paige Bennett, MD SECTION 14: SAFETY
426 Small Cell Lung Cancer
Anita Thomas, MD MEDICAL USE OF BYPRODUCT MATERIAL
430 Thymoma and Thymic Carcinoma 512 Medical Use of Byproduct Material
Anita Thomas, MD Umesh D. Oza, MD
434 Solitary Pulmonary Nodule 516 General Administrative Requirements
Pavani Thotakura, MD and Hollins Clark, MD Umesh D. Oza, MD
520 General Technical Requirements
THYROID Umesh D. Oza, MD
440 Papillary and Follicular Thyroid Cancer 524 Radioactive Spills
Ashley C. Mays, MD and Paige Bennett, MD Umesh D. Oza, MD
526 Records and Reports
URINARY TRACT Umesh D. Oza, MD
444 Renal Cell Carcinoma 530 Written Directive Requirements
Paige Bennett, MD and Brad Perry, MD Umesh D. Oza, MD
448 Transitional Cell Carcinoma
Paige Bennett, MD and Brad Perry, MD STANDARDS FOR PROTECTION AGAINST
RADIATION
PEDIATRICS 532 Standards for Protection Against Radiation
452 Ewing Sarcoma Umesh D. Oza, MD
Andrew T. Trout, MD 536 Dose Limits
456 Neuroblastoma Umesh D. Oza, MD
Andrew T. Trout, MD 540 Radiopharmaceutical Administration
460 Osteosarcoma Umesh D. Oza, MD
Andrew T. Trout, MD 542 Records and Reports
Umesh D. Oza, MD
SECTION 12: NUCLEAR MEDICINE 546 Restricted Areas and Precautionary Procedures
THERAPY Umesh D. Oza, MD
548 Surveys and Monitoring
468 I-131 Therapy for Thyroid Cancer
Umesh D. Oza, MD
Paige Bennett, MD
472 I-131 Therapy for Hyperthyroidism TRANSPORTATION OF BYPRODUCT
Paige Bennett, MD MATERIALS
476 Lymphoma Therapy
Virginia Barnes Planz, MD and Hollins Clark, MD 550 Waste Disposal
Umesh D. Oza, MD

xvii
 TABLE OF CONTENTS
554 Ordering, Receiving, and Opening of Packages
Umesh D. Oza, MD

