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THE REQUISITES
Emergency
Radiology
SERIES EDITOR OTHER VOLUMES IN THE REQUISITES
RADIOLOGY SERIES
James H. Thrall, MD
Radiologist-in-Chief Emeritus Breast Imaging
Department of Radiology Cardiac Imaging
Massachusetts General Hospital Gastrointestinal Imaging
Distinguished Juan M.Taveras Professor of Radiology Genitourinary Imaging
Harvard Medical School Musculoskeletal Imaging
Boston, Massachusetts Neuroradiology
Nuclear Medicine
Pediatric Radiology
Thoracic Radiology
Ultrasound
Vascular and Interventional Radiology
THE REQUISITES
Emergency
Radiology
SECOND EDITION
Jorge A. Soto, MD
Professor of Radiology
Department of Radiology
Boston University School of Medicine;
Vice Chairman
Boston Medical Center
Boston, Massachusetts
Brian C. Lucey, MD
Associate Professor
Boston University School of Medicine
Boston, Massachusetts;
Clinical Director
The Galway Clinic
Doughiska, County Galway, Ireland
1600 John F. Kennedy Blvd.
Ste 1800
Philadelphia, PA 19103-2899
EMERGENCY RADIOLOGY:THE REQUISITES, SECOND EDITION ISBN: 978-0-323-37640-2
Copyright © 2017 by Elsevier, Inc. 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
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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
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contained in the material herein.
Previous edition copyright © 2009 by Mosby, Inc., an affiliate of Elsevier, Inc.
Library of Congress Cataloging-in-Publication Data
Soto, Jorge A., editor.

Lucey, Brian C., editor.
Emergency radiology / [edited by] Jorge A. Soto, Brian C. Lucey.
Emergency radiology (Soto) | Requisites in radiology. | Requisites series.
Second edition. | Philadelphia, PA : Elsevier, [2017] | Requisites |Requisites radiology series
Includes bibliographical references and index.
LCCN 2015037285
ISBN 9780323376402 (hardcover : alk. paper)
MESH: Diagnostic Imaging. | Emergency Medical Services.
LCC RC78 | NLM WN 180 | DDC 616.07/572--dc23 LC record available at http://lccn.loc.gov/2015037285
Executive Content Strategist: Robin Carter

Content Development Specialist: Amy Meros
Publishing Services Manager: Patricia Tannian
Project Manager: Stephanie Turza
Senior Book Designer: Amy Buxton
Printed in China
Last digit is the print number: 9 8 7 6 5 4 3 2 1

To my parents, Jorge Sr. and Socorro, for their example and guidance, and to my
wife, Ana, and children, Andrea and Alejandro, for their sustained support and
patience as I devote my time to academic radiology.
J.A.S.
To my parents, James and Anne; sister, Suzanne; wife, Ciara; and son, James.
Thanks for the unconditional support.
B.C.L.
This page intentionally left blank

Contributors
Carlos A. Anaya, MD Ana Maria Gomez, MD
Medical Director Department of Radiology
Cardiovascular Interventional Institute Manati Medical Center
Department of Radiology Manati, Puerto Rico
Manati Medical Center
Manati, Puerto Rico Rathachai Kaewlai, MD
Instructor
Stephan W. Anderson, MD Division of Emergency Radiology
Associate Professor of Radiology Department of Diagnostic and Therapeutic Radiology
Boston University Medical Center Ramathibodi Hospital
Boston, Massachusetts Faculty of Medicine
Mahidol University
Laura L. Avery, MD Bangkok,Thailand
Assistant Professor
Massachusetts General Hospital Russ Kuker, MD
Harvard Medical School Department of Radiology
Boston, Massachusetts University of Miami Hospital
Miami, Florida
Glenn D. Barest, MD
Assistant Professor of Radiology Christina A. LeBedis, MD
Boston Medical Center Assistant Professor
Boston, Massachusetts Boston University Medical Center
Sarah D. Bixby, MD
Assistant Professor of Radiology Brian C. Lucey, MD
Harvard Medical School; Associate Professor
Pediatric Radiologist Department of Radiology
Department of Radiology Boston University School of Medicine
Boston Children’s Hospital Boston, Massachusetts;
Boston, Massachusetts Clinical Director
Anna K. Chacko, MD The Galway Clinic
Adjunct Professor of Radiology Doughiska, County Galway, Ireland
Boston University
Boston, Massachusetts; Asim Z. Mian, MD
Professor of Telemedicine Assistant Professor of Radiology
John A. Burns School of Medicine Boston Medical Center
University of Hawaii Boston University
Honolulu, Hawaii Boston, Massachusetts
Margaret N. Chapman, MD Sarah S. Milla, MD

Chief of Neuroradiology Associate Professor
Boston VA Healthcare System; Department of Radiology and Imaging Sciences
Assistant Professor of Radiology Emory University;
Boston Medical Center Attending Pediatric Radiologist and Neuroradiologist
Boston University School of Medicine Children’s Healthcare of Atlanta
Boston, Massachusetts Egleston Hospital
Atlanta, Georgia
Luis E. Diaz, MD
Associate Chief of Radiology Felipe Munera, MD
VA Boston Health Care System; Department of Radiology
Associate Professor of Radiology University of Miami Hospital
Boston University Miami, Florida
Rohini N. Nadgir, MD
Alejandra Duran-Mendicuti, MD Assistant Professor of Radiology and Radiological Science
Department of Radiology Johns Hopkins Medical Institutions
Brigham and Women’s Hospital Baltimore, Maryland
vii
viii Contributors
Osamu Sakai, MD, PhD Joshua W. Stuhlfaut, MD

Chief of Neuroradiology Beth Israel Deaconess Hospital
Professor of Radiology, Otolaryngology–Head and Neck Plymouth, Massachusetts
Surgery and Radiation Oncology
Boston Medical Center Jennifer C. Talmadge, MD
Boston University School of Medicine Department of Radiology
Boston, Massachusetts Children’s Hospital Boston
Rashmikant B. Shah, MD
Diagnostic Radiology Salvatore G. Viscomi, MD
St. James Healthcare Clinical Instructor
Butte, Montana Harvard Medical School;
Attending Radiologist
Ajay Singh, MD Department of Radiology
Department of Radiology Brigham and Women’s Hospital
Massachusetts General Hospital Boston, Massachusetts;
Boston, Massachusetts Chairman
Aaron D. Sodickson, MD, PhD Cape Cod Hospital
Department of Radiology Hyannis, Massachusetts
Brigham and Women’s Hospital
Boston, Massachusetts Scott White, MD
Jorge A. Soto, MD Brigham and Women’s Hospital
Professor of Radiology Boston, Massachusetts
Boston University School of Medicine; Ryan T. Whitesell, MD
Vice Chairman St. Paul Radiology
Department of Radiology Regions Hospital
Boston Medical Center St. Paul, Minnesota
Michael Stella, MD
Brigham and Women’s Hospital
Foreword
Time passes quickly, and it is now time to introduce the THE REQUISITES books have become old friends to
second edition of Emergency Radiology: THE REQUI- imagers for over 25 years. We have tried to remain true
SITES. Drs. Soto and Lucey, along with their coauthors, to the original philosophy of the series, which was to pro-
have once again created an excellent text that captures vide residents, fellows, and practicing radiologists with
the fundamental building blocks of emergency radiology a text that might be read within several days. From feed-
practice. back I have received, many residents do exactly that at
Drs. Soto and Lucey have maintained the logical division the beginning of each rotation. During first rotations this
of their book by both body part and indication—trauma allows them to acquire enough knowledge to really ben-
versus nontrauma with separate chapters for special con- efit from their day-to-day exposure to clinical material and
siderations in children and for nuclear medicine applica- the conditions about which they have just read. During
tions.This allows the reader of Emergency Radiology: THE subsequent rotations, a rereading imprints the knowledge
REQUISITES to go immediately to the material of interest. they will need subsequently for upcoming certification
As a side note, only two or so decades ago, nontrauma emer- exams. For the practicing radiologist, it serves as a useful
gency patients were not imaged nearly as often as they are refresher, like a booster shot.At the workstation, the books
today.Today, emergency applications for the nontrauma pain THE REQUISITES series are useful as a first reference
tient are just as important as the historic role of imaging source and guide to differential diagnosis.
in trauma. Imaging is truly the “guiding hand” of medical THE REQUISITES books are not intended to be exhaus-
practice, making possible rapid diagnosis, triage, and dispo- tive. There are other large reference books to catalog rare
sition, which are vitally important given the time and re- and unusual cases and to present different sides of con-
source constraints faced by busy emergency departments. troversies. Rather, THE REQUISITES books are intended
In the years between the preparation of the first edition to provide information on the vast majority of conditions
and the current work, much has happened to enhance that radiologists see every day, the ones that are at the core
the role of radiology in the emergency department and of radiology practice. In fact, one of the requests to authors
to reshape our thinking. These changes affect every area is to not look up anything they do not know but to put
of application and include, among many others, optimiza- in the book what they teach their own residents at the
tion of computed tomographic (CT ) protocols in every workstation. Since the authors are experienced experts in
organ system for lower radiation exposure, taking advan- their respective areas, this is predictably the most impor-
tage of fast CT scanning capabilities to reduce contrast us- tant material.
age and an increasing appreciation for the potential roles Drs. Soto and Lucey and their coauthors have again
of MRI for both traumatic and nontraumatic indications. done an outstanding job in sustaining the philosophy
Conventional radiography continues to play an important and excellence of THE REQUISITES series and deserve
role, especially for extremity trauma and some thoracic congratulations. Their book reflects the contemporary
imaging applications such as pneumonia and congestive practice of emergency imaging and should serve radiolo-
heart failure. However, for most applications, radiography gists, emergency medicine specialists, and other physi-
is being inexorably replaced by cross-sectional imaging. cians who deal with emergencies as a concise and useful
Drs. Soto and Lucey have again assembled an outstand- foundation for understanding the indications for imaging
ing team of coauthors to help ensure that Emergency and the significance of imaging findings in the emergency
Radiology: THE REQUISITES is as up to date as possible. setting.
Thanks to all the authors for their contributions.
Each chapter presents a different challenge in present- James H. Thrall, MD
ing material. All share a rich opportunity for illustrations, Chairman Emeritus
and Emergency Radiology: THE REQUISITES is extremely Department of Radiology
well illustrated. Otherwise the use of outline lists, boxes, Massachusetts General Hospital
and tables has been dictated by the material requiring Distinguished Taveras Professor of Radiology
presentation. Harvard Medical School
ix

Preface
Emergency Radiology is a unique title in THE REQUI- including CT angiography in the emergency department
SITES series. Although both the organ system–based and for coronary, aorta, brain/neck, visceral, and extremity ar-
modality-based divisions of radiology have existed for
teries, updated CT protocols in trauma and nontraumatic
some time, this REQUISITES title is the first to embrace a emergencies, and new and better quality images obtained
multimodality, multisystem approach to radiology. There with the latest imaging technology. Stepping away from
is an ongoing paradigm shift in medical management over the organ- and modality-based divisions, we acknowledge
the past 25 years or so, away from inpatient-oriented health that there is potential for overlap among this text and
care toward an increasingly outpatient-based system. No- others in THE REQUISITES series. However, to avoid this,
where is this more apparent than in emergency depart- we have endeavored to confine the text to medical and
ments across the United States and around the world. The surgical conditions that commonly present through the
reliance on imaging for diagnosis and guiding management emergency department rather than including every imag-
decisions throughout medicine has been increasing, and ing possibility that may present. We apologize in advance
this is exemplified in the emergency setting. All imaging if any overlap is identified—it was included for complete-
modalities are available to the emergency physician. More ness—or for any deficiencies; some rare entities may have
than in any other modality, the massive increase in the use been omitted for the sake of brevity.The fundamental divi-
of computed tomograpy (CT ) has led to the development sion of the book is in two parts, one dealing with acute
and growth of the specialty of emergency radiology. The trauma and the other with nontraumatic acute processes,
value of CT in the setting of trauma, investigation of severe and the division of the chapters reflects this. This makes it
headache, abdominal pain, and the evaluation of patients possible to easily select those chapters relevant to an in-
with suspected pulmonary embolus forms the bedrock of dividual radiology practice. Some departments, especially
emergency imaging, although there is an increasing role large academic departments with residency programs, will
for MR and ultrasound imaging in the emergency setting, have trauma units, whereas some community practices
particularly for the rapid evaluation of musculoskeletal in- may run an emergency department without dealing with
jury and emergent neurologic evaluation. The book is an acute trauma.
attempt to collate all the radiology information required We are pleased with how this revision has developed
in today’s emergency department setting into one suc- from an abstract concept into reality and built upon the
cinct, practical, and current text that can be used by both first edition. It has taken substantial effort, and we fully ap-
residents in training and general radiologists in practice, preciate the contributions from the authors, all of whom
as well as emergency department physicians and trauma have considerable experience in emergency imaging. We
surgeons. hope that the revision will be as well received as the first
The goal of this revision is to provide updates to address edition and will act as an integral resource for all radiology
the rapid changes in emergency imaging requirements, departments and training programs.
xi

Acknowledgments
We would like to thank many people who helped trans- are experienced radiologists with extensive knowledge
form the concept of this book into a reality. First, we owe in the various aspects of emergency radiology. Each au-
thanks to innumerable individuals (staff, residents, fel- thor has added his or her own subspecialty expertise
lows, technologists, and nurses) at the Boston University to the chapters, which has resulted in the final product,
Medical Center who helped us and our colleagues build a textbook that we believe they should all be proud of.
multidisciplinary groups for the care of the acutely ill Finally, thanks to all the staff at Elsevier, especially Amy
patient. This was the principal driving force behind our Meros and Robin Carter, who waited patiently for us to
growing interest in the field of emergency radiology. We deliver the various parts of the book, sometimes at a
would also like to thank Dr. James Thrall for insisting on slower-than-hoped-for pace.
the timeliness and necessity of this text to add to THE J.A.S.
REQUISITES series. We would also like to extend a sin- B.C.L.
cere thank you to the contributing authors, all of whom
xiii

Contents
Chapter 1 Chapter 8
Traumatic and Nontraumatic Emergencies of the Nontraumatic Emergency Radiology of the
Brain, Head, and Neck 1 Thorax 243
Glenn D. Barest, Asim Z. Mian, Rohini N. Nadgir, and Osamu Sakai Alejandra Duran-Mendicuti, Scott White, Salvatore G. Viscomi,
Michael Stella, and Aaron D. Sodickson
Chapter 2
Chest Trauma 61 Chapter 9
Ryan T. Whitesell and Laura L. Avery Nontrauma Abdomen 281
Stephan W. Anderson, Brian C. Lucey, and Jorge A. Soto
Chapter 3
Abdomen Trauma 81 Chapter 10
Joshua W. Stuhlfaut, Christina A. LeBedis, and Jorge A. Soto Pelvic Emergencies 316
Brian C. Lucey
Chapter 4
Extremity Trauma 115 Chapter 11
Rathachai Kaewlai and Ajay Singh Vascular Emergencies 327
Russ Kuker, Carlos A. Anaya, Ana Maria Gomez, and Felipe Munera
Chapter 5
Extremities: Nontrauma 165 Chapter 12
Luis E. Diaz Emergency Nuclear Radiology 369
Anna K. Chacko and Rashmikant B. Shah
Chapter 6
Imaging Evaluation of Common Pediatric Index 395
Emergencies 186
Jennifer C. Talmadge, Sarah S. Milla, and Sarah D. Bixby
Chapter 7
Traumatic and Nontraumatic Spine
Emergencies 221
Glenn D. Barest and Margaret N. Chapman
xv

THE REQUISITES
Emergency
Radiology

Chapter 1
Traumatic and Nontraumatic
Emergencies of the Brain,
Head, and Neck
Glenn D. Barest, Asim Z. Mian, Rohini N. Nadgir, and Osamu Sakai
Imagine you are asked to create a list of the disorders of to study the other volumes in the Requisites series (es-
the brain, head, and neck that one might commonly expect pecially Neuroradiology, Musculoskeletal Imaging, and
to encounter at an emergency department (ED) and de- Pediatric Radiology), which cover this material in great
scribe the typical imaging features. At first, this challenge detail. In this attempt at condensing so much material
seems straightforward enough. However, upon beginning into one useful volume, important topics inevitably have
the task, it soon becomes clear that almost every disorder been neglected. We hope that this volume can serve as
within the realm of neuroradiology/head and neck radi- a starting point for further study and become a valuable
ology might at one time or another present as an acute reference to on-call radiologists, emergency department
emergency. Inclusion of certain diagnoses such as stroke, physicians, and residents of both specialties.
fractures, and epiglottitis is a must. Other diagnoses, such
as oligodendroglioma or perhaps a slowly growing le- INTRACRANIAL HEMORRHAGE AND
sion, might seem less clear-cut. Ultimately, it is important TRAUMATIC BRAIN INJURY
to realize that a wide variety of processes will result in
an alteration in mental status leading to an ED visit, with Whether in the setting of head trauma, spontaneous de-
imaging playing a key role in diagnosis and appropriate velopment of headache, or alteration of mental status, the
management. ability to diagnose intracranial hemorrhage (ICH) is of
Upon admission, inpatient workups now occur on a primary importance for all practitioners. These presenta-
24/7 basis, with many complex examinations completed tions are some of the most common indications for brain
during the night shift. On-call radiologists (often residents imaging in the emergency setting. Almost invariably, the
or fellows) are expected to provide “wet readings” or requisition will read, “Rule out bleed.” An understanding
complete interpretations for complex cases covering the of traumatic and nontraumatic causes of ICH, the usual
full spectrum of medicine, pediatrics, surgery, and related workup, and recognition of ICH is therefore important
subspecialties. It was not that many years ago that the ra- and seems like a natural starting point. A discussion of the
diologist was faced with a seemingly never-ending stack important types of mass effect resulting from ICH and
of plain films from the ED, inpatient wards, and intensive traumatic brain injury is also included in this section. An
care units requiring rapid interpretations. This work was understanding of hemorrhage and herniation syndromes
interrupted by an occasional computed tomography (CT) is central to the discussion of other topics that follow, such
scan. In this new millennium, during a typical shift the radi- as stroke and neoplasms.
ologist must maintain a rapid pace to review thousands of The word hemorrhage has Greek origins: the prefix
cross-sectional CT and magnetic resonance images (MRI) haima-, meaning “blood,” and the suffix -rrhage, meaning
with two-dimensional (2D) and three-dimensional (3D) re- “to gush or burst forth.” Incidence of ICH is approximate-
formats. For this reason, the majority of the discussion and ly 25 to 30 per 100,000 adults in the United States, with a
most of the examples in this chapter are based on these higher incidence in elderly hypertensive patients. ICH is
modalities and the latest techniques. typically more common in the African American and Asian
The most daunting part of preparing this chapter was populations. Bleeding may take place within the substance
to boil down all of the disorders and details to a set of req- of the brain (intraaxial) or along the surface of the brain
uisites. Division of this chapter into sections is not quite (extraaxial). Intraaxial hemorrhage implies parenchymal
as neat as one might think. For example, it is not possible hemorrhage located in the cerebrum, cerebellum, or brain-
to separate the vascular system from discussion of the stem. Extraaxial hemorrhages include epidural, subdural,
brain, head and neck, or spine, and the imaging methods and subarachnoid hemorrhages, and intraventricular hem-
applied to the extracranial vessels in the setting of stroke orrhage can be considered in this group as well. Hem-
are similar to those used for blunt or penetrating trauma orrhages can lead to different types of brain herniation,
to the neck. One may therefore notice mention of similar from direct mass effect and associated edema or develop-
techniques and findings in several places with examples ment of hydrocephalus, causing significant morbidity and
appropriate to the context. All readers would do well mortality.
1
2 Chapter 1 Traumatic and Nontraumatic Emergencies of the Brain, Head, and Neck
TABLE 1-1 Usual Magnetic Resonance Signal Characteristics of Hemorrhage