xviii
SECOND EDITION
Another random document with
no related content on Scribd:
for this in the past because of the lack of general knowledge of bone
infections; now there is none. The majority of cases of necrosis
following osteomyelitis which have come under the writer’s
observation were the result of errors in diagnosis.
Rheumatism is never followed by suppuration and seldom
produces a septic type of disease; its painful lesions are rarely so
painful as those due to osteomyelitis. Lesions of rheumatism are
usually multiple; those of bone infection are mostly single. The first
complaint of pain in the latter is generally along the shaft of a bone
than at the joint end, while this is not true of rheumatism. Moreover
in acute osteomyelitis the disease assumes from the outset a
seriousness which is seldom approximated by acute inflammatory
rheumatism.
Treatment.—The treatment for acute osteomyelitis is essentially
surgical. Anodynes may be necessary for relief of pain, but no time
should be lost, when once the diagnosis is made, in making incisions
to expose the bone involved, and then opening to its interior to
relieve tension and to remove septic products. The incision over the
femur or tibia, for instance, may be ten or twelve inches in length.
The tissues will invariably be found edematous or infiltrated, with
evidence of the proximity of pus; the periosteum will be thickened
and infected, and between it and the bone, as well as outside of it,
there may be collections of pus. If seen late the characteristic
muscle appearances already described may be noted. The
periosteum should be incised to the bone throughout the length of
the incision, and then an ordinary bone drill may be used to
perforate the bone for exploratory purposes. From the punctures in
the bone thus involved will exude purulent fluid, often sanious, thus
indicating the condition within. A deep groove or channel should
now be cut, opening into the marrow cavity, in which numerous foci
will be found, or in which all distinctive structure of bone-marrow
may be lost, the cavity being filled with pus. The pus cavity should
be scraped and disinfected with hydrogen peroxide and cauterized
with zinc chloride or its equivalent, and then packed, the wound
being left open. Even this may not be sufficient, but if there be
epiphyseal separation, or evidences of joint infection, the
neighboring joints should be explored under aseptic precautions; if
pus be found they should be opened, washed out, and drained.
Meanwhile if in the soft tissues exposed by the incision the parosteal
veins are found filled with septic thrombi, they should be opened as
far as exposed and their contents removed.
These operations are often severe, but nothing in the way of
operative treatment can be so severe nor so serious as the disease
itself when left unoperated; the rule is stringent that every infected
tissue, and especially every infected bone interior, should be exposed
and cleaned out. Only in this way can lives be saved. Moreover, it is
necessary to carry out this treatment in the fulminant cases as early
as possible; and errors in diagnosis by which it may be postponed
until metastatic infection or grave pulmonary and cardiac
complications have set in are unfortunate. So long as the local
indications are as above described, surgical treatment is desirable,
whether the systemic complications are pronounced or not. The
immediate effect of the operation having passed the relief thus
afforded will often be so pronounced that within twenty-four hours
patients may be out of danger.
The results of this operation are a wound which will discharge at
first freely, and which so soon as septic material is out of the way
will begin to granulate. Ordinarily no attempt should be made to
close such a wound, though much may be done to favor rapidity of
granulation. While some antiseptic dressing is always employed, it
will be of advantage occasionally to change the character of the
same, and to alternate between various antiseptics, the effect of any
one drug being apparently lost after it has been used for some time.
There are some cases where an entire diaphysis or bone shaft will
be found separated from one or both epiphyseal terminations, lying
in a subperiosteal abscess cavity, bathed in pus, and dead beyond
possibility of repair. This is total necrosis of the shaft from an acute
infectious process, and is to be treated by complete removal of all
dead and dying tissue. In the case of the forearm or leg it may be
that the remaining bone, when only one is involved, as is usual, will
be sufficient to maintain the integrity of the limb until new bone can
be reproduced within the periosteal bed occupied by the old one.
 Fig. 225
More or less complete
regeneration of bone
is possible,
particularly in the
young, and in
connection with
compensatory
hypertrophy of the
parallel bone will
permit the restoration
of the leg to partial or
complete usefulness.
On the other hand,
should this later
prove a complete
failure, amputation
and substitution of an
artificial limb may be
required.
When the disease
has involved the
articular side of an
epiphyseal line, and
when there is
complete epiphyseal
separation with
consequent
pyarthrosis, the
probable
consequence will be
necessity for a
complete or partial
resection of the joint
Total necrosis of humerus, as seen by aid of the and the probability of
cathode rays. (Lexer.) subsequent ankylosis.
Patients may find
later that a modern artificial limb with its possibilities will be
preferable to such a condition, and may readily consent later to an
amputation which they would at first refuse.
Acute Infectious Periostitis.—This is an infection of the same
general character and type as the osteomyelitis just described, but
refers to those cases where the disease apparently is confined to the
periosteum and the outermost layer of the bone. In its possibilities
for harm it is scarcely less serious, although in its tendency to
spontaneous perforation and escape of pus it is less likely to prove
fatal.
Causes.—The causes and the general clinical manifestations are
practically identical. The disease is perhaps less grave in its acute
manifestations, the localization of pain more exact, with ordinarily
less tendency to joint complications. Local tenderness is exquisite,
and particularly in those bones which lie near the surface—e. g., the
tibia—and early recognition of fluctuating areas is easy. It may be
localized over a small area, or the entire periosteum of the shaft may
be involved; in which case, so soon as pus forms and the periosteum
is separated from the bone, there is probability of acute necrosis of
the shaft. Here, again, there may be a tendency to mistake at least
the first signs of the disease for acute rheumatism, from which it
must necessarily be early differentiated as above.
Treatment.—Here also there is the same necessity for immediate
intervention, if possible before pus be formed, in order that there
may be little or no periosteal separation and encouragement to
necrosis. Anesthesia is necessary, with prompt incision, the use of
the sharp spoon, and disinfecting agents: no attempt should be
made to close the wound, but drainage should be favored in every
way. The intensity of the pain is promptly relieved and the whole
clinical picture immediately changed by such a procedure.
The ordinary bone felon upon a terminal phalanx is practically an