Stage Time Component T1 T2
Hyperacute (0-12 h) Oxyhemoglobin Isointense Hyperintense

Acute (12 h-3 days) Deoxyhemoglobin Isointense Hypointense
Early subacute (3-7 days) Methemoglobin Hyperintense Hypointense
(intracellular)
Late subacute (1 wk-1 mo) Methemoglobin Hyperintense Hyperintense
(extracellular)
Chronic (>1 mo) Hemosiderin Hypointense Hypointense
General Imaging Characteristics of the injury. Although it is beyond the scope of this
of Hemorrhage chapter, a description of the physics of the signal char-
acteristics of blood products on MRI is generally based
The appearance of ICH on a CT scan can vary depending on the paramagnetic effects of iron and the diamagnetic
on the age of the hemorrhage and the hemoglobin level. effects of protein in the hemoglobin molecule. The usual
The attenuation of blood is typically based on the protein signal characteristics of hemorrhage and the general time
content, of which hemoglobin contributes a major por- course over which hemorrhages evolve are summarized
tion. Therefore the appearance of hyperacute/acute blood in Table 1-1.
is easily detected on a CT scan in patients with normal
hemoglobin levels (approximately 15 g/dL) and typically EXTRAAXIAL HEMORRHAGE
appears as a hyperattenuating mass. This appearance is
typical because, immediately after extravasation, clot for- Extraaxial hemorrhage occurs within the cranial vault but
mation occurs with a progressive increase in attenuation outside of brain tissue. Hemorrhage can collect in the epi-
over 72 hours as a result of increased hemoglobin concen- dural, subdural, or subarachnoid spaces and may be trau-
tration and separation of low-density serum. On the other matic or spontaneous. It is important to recognize these
hand, in anemic patients with a hemoglobin level less than entities because of their potential for significant morbidity
10 g/dL, acute hemorrhage can appear isoattenuating to and mortality. Poor clinical outcomes are usually the result
the brain and can make detection difficult. Subsequently, of mass effect from the hemorrhage, which can lead to
after breakdown and hemolysis, the attenuation of the clot herniation, increased intracranial pressure, and ischemia.
decreases until it becomes nearly isoattenuating to cere- Intraventricular hemorrhage will be considered with these
brospinal fluid (CSF) by approximately 2 months. In the other types of extracerebral hemorrhage.
emergency setting, one should be aware of the “swirl” sign
with an unretracted clot that appears to be hypoattenuat-
Epidural Hemorrhage
ing and resembles a whirlpool; this sign may indicate ac-
tive bleeding and typically occurs in a posttraumatic set- Epidural hematoma is the term generally applied to a
ting. It is important to recognize this sign, because prompt hemorrhage that forms between the inner table of the cal-
surgical evacuation may be required. The amount of mass varium and the outer layer of the dura because of its mass-
effect on nearby tissues will depend on the size and loca- like behavior. More than 90% of epidural hematomas are
tion of the hemorrhage, as well as the amount of second- associated with fractures in the temporoparietal, frontal,
ary vasogenic edema that develops. and parieto-occipital regions. CT is usually the most effi-
Use of an intravenous contrast agent usually is not nec- cient method for evaluation of this type of hemorrhage.An
essary for CT detection of ICH. If a contrast agent is used, epidural hematoma typically has a hyperdense, biconvex
an intraaxial hemorrhage can demonstrate an enhancing appearance. It may cross the midline but generally does
ring that is usually due to reactive changes and formation not cross sutures (because the dura has its attachment at
of a vascularized capsule, which typically occurs 5 to 7 the sutures), although this might not hold true if a fracture
days after the event and can last up to 6 months. Subacute disrupts the suture. Epidural hematomas usually have an
and chronic extraaxial hematomas also can demonstrate arterial source, commonly a tear of the middle meningeal
peripheral enhancement, usually because of reactive artery, and much less commonly (in less than 10% of cases)
changes and formation of granulation tissue. Unexpected a tear of the middle meningeal vein, diploic vein, or ve-
areas of enhancement should raise concern, because ac- nous sinus (Figs. 1-1 and 1-2). The classic clinical presenta-
tive bleeding can appear as contrast pooling. Refer to the tion describes a patient with a “lucid” interval, although
section on aneurysms and vascular malformations in this the incidence of this finding varies from 5% to 50% in the
chapter for a discussion of CT angiography in the setting literature. Prompt identification of an epidural hematoma
of acute ICH. is critical, because evacuation or early reevaluation may
MRI has greatly revolutionized the evaluation of ICH. be required. Management is based on clinical status, and
The evolution of hemorrhage from the hyperacute to therefore alert and oriented patients with small hemato-
the chronic stage will have corresponding signal chang- mas may be safely observed. The timing of follow-up CT
es on T1-weighted images (T1WIs), T2-weighted images depends on the patient’s condition, but generally the first
(T2WIs), fluid-attenuated inversion recovery (FLAIR) im- follow-up CT scan may be obtained after 6 to 8 hours and,
ages, and gradient-echo sequences. These properties can if the patient is stable, follow-up may be extended to 24
assist in detection and understanding of the time course hours or more afterward.
Chapter 1 Traumatic and Nontraumatic Emergencies of the Brain, Head, and Neck 3
A B
C
FIGURE 1-1 An epidural hematoma. A, Computed tomography (CT) shows a usual biconvex, hyperdense acute
epidural hematoma causing effacement of sulci and lateral ventricles and shift of midline structures. B, A CT
volume-rendered image shows a nondisplaced fracture at the vertex involving the coronal suture. C, Coronal
multiplanar reconstruction shows a biconvex epidural hematoma crossing midline over the superior sagittal sinus
(arrows).
Subdural Collections
hyperattenuating, crescentic appearance overlying the ce-
Subdural hematoma (SDH) is the term generally applied rebral hemisphere (Fig. 1-3).These hemorrhages can cross
to a hemorrhage that collects in the potential space sutures and may track along the falx and tentorium but do
between the inner layer of the dura and the arachnoid not cross the midline. Inward displacement of the cortical
membrane. It is typically the result of trauma (e.g., mo- vessels may be noted on a contrast-enhanced scan. SDHs
tor vehicle collisions [MVCs], assaults, and falls, with the have a high association with subarachnoid hemorrhage.
latter especially occurring in the elderly population). Acute SDHs thicker than 2 cm that occur with other pa-
An SDH causes a tear of the bridging vein(s) and has a renchymal injuries are associated with greater than 50%
mortality. As the SDH evolves to the subacute stage (with- isoattenuating SDHs can be especially challenging be-
in 5 days to 3 weeks) and then to the chronic stage (after cause findings are symmetric. One should beware of bilat-
more than 3 weeks), it decreases in attenuation, becoming eral isoattenuating SDHs, particularly in elderly patients
isodense to the brain and finally to CSF. A subacute SDH who do not have generous sulci and ventricles. At this
can have a layered appearance as a result of separation stage, the SDH should be conspicuous on MRI, especially
of formed elements from serum. Subacute hemorrhages on FLAIR sequences. A subacute SDH also may be very
may be relatively inconspicuous when they are isodense, conspicuous on T1WIs because of the hyperintensity of
and therefore it is especially important to recognize signs methemoglobin.
of mass effect, such as sulcal effacement, asymmetry of Chronic subdural hematomas are collections that have
lateral ventricles, and shift of midline structures, as well been present for more than 3 weeks. Even a chronic he-
as sulci that do not extend to the skull (Fig. 1-4). Bilateral matoma may present in the emergency setting, such as
A B
C D
FIGURE 1-2 An epidural hematoma and complications demonstrate on noncontrast CT. A, The “swirl” sign in
this large epidural hematoma suggests continued bleeding. B, A pontine (Duret) hemorrhage (arrow) and efface-
ment of the basal cisterns as a result of downward herniation. C, Uncal herniation (the arrow shows the margin
of the left temporal lobe) and a resultant left posterior cerebral artery territory infarct. The brainstem is distorted
and also abnormally hypodense. D, Infarcts in bilateral anterior cerebral, left middle cerebral, and left posterior
cerebral artery territories as a result of herniations.
in a patient prone to repeated falls who is brought in a contrast agent. Calcification of chronic SDH can occur
because of a change in mental status. On both CT and and may be quite extensive (Fig. 1-5). Areas of hyperden-
MRI, these collections typically have a crescentic shape sity within a larger hypodense SDH may indicate an acute
and may demonstrate enhancing septations and mem- component due to recurrent bleeding, termed an “acute
branes surrounding the collection after administration of on chronic subdural hematoma.” Mixed density collec-
tions also may be acute as a result of active bleeding or
CSF accumulation as a result of tearing of the arachnoid
membrane. A chronic SDH is usually isointense to CSF on
both T1WIs and T2WIs, but the appearance can be vari-
able depending on any recurrent bleeding within the col-
lection.The FLAIR sequence is typically very sensitive for
detection of chronic SDH as a result of hyperintensity
based on protein content. Hemosiderin within the hema-
toma will cause a signal void because of the susceptibility
effect, and “blooming” (i.e., the hematoma appears to be
larger than its true size) will be noted on a gradient-echo
sequence.
A subdural hygroma is another type of collection that
is commonly thought to be synonymous with a chronic
subdural hematoma. The actual definition of a hygroma
is an accumulation of fluid due to a tear in the arachnoid
membrane, usually by some type of trauma or from rapid
ventricular decompression with associated accumulation
of CSF within the subdural space. Many persons still use
this term interchangeably with chronic subdural hema-
toma. CT demonstrates a fluid collection isodense to CSF
in the subdural space. MRI can be useful in differentiat-
ing CSF from a chronic hematoma based on the imaging
characteristics of the fluid on all sequences. Occasionally
hygromas are difficult to differentiate from the promi-
nence of the extraaxial CSF space associated with cere-
bral atrophy. The position of the cortical veins can be a
FIGURE 1-3 A subdural hematoma with a mixed density layered helpful clue. In the presence of atrophy, the cortical veins
pattern due to recurrent hemorrhages. The image (arrow) shows are visible traversing the subarachnoid space, whereas
one method of measuring midline shift.
A B
FIGURE 1-4 An isodense subdural hematoma. A, Sulcal effacement and a midline shift to the right are clues to
the presence of a left-sided subdural hematoma. B, Reexpansion of the left Sylvian fissure and a reduction in
midline shift after evacuation.
A B
FIGURE 1-5 Calcified subdural hematomas. A, Colpocephaly configuration of the lateral ventricles. B, Bone
window/level settings more clearly show the calcified subdurals in this adult patient who, as a child, had a shunt
implanted because of congenital hydrocephalus.
with a hygroma, they are displaced inward along with the be confounded by artifacts from CSF pulsations, an el-
arachnoid membrane by the fluid in the subdural space. evated level of protein (meningitis), or oxygen concen-
tration (i.e., a high fraction of inspired oxygen) in CSF
Subarachnoid Hemorrhage on FLAIR images and the presence of blood products
from previous microhemorrhages on gradient-echo
Subarachnoid hemorrhage (SAH) fills the space between images.
the pia and the arachnoid membrane, outlining the sulci
and basilar cisterns. SAH can be due to a variety of causes, Intraventricular Hemorrhage
including trauma, a ruptured aneurysm, hypertension, ar-
teriovenous malformation, occult spinal vascular malfor- In the adult population, intraventricular hemorrhage
mation, and hemorrhagic transformation of an ischemic (IVH) is typically caused by trauma. It can result from ex-
infarction. SAH is often associated with overlying traumat- tension of a parenchymal hemorrhage into the ventricles
ic SDH. SAHs generally do not cause mass effect or focal or from redistribution of SAH. Primary IVH is uncommon
regions of edema. However, in patients presenting with and is usually caused by a ruptured aneurysm, an intra-
ominous signs on clinical grading scales, such as stupor or ventricular tumor, vascular malformation, or coagulopa-
coma, diffuse cerebral edema may be evident. On CT, hy- thy (Fig. 1-8). Large IVHs are quite conspicuous on CT or
perdensity is seen within the sulci and/or basilar cisterns MRI. They may occupy a majority of the ventricle(s) and
(Figs. 1-6 and 1-7). may result in hydrocephalus and increased intracranial
Although MRI may be as sensitive as CT for the de- pressure. Small amounts of IVH may be difficult to de-
tection of acute parenchymal hemorrhage and SAH, CT tect; one must check carefully for dependent densities
generally remains the modality of choice (and the im- within the atria and occipital horns of the lateral ventri-
aging gold standard). The sensitivity of CT for the de- cles. Normal choroid plexus calcifications in the atria of
tection of SAH compared with CSF analysis can vary lateral ventricles, in the fourth ventricle, and extending
from up to 98% to 100% within 12 hours to approxi- through the foramina of Luschka should not be mistaken
mately 85% to 90% after 24 hours of symptom onset. for acute IVH.
Other factors affecting sensitivity are the hemoglobin Another less common type of extracerebral ICH that
concentration and the size and location of the hemor- may present acutely is a pituitary hemorrhage, which is
rhage. CT is widely available, can be performed rapidly, usually associated with pituitary apoplexy due to pituitary
and is relatively inexpensive. In several small studies, necrosis that may become hemorrhagic. Presenting symp-
MRI has demonstrated sensitivity equivalent to CT for toms may include headache, visual loss, ophthalmoplegia,
detection of acute parenchymal hemorrhage and SAH. nausea, and vomiting. Other causes of pituitary hemor-
In some cases of “CT-negative” (subacute) hemorrhage, rhage include tumors (e.g., macroadenoma and germino-
MRI has shown greater sensitivity. However, results may ma) and, less commonly, trauma.
A B
C
FIGURE 1-6 Subarachnoid hemorrhage from a ruptured aneurysm. A, Noncontrast computed tomography (CT)
shows ill-defined hyperdense subarachnoid hemorrhage in the left Sylvian cistern (black arrow) and rim calcifica-
tion in the wall of the aneurysm (white arrow). B, A volume-rendered image from CT angiography shows a large
aneurysm (arrow) projecting above the lesser sphenoid wing. C, Reconstruction from a three-dimensional rota-
tional digital subtraction angiogram shows the carotid-ophthalmic aneurysm to the best advantage.
INTRAAXIAL HEMORRHAGE Contusion