expression of this type of disease, and experience corroborates the
wisdom of deep and early incision, even in the case of so small a
bone entity as a phalanx.
Acute Epiphysitis.—This is a term applied rather indiscriminately
to a form of acute osteomyelitis involving primarily and especially the
epiphyseal lines, or to a condition of hyperemia and neurovascular
excitement at epiphyseal junctions stopping short of suppuration,
but giving rise to intense pain, muscle contraction, joint tenderness,
etc. It is often seen at the upper end of the tibia. Sympathetic
disturbance may extend even to serous effusion into a joint,
although this is not necessarily the case. The limbs are early drawn
up, and every attempt to extend them simply aggravates the
distress. So long as there are no evidences of suppuration, it is
sufficient in these cases to apply a sufficient degree of traction to
overcome muscular contracture and to straighten the limbs. This
should be applied first under anesthesia, and the patient kept under
anodynes for a few hours thereafter. So soon, however, as the
muscles are tired out by the steady traction, pain subsides, and the
intensity of the condition may be thus relieved within forty-eight
hours or less. It would be well to continue physiological rest and
traction as long as there remains the slightest tenderness. Should
evidences of suppuration at any time supervene, incision and
evacuation of pus and exudate should be practised. Should
epiphysitis occur in one of two parallel bones, there may result such
failure of growth of that bone as shall cause marked deformity in the
attacked hand or foot. In some of these cases, should operation be
required on one bone, the other may be shortened at the time, or
later, by exsection of a portion of the shaft, or even of the
epiphyseal junction.
—This is a rare manifestation of bone disease, only given an identity
of its own since 1868, when Ollier first distinguished it, since which
time it has been the subject of considerable controversy. The name
refers to a condition less acute than the infectious periostitis just
described, almost always localized in a single bone, necessitating
incision and evacuation of a fluid which is gelatinous or mucoid in
appearance rather than purulent. It is because of the peculiarity of
the subperiosteal collection of fluid that it received the name
periostitis albuminosa, and it was not generally regarded until
recently as a variety of the infectious form of periostitis. It is,
however, now conceded as being a mitigated form of infection, in
which the products of exudation assume the serous rather than the
 Periostitis Albuminosa.puru Fig. 226
lent type. In some instances it
appears to be the tubercle bacilli
which are at fault. At all events,
the organisms which produce the
disease are more or less virulent,
else the clinical form of the
disease would be less serious
than it really is. Cultures made
from these subperiosteal
collections have in almost all
recent instances revealed the
presence of some one of the
numerous pyogenic organisms.
Quite recently Dor has described
a polymorphic microbe, in
instances of this kind, which he
has called the Bacillus cereus
citreus, with which he claims to
have been able to reproduce the
disease in animals.
—As in the lungs, however,
chronic lesions are met with, and
as in the lungs, again, it is
possible for collections of
microörganisms to become more
or less encapsulated and for a
long time to lie latent until some
provoking cause excites them
again into activity. In this way
are to be explained the
numerous instances of recurring Osteogenesis and osteosclerosis in slow
abscesses within the bone infective processes. (Buffalo Museum.)
Chronic and Latent Osteomyelitis.necessitating repeated
operations, often at long intervals. (See Plate XXXVI.)
 Possible Consequences of Any and All of the Bone
Infections.
—Bone is a living tissue, calcified and stiffened by inorganic material
for the purpose of giving it strength; it may suffer remotely from the
consequences of local infections, the same as other tissue. Thus it
may have its nutrition impaired so as to produce atrophy on one
hand, or increased so as to lead on the other to hypertrophy, either
regular or irregular in outline. Again in its texture it may be altered
to a wide extent between the sponginess or porosity on one side
(osteoporosis), or to the density attained by ivory (osteosclerosis) on
the other. Similar changes are also noted in cases of bone
tuberculosis, which is to be considered by itself. The densest bone
has sufficient vitality to permit its nutrition and life, and may assume
dimensions much larger than that of the original, and a hardness
which will defy the best steel instruments should it become
necessary to operate upon it. The other extreme of osteoporosis
includes a condition where the bone has barely sufficient inorganic
material to permit it to retain its shape and ordinary proportions.
Such bone is fragile in the extreme and scarcely serviceable as a
supporting tissue. The principal portion of its bulk is constituted by
marrow tissue, which makes it extremely vascular, but far from
strong. When spongy it is ordinarily unserviceable for its proper
function. Astonishing pictures of osteosclerosis and osteoporosis side
by side are present in many instances of disease, the latter being
often evidence of more or less ossification of new-formed
granulation tissue. This is often a happy combination, because the
bone, which has been sadly weakened by disappearance of its
calcareous material by liquefaction and by absorption, is reinforced
along some of its lines by a pillar of osteosclerotic tissue, by means
of which it still functionates as a more or less useful support (Fig.
226).
The operating surgeon should familiarize himself with the density
of normal bone in various locations, as in many operations upon the
deeper bones he detects healthy bone rather by the sense of touch
and of hearing, and the resistance which it offers to his instruments,
than by sense of sight.
 TUBERCULOSIS OF BONE.
In Chapter IX, on Tuberculosis in general, we entered into
considerable detail in regard to the nature of tuberculous lesions,
which were stated to be essentially the same whether occurring in
hard or soft tissue, the active agent being the now well-known
Bacillus tuberculosis, which, finding lodgement, for instance, in the
osseous tissue, acts as a specific irritant, and so provokes the
production, first, of a typical tubercle, and, later, of typical
granulation tissue, by whose ravages the distinctive signs of bone
tuberculosis are produced. This process, then, is in no respect
different in bones from similar lesions in other parts, though
modified to a slight extent pathologically, to a greater extent
clinically, by the dense environment. Nevertheless, trifling or most
extensive destruction of bone substance is produced by this tissue,
while by continuity or by metastasis there is more or less
involvement of the adjoining textures, either parosteal or articular. It
is by granulation tissue that so-called caries is produced, and it is by
the same tissue that distinct portions of bone are sometimes
completely segregated from their vascular surroundings and shut off
from nutrition, so that they die and form what are known as
sequestra. Necrosis may then be the result of tuberculous disease.
 PLATE XXXVI