The cause of intraaxial (parenchymal) hemorrhages can Parenchymal contusions result from blunt trauma and can
generally be categorized as spontaneous or traumatic.Trau- occur in the cortex or white matter. Their locations are
matic causes include blunt injury from MVCs, assault, and typically at the site of greatest impact of brain on bone,
penetrating injuries such as gunshot wounds. Intraaxial including the anterior/inferior frontal lobes and the tem-
hemorrhages have many spontaneous causes, which are poral lobes. They can be considered coup (occurring at
discussed in the section on hemorrhagic stroke. the site of impact) or contrecoup (opposite the site of
B
FIGURE 1-7 Subarachnoid hemorrhage and complications. A, Three computed tomography (CT) images show
diffuse hyperdense subarachnoid hemorrhage filling basal cisterns and cerebral sulci bilaterally. Diffuse loss of
gray–white differentiation and effacement of the sulci and cisterns probably preclude the need for further work-
up. B, A volume-rendered image from CT angiography demonstrates lack of enhancement of intracranial vessels
suggesting poor intracranial flow consistent with the expected elevation of intracranial pressure.
impact) types. On CT, a contusion typically appears as an Diffuse Axonal Injury

area of hyperdensity with a surrounding rim of hypodense
edema. A parenchymal contusion can initially appear as a Diffuse axonal injury (DAI) is another type of traumatic
focal area of subtle hypodensity and may blossom on fol- brain injury that may present with parenchymal hemor-
low-up examination at 12 to 24 hours with development rhages and is distinct from a parenchymal contusion. DAI
of an obvious central area of hyperdensity and a larger sur- is an injury to the axons caused by acceleration/decelera-
rounding zone of hypodense edema (Fig. 1-9). On MRI, sig- tion injury with a rotational component (usually from an
nal characteristics reflect the hemorrhagic and edematous MVC or other blunt trauma to the head). Complete tran-
components. Over time, the density and signal character- section of axons may occur with injury to the associated
istics of the hemorrhage will evolve in a fashion similar capillaries, or partial disruption of the axons may occur.
to a spontaneous hemorrhage. Parenchymal hemorrhage DAI lesions typically occur at the interfaces of gray and
due to penetrating trauma, such as from a gunshot wound white matter in the cerebral hemispheres, the body and
or impalement, will follow the same general pattern of splenium of the corpus callosum, the midbrain, and the
evolution. upper pons. Lesions also may be seen in the basal ganglia.
A B
FIGURE 1-8 Intraventricular hemorrhage. A, A fluid-attenuated inversion recovery magnetic resonance image
shows a hyperintense hemorrhage isolated to the frontal horn of the right lateral ventricle. B, An image from a
right internal carotid artery digital subtraction angiogram in the late arterial phase shows a nidus (arrow) and an
early draining vein (arrowhead) diagnostic of an arteriovenous malformation.
A B
FIGURE 1-9 Blossoming of a contusion. A, Computed tomography (CT) shows a thin left frontoparietal subdural
hematoma tracking along the anterior falx and mild sulcal effacement. B, A follow-up CT scan after 24 hours
shows a hyperdense parenchymal hemorrhage and surrounding edema in left frontal lobe and a stable subdural
hematoma. Notice the mass effect on the left lateral ventricle.
Patients sustaining DAI typically lose consciousness who recover usually demonstrate lingering effects such
at the moment of impact. DAI may be suspected when as headaches and cognitive deficits. Initial CT scans in
the clinical examination is worse than expected based more than half of patients with DAI may be negative. CT
on the findings of an initial CT scan. Usually, the greater findings include hypodense foci due to edema in areas of
the number of lesions, the worse the prognosis. Persons incomplete axonal disruption and hyperdense foci due
to petechial hemorrhage where complete transection (Fig. 1-11). Lesions may appear hyperintense on diffu-
of the axons and associated capillaries has occurred (Fig. sion-weighted images. It is estimated that more than 80%
1-10). MRI is more sensitive than CT for detection of DAI. of DAI lesions are nonhemorrhagic. Generally, if imaging
Approximately 30% of persons with negative CT find- is repeated within 3 to 5 days, more lesions will become
ings will demonstrate abnormal findings on MRI. These apparent as the process evolves.
findings include FLAIR and T2WI hyperintensities (ede- A staging system for DAI based on locations of lesions
ma) and gradient-echo hypointensities (hemorrhages) on histopathology may be applied to MRI findings. Stage
1 is based on subcortical lesions in the frontal and tem-
poral lobes. Stage 2 will also show lesions in the corpus
callosum and lobar white matter, and stage 3 will have le-
sions in the midbrain and pons. Diffusion tensor imaging is
well suited to the evaluation of white matter tracts and has
been shown to be more sensitive than conventional MRI
for detection of DAI and correlates more closely with clini-
cal outcomes. Diffusion tensor imaging may be helpful for
long-term diagnostic evaluation of patients with mild trau-
matic brain injury more so than in the initial emergency
setting.
BRAIN HERNIATIONS
Brain herniation is a potentially devastating complica-
tion of increased intracranial pressure. The most common
causes include ICHs, brain tumors, and cerebral edema
from stroke or anoxic injury. To explain this concept, a
common example from the literature describes the brain
as being separated into multiple compartments within a
rigid container. Any shift of the brain from one compart-
ment to another is considered herniation. With shift of
the brain, there can be mass effect on adjacent and con-
tralateral parenchyma, the brainstem, major intracranial
FIGURE 1-10 Shear hemorrhages of diffuse axonal injury. Non- vessels, and cranial nerves. As a result, the feared compli-
contrast computed tomography shows three small hemorrhages cations of herniations include ischemic infarcts due to
in the left superior frontal gyrus after blunt head trauma. Note a compression of the major intracranial vessels (commonly,
subdural hematoma along the falx (arrow). the anterior and posterior cerebral arteries), cranial nerve
A B
FIGURE 1-11 Diffuse axonal injury. A, Fluid-attenuated inversion recovery hyperintensities in the posterior limb
of the internal capsule (arrow) and subcortical white matter (arrowhead). B, Gradient-echo hypointensities in the
subcortical white matter indicative of hemorrhages (arrows) were not evident on other sequences. Note intraven-
tricular hemorrhage in the occipital horns of the lateral ventricles.
palsies, and “brain death” due to compression and infarc- midbrain with associated effacement of the ambient and
tion of the brainstem. The major types of intracranial her- quadrigeminal plate cisterns. Hydrocephalus is usually
niations include subfalcine, transtentorial, tonsillar hernia- present as a result of obstruction at the level of the cere-
tion through the foramen magnum, extracranial herniation bral aqueduct of Sylvius.
(through a defect in the skull), and, less commonly, transa-
lar herniation. Once the complications of herniation have Tonsillar Herniation
developed, it is often too late to intervene. Thus it is best
to recognize the signs of impending herniation, when Tonsillar herniation is caused by downward displacement
prompt neurosurgical intervention may avert disaster. of the cerebellar tonsils through the foramen magnum into
the spinal canal (generally by more than 5 mm). Imaging
shows a peg-like configuration to the tonsils with oblitera-
Subfalcine Herniation
tion of the CSF space in the foramen magnum (Fig. 1-12).
Subfalcine herniation occurs as a result of displacement Complications include obstructive hydrocephalus from
and impingement of the cingulate gyrus underneath the compression of the fourth ventricle. Mild tonsillar ectopia,
falx. It is usually caused by mass effect on the frontal lobe Chiari I malformations, and sagging tonsils due to intracra-
and is associated with ipsilateral lateral ventricle compres- nial hypotension should not be mistaken for acute tonsil-
sion and obstruction of the foramen of Monro with dila- lar herniation, but it should be considered seriously when
tation of the contralateral ventricle (“trapped ventricle”). downward mass effect is expected based on brain edema,
The degree of midline shift (not synonymous with subfal- mass, or hemorrhage.
cine herniation) can be estimated by drawing a line be-
tween the anterior and posterior attachments of the falx Extracranial Herniation
and measuring the shift of the septum pellucidum relative
to this line (see Fig. 1-3). Anterior cerebral artery territory An extracranial herniation is the displacement of brain pa-
infarct(s) may result from this type of herniation. renchyma through a cranial and dural defect that is usually
caused by trauma or a craniectomy (usually performed to
prevent downward herniation from acute cerebral ede-
Transtentorial Herniation
ma). Complications may include infarction of the herni-
Transtentorial herniations include two major types: de- ated brain tissue.
scending transtentorial herniation (DTH) and ascending
transtentorial herniation (ATH). An early DTH is known Transalar Herniation
as uncal herniation, in which the uncus (i.e., the ante-
rior portion of the parahippocampal gyrus) is displaced Transalar herniation is uncommon and, by itself, does not
medially and occupies the ipsilateral suprasellar cistern. A cause symptoms. It is usually associated with subfalcine
later-stage DTH is caused by continued mass effect with and transtentorial herniations. This type of herniation is
displacement of the remainder of the medial temporal caused by displacement of the temporal lobe anteriorly
lobe through the tentorial incisura, which completely oc- or of the frontal lobe posteriorly across the sphenoid
cupies the suprasellar cistern (along with the uncus) and wing. One should look for anterior or posterior displace-
causes enlargement of the ipsilateral and effacement of ment of the middle cerebral artery to identify this type of
the contralateral ambient cisterns. This phenomenon oc- herniation.
curs because, as there is marked shifting of brain in the In the setting of severe head trauma, many of these dif-
supratentorial compartment, the brainstem shifts in the ferent types of injuries may coexist. The mechanism of in-
same direction. Occasionally, when marked mass effect jury should correspond with the degree of injury. In cases
is present, there can be compression of the contralateral when the reported mechanism is mild, nonaccidental trau-
cerebral peduncle against the tentorium, or “Kernohan’s ma (e.g., “Trauma X” and “shaken-baby syndrome”) should
notch,” which leads to ipsilateral motor weakness (this be considered. Infants, children, persons with mental or
phenomenon may be a false localizing sign). Other im- physical disabilities, and elderly persons are particularly at
aging findings include a “trapped” temporal horn of the risk. Skull fractures, SAH, SDH, contusions, shear injuries,
lateral ventricle contralateral to the side of the mass and infarcts, vertebral compression fractures, and retinal hem-
Duret hemorrhages—that is, hemorrhages of the midbrain orrhages constitute the usual neuroradiologic spectrum of
and pons caused by stretching and tearing of the arterial abnormalities. Injuries of different ages, metaphyseal and
perforators. In cases of bilateral mass effect, displacement rib fractures, and visceral injuries are other common find-
of both temporal lobes and midbrain can occur through ings of child abuse.
the incisura, leading to effacement of the basilar cisterns
bilaterally. Complications of this type of herniation include ACUTE CEREBROVASCULAR DISORDERS
compression of the posterior cerebral artery and penetrat-
ing basal arteries with associated infarcts in these vascular Although acute cerebrovascular disorders usually do not
distributions (see Fig. 1-2). In addition, compression of the occur as a result of trauma, they are treated with the same
oculomotor nerve (cranial nerve [CN] III) can occur with urgency as traumatic injuries or spontaneous ICH.Accord-
an associated palsy. ATH is less common and is caused by ing to the American Heart Association update for 2015, in
superior displacement of the cerebellum and brainstem the United States, approximately 800,000 strokes occur
through the incisura. ATH is usually due to mass effect in each year (on average, about one stroke occurs every 40
the posterior fossa (as from hemorrhage, tumor, or infarct), seconds, resulting in one death every 4 minutes). Almost
and imaging shows compression on the posterolateral 25% are recurrent, and 75% occur in persons older than
A B
FIGURE 1-12 Tonsillar herniation. A, A sagittal T1-weighted image shows the pegged appearance of the cerebel-
lar tonsils extending through the foramen magnum, simulating a Chiari I malformation (representing a dramatic
change from a previous examination). B, A postgadolinium T1-weighted image shows cerebellar leptomeningeal
enhancement due to cryptococcal meningoencephalitis in this patient with acquired immunodeficiency syn-
drome.
65 years. The 20% mortality rate is surpassed only by car-

diac disease, cancer, and chronic lung disease. Stroke is
the leading cause of severe, long-term disability and long-
term care. Estimates of annual cost exceed $50 billion.
One clinical definition of stroke is a neurologic deficit
caused by inadequate supply of oxygen to a region of the
brain. Stroke can be due to a low flow state or rupture of
a vessel and thus may be divided into ischemic and hem-
orrhagic varieties. The definition of stroke used for cur-
rent clinical trials requires symptoms lasting more than
24 hours or imaging of an acute clinically relevant brain
lesion in a patient with rapidly vanishing symptoms. In the
past, a transient ischemic attack (TIA) implied resolution
of the deficit within a 24-hour period. The current defi-
nition of TIA is a brief episode of neurologic dysfunction
caused by a focal disturbance of brain or retinal ischemia,
with clinical symptoms typically lasting less than 1 hour,
and without evidence of infarction. Estimates of the annual
incidence of TIA in the United States vary from 200,000
to 500,000. The 1-year mortality rate after TIA has been
reported to be 12%. Evidence of acute infarction may be
identified by MRI (tissue-based case definition) in up to
30% of patients who meet the clinical criteria for a TIA.
Semantics can be unclear when an abnormality is detected FIGURE 1-13 A spontaneous parenchymal hemorrhage as a result
on imaging in the absence of symptoms. of uncontrolled hypertension. Noncontrast computed tomogra-
phy in a patient with uncontrolled hypertension shows a large
hyperdense parenchymal hemorrhage arising in the basal ganglia
Hemorrhagic Stroke: Spontaneous with intraventricular extension. Note the ventriculostomy catheter
Parenchymal Hemorrhage in the right lateral ventricle.
Approximately 10% to 15% of strokes present with an

acute parenchymal hemorrhage. The most common causes. (Refer to the section on aneurysms and vascular
cause is hypertension (Fig. 1-13). Coagulopathies, hema- malformations in this chapter for a discussion of CT angi-
tologic disorders including hypercoagulable states, amy- ography in the setting of acute ICH.) Hemorrhages result-
loid angiopathy, drugs, vascular malformations and aneu- ing from use of illicit drugs and vascular malformations
rysms, vasculitides, and tumors round out the usual list of are commonly found in young adults (Fig. 1-14). Sickle
A B
C D
E
FIGURE 1-14 A parenchymal hemorrhage due to use of an illicit drug—Ecstasy (3,4 methylenedioxymethamphetamine). A, Computed
tomography shows a hyperdense acute hemorrhage with minimal surrounding hypodense edema. B, A T1-weighted image shows iso- to
mild hyperintensity with hypointense edema. Fluid-attenuated inversion recovery (C) and fat-suppressed T2-weighted gradient and spin
echo (D) show hypointensity with surrounding hyperintense edema. E, Gradient echo shows a peripheral rim of signal loss and bloom-
ing. In summary, signal changes on T1- and T2-weighted images are consistent with deoxyhemoglobin, although the gradient echo
suggests only a rim of deoxyhemoglobin.
cell disease and venous infarcts also may present with score has been shown to correlate with the initial Na-
parenchymal hemorrhage. A ruptured intracranial aneu- tional Institutes of Health stroke score and is one piece
rysm occasionally may cause a parenchymal hemorrhage of data that may be considered in determining patient
in association with SAH. Hypertensive hemorrhages most management.
commonly occur in the basal ganglia and thalamus but
also may primarily arise within the cerebral hemispheres, Magnetic Resonance: Diffusion-Weighted Imaging
brainstem, or cerebellum. Cerebral amyloid angiopathy MRI with diffusion-weighted imaging (DWI), which be-
(CAA) is another common cause of ICH in patients older came widely available in routine clinical practice in the
than 65 years. CAA can be found in patients with mild cog- late 1990s, offers significantly greater sensitivity and
nitive impairment, Alzheimer-type dementia, and Down specificity for the detection of acute stroke (greater
syndrome with extracellular deposition of β-amyloid oc- than 90% compared with approximately 60% for CT).
curring in the cortex and subcortical white matter. CAA Energy depletion will trigger a cascade that alters the
can be hereditary (autosomal dominant, Dutch type), spo- internal cellular milieu, such as the glutamate excito-
radic (with the presence of the Apoε4 allele), or acquired toxic pathway, in which reduced energy-dependent
(as from hemodialysis). The lobar hemorrhages of CAA glutamate reuptake within the synaptic clefts results in
typically occur in the frontal and parietal regions. MRI is the development of cytotoxic edema. The restriction of
sensitive for the detection of hemosiderin deposition re- water molecule diffusion appears as hyperintensity on
sulting from multiple microhemorrhages over the course diffusion-weighted images. The diffusion “experiment”
of time that appear as small hypointense foci on gradient- can be performed with a variety of rapid imaging tech-
echo sequences. niques, such as echo planar imaging, and can acquire im-
ages of the entire brain in half a minute. This approach
Imaging of Acute Ischemic Stroke minimizes the effects of patient motion, which is espe-
cially important when the clinical presentation includes
Computed Tomography alteration of mental status. The apparent diffusion coef-
The role of imaging in acute stroke diagnosis and man- ficient (ADC) value is a quantitative measure that may be
agement continues to evolve. Since the mid 1970s, unen- calculated from the diffusion-weighted images. Because
hanced CT has been the first-line modality to determine diffusion-weighted images rely on both diffusion and
the cause of acute neurologic deficits. CT can offer the T2 effects, it is wise to confirm that the ADC values are
chance to detect an ischemic infarct, generally in the indeed reduced before diagnosing an acute infarct. This
middle cerebral artery territory, within 3 hours in up to confirmation will reduce the number of false-positive
one third of cases based on findings of subtle parenchy- results due to the “T2 shine-through” effect from old in-
mal hypodensity, loss of gray–white matter differentia- farcts (gliosis) or other T2 hyperintense processes such
tion (including loss of the insular ribbon or margins of as vasogenic edema.
basal ganglia; Fig. 1-15), and effacement of sulci. A hyper- Acute ischemic infarcts appear as hyperintense regions
dense vessel sign may indicate the presence of an acute on DWI (see Fig. 1-15) as quickly as 30 minutes after on-
thrombus and support the diagnosis. The sensitivity for set. Up to 100% sensitivity has been demonstrated in clini-
detection of acute stroke has been shown to increase cal studies. However, in routine practice, small lesions in
with the use of the “acute stroke” window and level set- the brainstem may not be perceived initially, only to be
tings (see Fig. 1-15). A very narrow window width of 8 detected on a follow-up examination prompted by persis-
Hounsfield units (HUs) and a level of 32 HUs (compared tent symptoms. It is also possible that a region of ischemia
with 80 and 40 HUs, respectively) may increase the sen- (prior to a completed infarction) may not be detected on
sitivity of CT to approximately 70% without a loss of an initial imaging study, thus providing a false-negative re-
specificity. sult. False-positive results on DWI can be due to processes
CT is currently used to screen patients who may be that mimic stroke and also cause diffusion restriction, such
considered for treatment with intravenous recombinant as certain neoplasms, multifocal metastatic disease, and ab-
tissue plasminogen activator (rt-PA). This medication is scesses. The presence or absence of associated findings on
currently approved by the Food and Drug Administra- conventional MRI sequences—such as loss of gray–white
tion for use within 3 hours of onset based on guidelines matter differentiation on T1WIs and hyperintense edema
from the National Institute of Neurologic Disorders and on FLAIR and T2WIs—may help with diagnosis, although
Stroke rt-PA trial. Since 2013, its use within 4.5 hours of these signs may be inconspicuous for 6 to 12 hours after
stroke onset in selected patients has been endorsed in a stroke onset. Blooming on gradient-echo sequences due to
joint clinical policy statement of the American College of intravascular thrombus and loss of expected vascular flow
Emergency Physicians, American Academy of Neurology, voids are other useful clues.
and Neurocritical Care Society. Beyond this time, the risk Lacunar infarcts are generally less than 1 cm in diameter
of ICH due to intravenous thrombolysis was shown to and are presumed to be due to occlusion of small perfo-
outweigh potential benefits. An association between larg- rating branches as a result of embolic, atheromatous, or
er stroke volumes (greater than one third of the middle thrombotic lesions. Lacunar infarcts occur most commonly
cerebral artery territory) and reperfusion hemorrhage in the basal ganglia, internal and external capsules, immedi-
was initially reported.This criterion for the use of 100 mL ate periventricular white matter (corona radiata), and, less
estimated infarct volume has commonly been applied in frequently, in the centrum semiovale. Occlusion of basilar
stroke trials. The Alberta Stroke Program early CT score, artery perforators will result in lacunes in the brainstem.
a 10-point topographic scoring system, was developed Diffusion imaging offers the ability to identify very small,
to try to more easily quantify initial stroke volumes. This acute infarcts even in the background of chronic white
A B
C
FIGURE 1-15 A hyperacute infarct. A, Noncontrast computed tomography with a window/level of 80/40 shows
a subtle decrease in density of the right insular cortex. B, The insular “ribbon” sign is more conspicuous with
a stroke window/level of 40/40 (arrows). C, The infarct is much more conspicuous on a diffusion-weighted
image. D, Time-of-flight magnetic resonance angiography shows attenuation of right middle cerebral artery
distal branches.
matter disease and remote lacunes (Fig. 1-16). Although MRI Diffusion-weighted MRI is most sensitive for evaluating
is still considered a relatively expensive technique, it has the the different patterns of injury. In preterm infants sub-
potential to reduce the number of unnecessary hospital ad- jected to mild hypotension, the periventricular regions
missions for recurrent small vessel infarcts in many patients. are most often affected. With more severe hypotension,
It also may assist in selecting the most appropriate pathway the basal ganglia, brainstem, and cerebellum may be in-
for patients with central embolic sources of infarcts based volved. In full-term infants with mild hypotension, in-
on the detection of infarcts in different vascular territories. farcts in the border zones between anterior and middle
MRI is also valuable in the setting of neonatal hypoxic cerebral arteries or between middle and posterior cere-
ischemic encephalopathy. Cranial ultrasonography and bral arteries may result. Severe hypotension may result in
CT may be used to evaluate germinal matrix hemor- infarcts of basal ganglia, hippocampi, corticospinal tracts,
rhages, periventricular leukomalacia, and hydrocephalus. and sensorimotor cortex.
A B
C
FIGURE 1-16 An acute lacunar infarct. A, Computed tomography shows multifocal hypodensities. B, A fluid-at-
tenuated inversion recovery image shows corresponding hyperintensities due to chronic small vessel disease. C, A
diffusion-weighted image shows the acute infarct in the left lentiform nucleus/posterior limb of internal capsule in
a patient with acute onset of right-sided weakness. An apparent diffusion coefficient map (not shown) confirmed
restricted diffusion. Other periventricular white matter mild hyperintensities are the result of “T2 shine-through.”
Diffusion-weighted hyperintensity generally begins to Magnetic Resonance Angiography