Tuberculous Disease of Hip-joint and Pelvis,

involving the Muscles (rare). (Lannelongue.)
 o, rarefying ostitis (i. e., osteoporosis); f, fungus granulation tissue.

So long as the process is active, this granulation tissue tends to

enlarge its boundaries, and, like pus, to spread in the direction of
least resistance. When produced in the shaft of a long bone this may
lead to involvement of the entire shaft, or there may be liquefaction
and absorption of dense bone and the formation of a sinus from the
marrow cavity to the periosteum, beneath which the granulation
tissue will spread, and through which it will sooner or later perforate,
to resume its progress toward the surface, always in the direction of
least resistance. In this progress tendon sheaths or bursæ may be
involved, or dense aponeuroses may turn the granulation column
aside, causing it to perforate toward the surface at some remote
point; while it may spread out more or less beneath the skin before
finally causing its destruction. Sooner or later, if uninterrupted by
treatment, this escape will occur, and then we have the condition of
a tuberculous ulcer of the skin, from which leads down, by a devious
path, a sinus toward the original focus.
When this original focus has been juxta-epiphyseal there is
involvement of the epiphyseal cartilage and a pathological diastasis,
which may early lead to spontaneous or pathological luxation. Or,
again, a focus having once originated at an epiphyseal extremity,
tends usually to perforate quickly into a joint cavity, after which a
considerable length of time is usually expended in filling up this joint
cavity with exuberant granulation tissue. This is the material so often
found in tuberculous joints, and is well characterized by the name
given to it by the Germans, fungous tissue, they calling such joint
affections fungous joint inflammations. (See previous chapter.)
Seen thus in joints, after it has been long exposed to friction and
to more or less pressure, it may have lost some of its original
luxuriant features. It is best seen when it is freshest and has been
exposed to least disturbance. Under these circumstances it is
vascular, dark red in appearance, friable, and easily removed from
the tissue upon which it has grown. Ordinarily it is infectious, and by
its inoculation into animals is capable of reproducing the disease.
 Pathology.—The pathology of tuberculosis of bone may then be
virtually summed up in saying that it consists of the ravages
produced by the presence of this granulation tissue, with the
irritative hyperplasia of surrounding tissues which its presence
always excites, even though they be not actively infected. This is the
explanation for the majority of cases of caries, of tumor albus, of
Pott’s disease, of spina ventosa, and of the condition which has been
known under many other names.
Varieties. Acute Miliary Tuberculosis of Bone.—This corresponds to
a similar invasion of the lungs. It might be fittingly described as an
acute tuberculous form of osteomyelitis. It may run its destructive
course within a short time and cause such involvement of structures
as to necessitate amputation of a limb, or it may appear in the
truncal skeleton as a primary disease, spreading rapidly therefrom
and involving the viscera or the cerebrospinal membranes, and
causing an early death, perhaps within a few weeks after its onset.
This condition has been more prevalent than is generally
understood, and has not even yet received the attention it deserves.
It is less painful than the pyogenic forms of osteomyelitis, and may
assume less of the septic and more of the typhoid or meningeal type
of disease. The pain also may be less severe, though reflex
symptoms, especially muscle spasm, will be an early and marked
feature of these cases. When a limb is involved the case may not be
hopeless; but when involving the cranium, spine, or trunk it is fatal,
and little can be accomplished by treatment. The operative
treatment for parts which are accessible is given under Acute
Osteomyelitis.
Chronic Tuberculous Osteomyelitis.—This is the ordinary form of the
disease, and is exceedingly common. In some sections it constitutes
nearly one-third of the diseases necessitating surgical treatment in
clinics and hospitals. This is particularly so in the thickly settled
portions of the European continent. In Buffalo it constitutes from 15
to 20 per cent. of cases found in my wards and in my clinic. The
proportion some years has been larger.
Symptoms.—The essential symptoms of bone tuberculosis are
muscle atrophy, muscle spasm and pain, direct or referred, and
upon the existence of these, coupled with local tenderness and local
swelling, a diagnosis can almost always be made. Muscle atrophy is
distinct, and is not alone that of disuse, but is a distinctive evidence
of the tuberculous process. It involves the parts above and below
the lesions.
Muscle spasm is never lacking, but is most noticeable about the
spine and the joints of the extremities. In Pott’s disease, for
instance, the condition causes a stiffening of the back and an
inflexibility of the spine. About the joints it leads gradually to
fixation, usually in the condition of more or less flexion, the flexor
muscles being ordinarily stronger than the extensors in all parts of
the body. Thus we see the knee and the elbow drawn up, and most
other joints in a condition of flexion so far as it may be permitted.
It is characteristic also that muscle spasm is frequently
exaggerated, usually in a reflex way, by which pain is always
augmented. These sudden but brief contractures occur more often
during sleep than during the waking hours, and give rise to the so-
called starting pains, usually nocturnal, which are noted in nearly
every case of this kind.
The pain is in large measure the result of contracted muscles
pulling tender joint surfaces together, and is consequently
augmented during the muscle spasms just described to an extent
causing the patient to cry out even during sleep. There is also
usually a more or less deep-seated and constant pain or soreness,
manifested in increasing degree as the lesion advances. These pains
are also often referred, lesions in the upper ends of long bones
usually giving rise to pain which patients refer to the lower ends. In
hip-joint disease pain is often referred to the knee, and in Pott’s
disease to the anterior part of the trunk. Slight but slowly increasing
disturbance of function of a joint inaugurated by trifling muscle
spasm, with complaint of aching pain, is significant and needs
careful examination, it being a mistake to anesthetize patients for
this purpose, as by the anesthetic the pathognomonic muscle spasm
is abolished and mistakes in diagnosis favored.
 Fig. 227 Fig. 228

Tuberculous disease of the hip. Healed tuberculosis of the spine.

(Buffalo Museum.) (Buffalo Museum.)

It will be seen that these features are also met with in

tuberculous-joint disease, the fact being the conditions are not only
allied but often associated.
Treatment.—The treatment of tuberculosis of bone is
constitutional and local. The former consists in the best possible
hygiene and in those measures which are everywhere recognized as
helpful in similar conditions. I believe in the internal use of benzosol,
or its equivalents, in doses sufficiently large to influence the tissues.
In addition the tonics and evacuants should be judiciously used. But
it is mainly with local treatment that we shall here have to deal.
The local treatment may be divided into the non-operative and the
operative. The former consists in enforcing the general principles of
physiological rest, which is done partly by orthopedic apparatus
proper and partly by the general principles of traction, and is
resorted to mainly in a class of cases treated of under Orthopedic
Surgery, the best methods for the purpose, apparatus, etc., being
found in the next chapter.
Aside from this a hopeful method has been that suggested by Bier,
consisting of making an artificial chronic congestion, it having been
long known that tubercles do not thrive when bathed in much blood.
The congestion is secured by wearing an elastic bandage above the
point involved, elastic constriction being made to a degree as great
as may be comfortably borne. The result is venous congestion,
possibly edema of the parts below, which to be made effective
should be carried nearly to the tolerable extreme. Constriction may
be at first enforced for only a short time, but can be later borne for
longer periods, until a time is reached when the patient can wear a
bandage almost continuously. Marked improvement in many cases
follows this method.
The operative treatment consists in ignipuncture, curettage, or
formal extirpation. Ignipuncture is the insertion into the bone focus
of the glowing point of the thermocautery. It should be practised
under an anesthetic, and when the bone is superficial the cautery
should be plunged through the skin, making it burn its way into the
depth of the bone. This is not difficult when the cancellous tissue is
that at fault. If the bone be deep an incision may be made down to
it, after which the cautery is applied as above. The result in almost
every instance is relief from pain.
This effect seems to be brought about partly by relief of tension,
partly by destruction of diseased tissue, and by the acute congestion
which is the result of vigorous counterirritation. It need occasion no
fear nor difficulty, and is applicable to all accessible bones. It must
not be expected to cure every case, but is a measure which may be
confidently expected to relieve pain and to do good.
The radical form of treatment is necessary when it can be
determined that the carious process is advancing or that pus or
caseated deposits are present. This is made known in various ways;
but when reasonably sure of their presence it is best to begin the
operation as an exploration, going as far as the findings may justify.
This may include scraping out of a small focus, or it may entail
removal of a large portion of a bone or resection of a joint, or even
amputation, according to the severity of the deep lesion. It is best to
do whatever may be necessary, and to do it all at once. The operator
should not rest content with mere operative attack, but should
carefully disinfect the entire tract, cutting away or removing with the
spoon the sinus wall and fungous tissue, which he should follow
wherever it may lead, disinfecting freely with hydrogen peroxide or
caustic pyrozone, and then using an active caustic, like zinc chloride
or the actual cautery, unless caustic pyrozone has already been
used. In this way material may be destroyed which has escaped the
instruments used, and absorbents are eared or closed and protection
afforded. My personal preference is for a packing made of bismuth
subiodide gauze, soaked in a mixture of balsam of Peru containing
10 per cent. of guaiacol, which I find more advantageous than
anything I have used. There should be added to these measures,
however, whatever may be necessary in the way of after-treatment,
both local and constitutional, and the surgeon should be prepared to
operate once or twice again should latent foci subsequently manifest
themselves or should there be recrudescence of the active disease.

BONE ABSCESS.
Bone abscess is a term applied to deep and circumscribed
collections of pus within the bone, mainly within the shafts of long
bones. They are due either to the acute ravages of pyogenic cocci or
to the slower lesions produced by the tubercle bacillus. They are
frequently evidences of return of disease in its acute type after a
long period of latency. The manifestations are usually localized, in
this respect differing from those of acute osteomyelitis. The pain is
deep-seated and boring, while there is local tenderness, often with
considerable enlargement of the overlying bone. The lesion occurs
more often in the tibia than in all of the other bones together—at
least under those clinical conditions which entitle it to be called bone
abscess. The pain is frequently nocturnal or osteoscopic, and
patients may endure it for weeks or months before seeking relief.
The surgeon may always expect to find a layer of condensed,
sometimes extremely hard bone around these local foci, and it is due
to this that they do not either perforate or diffuse and cause
extensive trouble.
Treatment.—Treatment is always operative; it should consist in
anesthesia, exposure of the bone, effective exploration by means of
the bone drill, as the hypodermic needle would be used for
exploration in the soft parts, and then the free use of the bone chisel
or other instruments by which the area may be widely exposed. The
density and firmness of the bone under these conditions will
sometimes almost defy the best-tempered instruments. Care should
be taken to make the external opening nearly the size of the deep
focus, in order that the surface may not heal too readily and before
the deeper part is filled. The same directions with regard to
cauterization and packing the cavity obtain as given before.