decline after a few days, with the process of ADC pseudo- Noninvasive imaging of the vessels of the head and neck
normalization usually taking place during the next few with MR angiography (MRA) based on time-of-flight or
weeks. Final ADC values will vary based on the degree of phase-contrast MRA techniques can be used to locate ste-
gliosis or cavitation of the infarct. It should be noted that noses and occlusions in the extracranial and intracranial
infarct development depends on the magnitude and dura- arterial systems (see Fig. 1-15). Gadolinium-enhanced MRA
tion of ischemia and the metabolic demands of the affect- has become the standard of care at some institutions; this
ed tissue. Although diffusion restriction due to ischemia procedure requires consideration of renal function. Com-
almost always results in infarction, rare cases of spontane- plete brain MRI and head and neck MRA examinations can
ous reversible diffusion abnormalities have been reported, be acquired in less than 30 minutes and have become the
as well as those occurring in the setting of thrombolytic routine standard of care; they are often performed imme-
therapy. diately or soon after completion of CT. It must be stressed
that patient safety is a primary concern and therefore care- models with up to 320 rows are available. Analogous to
ful attention to screening for potential contraindications PWI, CTP is based on measurement of tissue density as a
prior to MR scanning is a requisite at all times. function of time during a first pass of an intravenous con-
trast agent and commonly uses deconvolution analysis. In
Magnetic Resonance: Perfusion Imaging contrast to PWI, as a result of the proportionate increase
It became clear from imaging-based stroke trials that final in tissue attenuation due to iodine concentration, quantita-
infarct volumes were often larger than those identified by tive (rather than relative) estimation of CBV (and therefore
imaging at the time of admission. Advances in rapid scan- CBF) can be obtained by CTP. Other parameters includ-
ning techniques soon led to the ability to obtain functional ing time to maximum enhancement (Tmax) also may be
images of brain perfusion. By demonstrating an ischemic measured.
zone at the periphery of an acute infarct, salvageable tissue CTP applied in the setting of acute stroke has been vali-
(the so-called penumbra) could be targeted with novel dated with clinical outcomes and follow-up imaging and
therapies. Dynamic gadolinium-enhanced T2* perfusion- also by comparison with DWI. Wintermark and colleagues
weighted imaging (PWI) is one available technique that is initially proposed that regions with a CBV less than 2.5
based on the decrease in tissue signal intensity as a func- mL/100 g be considered the “core infarct” and regions
tion of time during passage of a bolus of contrast mate- with a CBF reduction of more than 34% be defined as the
rial. Functional “maps” of different perfusion parameters penumbra. These values were based on correspondence
may be calculated from the time-signal intensity curves with initial DWI abnormality and final infarct size. Schaefer
obtained during a minute-long acquisition. Cerebral blood and colleagues later proposed other absolute values and
volume (CBV) and tissue mean transit time (MTT) can be the use of normalized CBV and CBF ratios to help distin-
estimated using different methods, most commonly decon- guish ischemic tissue likely to become infarcted from that
volution analysis. One limitation of MR-based techniques likely to survive after intraarterial recanalization therapy.
is that the blood volume estimate is a relative value. Cere- Perfusion maps can be visually compared to determine
bral blood flow (CBF) can be estimated by dividing CBV if a penumbra is present but may underestimate or over-
by MTT. A penumbra will be identified when a region of estimate the extent of tissue at risk (Fig. 1-17). Software
decreased CBF or prolonged MTT is larger than the infarct packages are available that can automatically segment the
detected by DWI—a perfusion mismatch. Based on the ex- processed perfusion maps into core infarct, penumbra, and
tent of the mismatch, aggressive therapies may be pursued normal regions based on thresholding techniques.
to limit the final infarct volume. Therapeutic trials of desmoteplase, a novel thrombo-
In some cases, the perfusion abnormality may exact- lytic drug, including the Desmoteplase in Acute Ischemic
ly match the diffusion abnormality, and thus there is no Stroke (DIAS) and Dose Escalation study of Desmoteplase
penumbra. The final infarct volume is not expected to in- in Acute Ischemic Stroke (DEDAS) trials, were based on
crease further. In other cases, when prompt reperfusion demonstration of a perfusion mismatch. Although clinical
has occurred, such as from early vessel recanalization, the outcomes were not promising, these trials demonstrated
perfusion abnormality may be smaller than the diffusion the value of advanced imaging compared with unen-
abnormality. In both of these situations, the risk of aggres- hanced CT and use of a strict time limit alone.
sive treatment is probably not warranted. The potential of Thrombolysis with intravenous rt-PA is limited by a
improved clinical outcomes from therapeutic strategies short time window after onset of symptoms and a recana-
based on perfusion imaging may result from either salvage lization rate of less than 50%. Stroke specialists had hoped
of tissue at risk or reduction of complications. that an endovascular approach to treatment of severe
Arterial spin labeling (ASL) is an MR perfusion tech- strokes would be a valuable addition or alternative to in-
nique that does not require injection of a contrast agent. travenous therapy. The paradigm of acute stroke imaging
ASL uses paramagnetic labeling of water in blood flowing has continued to evolve with clinical trials.
to the brain to produce measurements that are propor- Over the course of several trials without promising re-
tional to CBF. There are many varieties and technical limi- sults, including randomized, controlled trials of intraarte-
tations of ASL. Clinical utility will require determination of rial treatment (Interventional Management of Stroke III
appropriate clinical perfusion thresholds. ASL is becoming [IMS III], Synthesis, and Mechanical Retrieval and Recanali-
increasingly available but is not yet used routinely at most zation of Stroke Clots Using Embolectomy [MR RESCUE]),
centers. many lessons were learned. Improved outcomes were
demonstrated with enrollment of patients with severe
Computed Tomography: Perfusion Imaging strokes, proof of proximal vessel occlusion, early initiation
The advent and wide availability of multidetector CT of treatment, and use of modern thrombectomy devices
(MDCT) scanners has led to the use of CT angiography (i.e., retrievable stents). The recently published results of
(CTA) and CT perfusion (CTP) imaging in the workup of the Multicenter Randomized Clinical Trial of Endovascu-
suspected acute ischemic stroke. The ability to acquire a lar Treatment of Acute Ischemic Stroke in the Netherlands
large 3D volume of data rapidly during administration of (MR CLEAN), which required demonstration of a proximal
a bolus of contrast material combined with submillimeter vessel occlusion, ended the long drought of negative re-
spatial resolution results in CTA images that in many in- sults for endovascular treatment (Fig. 1-18).
stances approach the diagnostic quality of more invasive In the Extending the time for Thrombolysis in Emergen-
digital subtraction angiograms. Large detector arrays and cy Neurological Deficits–Intra-Arterial (EXTEND-IA) trial,
cine or shuttle modes of scanner operation allow for gen- the imaging inclusion criteria were a proximal intracranial
erous coverage of the brain during perfusion studies. De- occlusion, a perfusion mismatch (CTP Tmax >6-second
tector arrays with 64 rows are common now, and newer delay perfusion volume compared with CT-CBF or DWI
A B CBV CBF MTT
D
FIGURE 1-17 Perfusion computed tomography (CT)—large mismatch. A, Noncontrast CT shows decreased den-
sity of the left caudate head and putamen. B, Cerebral blood flow (CBF) and mean transit time (MTT) abnormali-
ties are much larger than core infarct (cerebral blood volume [CBV] abnormality). C, CT follow-up 1 week after
conservative management shows that the final infarct volume closely matches the initial CBV abnormality. D, An
initial CT angiogram showed abrupt occlusion of the left middle cerebral artery stem (arrow) but with filling of
distal branches as a result of robust leptomeningeal collateral circulation.
A B C
FIGURE 1-18 Mechanical thrombectomy. A, An acute right middle cerebral artery occlusion. B, A Merci retriever
is deployed distal to the thrombus. (Note that newer stent retrievers, such as the Solitaire revascularization device,
have supplanted use of this device.) C, Recanalization of the right middle cerebral artery after clot retrieval.
infarct core), and infarct core lesion volume less than 70