SYPHILIS OF BONE.
 Fig. 229 Fig. 230

Syphilitic gummas of head and face. Syphilitic ostitis and osteosclerosis.

(After Jullien.)

Syphilis of bone may assume the type of gummatous involvement

of the periosteum or of the bone itself or of syphilitic caries and
necrosis. The former appears usually as a distinct tumor, ordinarily
tender and exceedingly painful, especially at night, it being
characteristic of almost all cases of bone syphilis that the pain,
however great during the day, is exaggerated at night. The true
syphilitic gumma, or syphiloma, of bone is but little different from
gumma in other tissues, which may become secondarily infected and
then suppurate with the formation of sinuses, etc. Suppuration,
however, is rare. Central gumma, like central osteosarcoma, is
possible, and may lead to expansion of the surrounding bone.
Syphilitic necrosis, so far as the bone lesion is concerned, scarcely
differs from the other varieties. It is, however, almost always of the
slow form, and involves more often the flat than the long bones. It is
especially seen in the cranium and the sternum. Syphilis of bone is
often mistaken for rheumatism or pseudorheumatism because of the
deep-seated and somewhat indolent pain. Syphilitic disease of bone
permits occasional spontaneous fracture, the bone affected with this
disease being always more friable than natural. There is also another
form of bone syphilis—namely, the hereditary. It leads either to bone
enlargement or to caries and necrosis, the latter usually upon the
cranium, where extensive ulceration and sequestrum formation may
be observed, even the dura being exposed by breaking down of the
fungous tissue.
Hereditary bone syphilis is also characterized by osteophytic
formation, by the substitution of gelatinous for spongy bone tissue in
the neighborhood of epiphyses, and by early and easy epiphyseal
separations. It is characterized also by irregularity of ossification of
cartilage and consequent deformity of bone ends, especially about
the phalanges and the metacarpal and metatarsal bones. In almost
every case where doubt would in other respects arise the other
evidences of congenital or acquired syphilis are so plain as scarcely
to permit uncertainty (Fig. 230).
The possible combination of syphilis and tuberculosis in the same
subject may occur, the lesions partaking of one or the other
character according as the tuberculous or syphilitic taint may
predominate.
There is urgent necessity in all cases of syphilis in bone, whether
operated on or not, for the combination of suitable internal
treatment with surgical intervention. Only by this combination can
the efforts of the surgeon be Fig. 231
crowned with success. In failure
to appreciate this fact operation
often seems to be almost futile.

CARIES.
Caries is a term applied to
infiltration, and substitution in
healthy bone of granulation
tissue, which has been in use for
many centuries, from a time long
before the pathology of the
condition was understood. Caries
never occurs except in the
presence of a specific irritant,
which, in general, is tuberculous
and sometimes syphilitic in
character. The pure type of
caries is connected entirely with
the formation of granulation
tissue, and the slow ravages
connected with its presence in
and substitution for the original
bone. As long as septic infection
(pyogenic) is avoided it assumes
the dry type, as it used to be
known, called by the older
writers caries sicca. When the
fungous tissue is invaded by
putrefactive or pyogenic
organisms suppuration takes
place, and then occur the moist
forms of caries, the caries
humida of our forefathers,
connected with the presence of
pus. When closed areas of bone,
small or large, being thus shut
off from nourishment, die as the
result of its presence the
complicated condition used to be
known as caries necrotica.
Occurring under any
circumstances, caries is a result
and not a cause, and is to be
dealt with accordingly.
Peculiar alterations and
markings in bone are the
consequence of carious changes,
and bones are given a fantastic
and peculiar appearance in
consequence. The surface is
almost always irregular, tunnels
or canals are formed, and the
bone is often honeycombed, as it
were, by the excavations just
made. Along with the process of
osteoporosis and disappearance
of bone at one point may be
seen osteosclerosis in an
adjoining area, and the bone,
which is apparently much
weakened by the destructive
process, is strengthened in a
compensatory way by the
artificial density of the tissue
undestroyed.
The clinical evidences of caries
are those of joint and bone
tuberculosis or syphilis, which
have been already discussed,
and its operative treatment
consists always in surgical attack Caries of lower end of femur. (Buffalo
with bone chisel and sharp Clinic.)
spoon, according to the rules
already laid down. The bone which is completely carious calls for
extirpation—i. e., usually amputation. In the carpus and tarsus
resection will often suffice, and also when the disease is limited to
joint ends. Occurring in the pelvis, ribs, sternum, or cranium, more
or less extensive resections of flat bones are necessary, in the latter
place leading to exposure of the dura (of which one need have no
fear). The same rules with regard to cleansing and packing the
wound should be observed as in operation on tuberculous bones.

NECROSIS OF BONES.
Necrosis corresponds to gangrene of soft parts, and the term,
when used by itself, is limited to death of bone tissue. Necrosis by
itself is a distinct disease, but indicates the termination of some
preceding disease process. It may be considered as:
1. Traumatic;
2. Pathological—i. e., the result of disease; or
3. Toxic, due to the presence of specific poisons in the
system.
1. Traumatic Necrosis.—Traumatic necrosis is due to the
discontinuance of the blood supply by accident or by separation of
the whole or a part of a bone in the same way. Thus in consequence
of multiple fractures fragments occasionally die and require removal.
The same result has been ascribed to traumatic or non-traumatic
embolism of the principal nutrient artery of a bone, but the
possibility of this condition is doubtful, bone being too well supplied
by its surrounding periosteum. Necrosis in connection with fracture
is rare except in compound fractures, and, when a detached
fragment can be seen, may be anticipated by removal of the same.
2. The Pathological Form.—The pathological form is due to the
preëxistence either of tuberculosis, syphilis, or an acute infection,
such as osteomyelitis. It may also be the result of acute infectious
periostitis, where the periosteum is completely loosened from the
shaft of a long bone. These conditions are connected either with the
slow ravages produced by granulation tissue, or with the acute
septic processes by which infected exudates shut off large areas
from sufficient blood supply, or by which in consequence of septic
thrombosis a similar condition results. In consequence there may be
met bone dying in small visible particles, or the entire shaft of a long
bone or several smaller ones may be involved in the destructive
processes.
The portion which dies is known as the sequestrum, which may
assume irregular and unusual shapes, varying entirely with the area
involved. The general character and size of a sequestrum will
depend upon the nature of the cause. In acute osteomyelitis it is
either a bone shaft or an epiphysis which thus suddenly dies. In the
slower processes the fragments may be of almost any imaginable
size and form—irregular with jagged ends, or long, extending
completely through a bone, either from end to end or from side to
side.
3. The Toxic Forms Of Necrosis.—The toxic forms of necrosis
are due mainly to two substances used in the arts—mercury and
phosphorus—whose use seems to be inseparable from the
manufacture of many modern industrial products.
Mercurial necrosis may come either from the volatilization of the
metal in factories where mirrors are made or from refineries where
amalgam is distilled. It also occurs from the internal use of the drug.
Its effects are seen more frequently in the alveolar portion of the
lower and upper jaw than elsewhere. It is through some unknown
peculiarity that the jaws are the bones commonly involved in both of
these forms.
Phosphorus necrosis, on the other hand, manifests itself almost
entirely in the lower jaw, and occurs usually among the young, in
factories where matches are made. It is due to the vapors of
phosphorus, which cause a form of nearly distinct maxillary necrosis
—a fact which has been so widely recognized as to lead to State
legislation preventing the employment of the young in such work.
Phosphorus necrosis begins as a periostitis with the production of
osteophytes, and is completed as a nearly total necrosis of the entire
bone.
Treatment of the Toxic Forms.—The preventive treatment should
consist of supervision of the teeth, the use of alkaline mouth-
washes, inhalation of terebinthinate vapors, which neutralize those
of phosphorus, and the ventilation of establishments devoted to
match-making. The curative treatment consists of buccal antisepsis,
opening of abscesses, and the removal of diseased bone, especially
of dead bone, upon the first provocation. The occurrence of fistulas
should always be regarded as pathognomonic of diseased bone. In
aggravated cases, such as are rarely if ever seen since legislation
has been brought to bear upon the subject, practically complete
necrosis of the lower jaw, either en masse or in portions, was far
from unknown, and the possibility of regeneration of the bone was
for a long time discredited, until the late James R. Wood, of New
York, exhibited a specimen, both at home and abroad, which proved
its possibility. Since then we have learned that it is possible for bone
thus to regenerate, the cause of the disturbance having been
removed.
PLATE XXXVII
 Necrosis of Shaft of Femur with
Sequestra. (Life size.)

Fig. 232

Phosphorus necrosis of the lower jaw. (Musée Dupuytren.)

Sequestrum Formation.—To the portion of bone which dies is

given the name sequestrum, while multiple sequestra are by no
means uncommon. The sequestrum is white and ivory-like in
hardness when it consists of original compact structure. It is rare to
find a distinct sequestrum of spongy tissue, as this yields so readily
to the presence of granulation tissue and of pyogenic infection. A
sequestrum may include an entire bone shaft, or epiphysis, or only a
small fragment. A portion of the bone having lost its vitality becomes
a foreign body which the surrounding tissues endeavor to extrude or
to wall off and surround. The extrusive effort is the one which is
usually seen. This is done by the continued presence of granulation
tissue, which gradually perforates the surrounding bone at places of
least resistance, the result being the slow formation of a sinus or
several sinuses, ultimately connecting with the surface, and in which
in neglected cases the dead fragment of bone can be seen or felt, or
from which it can be withdrawn almost without operation. While this
weakening of bone is going on in certain portions a corresponding
strengthening process is also being put into effect; and the result is
a quantity of new bone, which is often wrapped around the
sequestrum and is simply the effort to atone for its pathological
weakness and to strengthen it. This new osseous tissue which so
often surrounds the sequestrum is called the involucrum, and in
many instances it is necessary to remove more or less of the
involucrum before the sequestrum can be lifted out of its bed or
removed. (See Plate XXXVII.)
The whole necrotic process is intelligible if read aright as an
endeavor on the part of Nature to get rid of dead and irritating
material. When this effort is properly interpreted the natural efforts
can be seconded by the interference of the surgeon at a time when
disturbance is limited to the minimum and before external sinuses
have had opportunity to form. On the other hand, ignorance and
neglect may lead to the extreme condition, and most fantastic
arrangements of sequestra and involucra are seen in all pathological
museums, some of which seem to partake almost of the perplexities
of Chinese puzzles. The explanation, however, is always as above
afforded. (See Figs. 233, 234 and 235.)
Treatment.—The treatment should be surgical, and consist in
removal of the dead portions and restoration of the parts to a
condition favoring rapid regeneration. It should always be radical,
but is sometimes made difficult by the inaccessibility of the fragment
or by the density of the involucrum and the necessity for large
external openings in order to remove the sequestrum.
Large and powerful forceps and strong and well-tempered bone
chisels are usually necessary, while, after making the necessary
opening for removal of the sequestrum, the sharp spoon should be
used thoroughly to scrape away all the lining material of cavities in
which fragments have been lying or all fungous tissue which may fill
sinus tracks. It will be well after this to thoroughly cauterize the wall
of the cavity, after which it is to be packed.
 Fig. 233 Fig. 234 Fig. 235

Central necrosis of the Sequestrum inside of a Necrosis of tibia, showing

tibia, long central core of new-bone sequestra after removal. (All
sequestrum. tissue, arranged much three specimens from the
like a puzzle. Buffalo Museum.)
 The packing of old bone cavities is of importance, and operators
should appreciate the reason for so treating them. The packing is
essentially a foreign material which the tissues will naturally
endeavor to extrude as they did the sequestrum. The method of
extrusion is by filling up beneath and around it with granulation
tissue, which later may ossify. The packing is therefore a constant
provocation to the formation of this tissue, which is now desirable,
and is used mainly for this purpose. It is antiseptic material, and will
serve to prevent decomposition of the pyoid material which would
otherwise fill such a cavity as the result of waste—Nature’s effort at
formative material gone to waste. A number of years ago Gunn
suggested the use of wax for this purpose, wax being plastic and
incapable of absorption. A piece of white wax was heated in hot
water, molded with the fingers to fit the cavity, where it served the
purpose of a packing, and was reduced in size with each dressing, as
was necessary to permit it still to remain. It is not now used as much
as it deserves to be. (See p. 431.)
In favorable cases it may be possible to so thoroughly cleanse the
bone cavity without the use of caustics as to justify the attempt,
after rigid asepsis, of allowing it to fill with blood, which will
coagulate and organize into connective tissue. When this effect is
desired the wound should be covered with green silk protective, over
which the other dressing may be snugly applied. This healing by the
aseptic blood clot is the ideal method when possible.
The extent to which regeneration of bone is possible is often
amazing, especially in the young. Thus after removal of the entire
shaft of a tibia there may result, in time, not a complete restoration
to former integrity, but, in addition, the formation of so much new
osseous material as to restore a great degree of strength, and which
shall, with the compensatorily hypertrophied fibula, make the leg as
useful as ever. In the thigh, however, complete necrosis of the femur
means amputation, as it will also in the arm unless the necrotic
portion is but a small proportion of the length of the humerus. The
treatment of necrosis of the skull, or, in fact, of any bone in the body
which is accessible, is based practically on the principles already laid
down.

BONE TRANSPLANTATION AND TRANSFERENCE.

In the effort to atone for extensive loss of bone many experiments
have been tried, first on animals and afterward on men, success
with the former having lent much prospect to the latter. It has been
learned, for instance, that portions of living bone can be removed
from some of the lower animals and transferred into a bed of more
or less healthy sterile human tissues, often with the result that a
fragment thus transplanted becomes vitalized and incorporated, and
serves the purpose for which it was intended; still these efforts do
not in all instances succeed. However, experience has led to the
effort to utilize some portion of the patient’s own osseous system.
This becomes more easily possible in the case of the forearm or leg
where, especially in the latter, a small or less important bone can be
utilized to take the place of the greater. Thus, when the entire shaft
of the tibia has been removed for necrosis resulting from acute
osteomyelitis, the fibula has been sawed across, opposite the site of
the ends of the lacking tibial shaft, and transplanted into the trough-
shaped depression, thus making it functionate for the lost tibia.
Huntington has recently reported a case in which not only was this
done, but later the upper and lower ends of the fibula attached to
the tibia, with good bony union and with an almost perfect
functional result. This will illustrate what elsewhere may be done in
this direction.

FILLING OF BONE CAVITIES.

Our methods for removal of sequestra and cleaning out of infected
bone cavities are now simplified and made safe. The difficulty which
is still universal is to secure a rapid filling or closure of these cavities.
If we could be certain of cleaning out every particle of infected
tissue and the removal of every germ which might excite