mL.The study demonstrated that early thrombectomy with
a stent retriever in this setting improved reperfusion, early
neurologic recovery, and functional outcome.
Another consideration in penumbral imaging is based on
assessment of collateral circulation by CTA, MRA, or digital
subtraction angiography (DSA). Good collateral circulation
has been associated with improved clinical outcomes after
treatment even when reperfusion was achieved. Different
methods of grading collaterals have been described based
on single or multiphase CTA techniques. In the multicenter
Endovascular Treatment for Small Core and Anterior Circu-
lation Proximal Occlusion with Emphasis on Minimizing
CT to Recanalization Times (ESCAPE) trial, imaging inclu-
sion/exclusion criteria were based on CTA identification
of the location of the occlusion, the extent of collateral
vessels, and the extent of CTP mismatch (CBV and CBF).
Rapid endovascular thrombectomy improved functional
outcomes and reduced mortality in patients with acute
strokes who had proximal vessel occlusion, a small infarct
core, and moderate to good collateral circulation.
A recent mismatch-based penumbral imaging paradigm
takes into consideration venous outflow based on MR
susceptibility-weighted imaging (SWI). An increase in

brain tissue demand for oxygen leads to an increase in con- FIGURE 1-19 Hemorrhagic transformation of an ischemic infarct.
centration of deoxyhemoglobin in capillaries and veins Noncontrast computed tomography 24 hours postictus shows a
and signal loss on SWI. Perfusion mismatch may be graded hyperdense hemorrhage within a large left middle cerebral artery
by the ratio of SWI abnormality to the DWI infarct core territory infarct.
volume.
Thus current paradigms may be based on identifica-
tion of tissue-based, collateral, or venous outflow–based
mismatches. Continued outcomes-based research will be
necessary to determine the best imaging protocol to iden-
tify the subset of patients who might benefit from aggres-
sive treatment with a reduced risk of symptomatic hemor-
rhage. It should be noted that great variety exists in the
application of these techniques in routine clinical practice.
Some authors have proposed that CT and MR perfusion
techniques should be limited to research patients and that
clinical decisions regarding pursuit of endovascular treat-
ment should be based on results of noncontrast CT, CTA,
and DWI examinations.
Hemorrhagic Transformation
Hemorrhagic transformation of an ischemic infarct that is
thought to result from reperfusion injury can be a dreaded
complication of therapy or may happen spontaneously
within hours or after a period of several weeks (Fig. 1-19).
If a large hematoma is present at the time of initial im-
aging, it may not be possible to distinguish a primary pa-
renchymal hemorrhage from hemorrhagic transformation.
The blood products generally cause substantial artifacts
on DWI. However, if the hemorrhage is confined within a FIGURE 1-20 Cortical laminar necrosis. A T1-weighted image
larger zone of restricted diffusion, the cause may be clear. shows gyriform hyperintensity in a peri-sylvian distribution 1 week
Petechial hemorrhages occur very commonly within an after a middle cerebral artery infarct.
ischemic infarct, are best detected by gradient-echo imag-
ing, and do not usually lead to increased morbidity. attributed to cortical laminar necrosis (Fig. 1-20). It seems
that gray matter is more vulnerable to ischemic necrosis
than white matter (especially the third layer of the six
Cortical Laminar Necrosis
cortical layers), and although the signal changes may lead
A pattern of gyriform T1-weighted hyperintensity devel- one to diagnose hemorrhage or calcification, in one histo-
oping a week or two after an ischemic infarct may be logic study neither was detected.The exact cause of the T1
the common variants is necessary to avoid diagnostic pit-

falls, especially false-positive results. On unenhanced CT,
normal venous structures may appear denser than usual
as a result of dehydration or elevated hematocrit, whereas
thrombosis should appear hyperdense relative to arteries.
A filling defect or occlusion may be detected on contrast-
enhanced CT. CT venography can be performed with a
thin-section, volumetric technique that allows the cre-
ation of 2D and 3D reconstructions. Normal and throm-
bosed venous sinuses take on many different appearances
on MRI depending on scan parameters, flow velocity,
and turbulence. Unexpected hyperintensity, loss of usual
flow voids, and blooming on gradient-echo sequence are
clues that flow-sensitive MR venography (MRV) should
be performed. Time-of-flight MRV may be less sensitive
than phase contrast technique because of shine-through
of methemoglobin in a thrombosed sinus, simulating flow
in the vessel. Contrast-enhanced MRV may be more sensi-
tive, although enhancement of chronic thrombus can be
misleading. Associated findings of edema, hemorrhage, or
ischemic infarct may help one arrive at the correct diagno-
sis, but brain swelling without signal changes has been re-
A ported in up to approximately 40% of patients. Cavernous
sinus thrombosis is discussed in relation to complex sinus
and orbit infections in the section on head and neck imag-
ing in this chapter. Prompt diagnosis of cerebral venous
thrombosis is critical, because many of the parenchymal
changes may be reversible. Systemic anticoagulation and
local catheter-based thrombolytic, mechanical, or rheolytic
(hydrodynamic) clot dissolution are treatment consider-
ations. Intracranial hypertension and collateral formation
leading to dural arteriovenous malformations are possible
long-term sequelae.
B C Imaging of the cerebral venous sinuses is also often
FIGURE 1-21 Venous sinus thrombosis. A, T1-weighted image performed in the workup of patients with papilledema or
shows loss of usual flow voids in the superior sagittal and straight suspected idiopathic intracranial hypertension (IIH). Many
sinuses (arrows). B, Two-dimensional phase contrast magnetic patients with IIH have venous hypertension and stenosis
resonance (MR) venography shows a corresponding lack of flow- of either the dominant or both transverse sinuses. One ret-
related signal. C, Three-dimensional phase contrast MR venogra- rospective study reported cure of IIH symptoms in 49 of
phy 1 week after systemic anticoagulation shows recanalization. 52 patients after transverse sinus stent placement.
ANEURYSMS, VASCULAR MALFORMATIONS,

shortening is uncertain, but it may be due to high concen- AND VASCULAR INJURIES
trations of proteins and macromolecules related to tissue
necrosis. Aneurysms and cerebral vascular malformations present
in various ways in the emergency setting. SAH resulting
Cerebral Venous Infarction and Sinus from a ruptured aneurysm and parenchymal hemorrhage
Thrombosis related to an arteriovenous malformation are dramatic ex-
amples of disorders that may present with headache as the
An uncommon (with annual incidence estimates of less chief complaint. Presenting symptoms of nausea and vom-
than 1 case per 100,000 population) but important cause iting are common with hemorrhages that arise in the pos-
of hemorrhage is cerebral venous thrombosis (Fig. 1-21), terior fossa. On routine noncontrast CT, large unruptured
which may affect cortical veins and other portions of the aneurysms may simulate other mass lesions and displace
superficial and deep venous drainage systems. Hypercoag- or compress adjacent structures. Arteriovenous malforma-
ulable states due to pregnancy and the postpartum period tions also may be conspicuous on routine CT based on
or oral contraceptive use, dehydration, regional infections, abnormally enlarged feeding arteries and draining veins or
and trauma are relatively common. Common presenting internal calcifications (Fig. 1-22).
symptoms include headache, seizure, and focal neurologic The traditional gold standard for diagnostic evaluation of
deficits. Fluctuating symptoms and intracranial hyperten- vascular lesions, both spontaneous and traumatic, is DSA.
sion are common as well. Bilateral parenchymal hemor- The risk of major complication from this invasive proce-
rhages or infarcts that do not obey usual arterial territory dure is low in experienced hands, and treatment (complete
borders can be clues to diagnosis. A working knowledge or partial) with endovascular techniques is possible for
of the normal anatomy of the major venous structures and many types of aneurysms and other vascular lesions. That
FIGURE 1-23 Subarachnoid hemorrhage due to a ruptured aneu-

rysm. Noncontrast computed tomography (CT) (upper left) shows
subarachnoid hemorrhage in the left Sylvian fissure and a round
FIGURE 1-22 An arteriovenous malformation. Noncontrast com- hyperdense mass. Images from a CT angiogram (coronal multi-
puted tomography shows a hyperdense lesion extending from the planar reconstruction, volume-rendered volume of interest, and
third ventricle to the right occipital lobe and associated hydro- volume created from a seed point) confirm a large left middle
cephalus (arrows). cerebral artery bifurcation aneurysm.
being said, the constantly improving technology and clini- the presence of dilated draining veins or from asymmet-
cal experience with CTA have led to a substantial decrease ric opacification of the cavernous sinuses, although this
in the number of diagnostic angiograms. CTA is commonly shunting might just as well be due to normal physiologic
applied in the setting of spine, facial, and skull base frac- variation. Evaluation of the smallest arteries is necessary
tures. One study of CTA in 2004 in the setting of acute SAH for the evaluation of cerebral vasculitis. Improvements in
reported a sensitivity of 89% and a specificity of 100% for spatial and temporal resolution and reconstruction tech-
detection of aneurysms. Dual-energy CT may provide ben- niques will certainly reduce the number of false-negative
efits compared with standard techniques. A more recent aneurysm hunts and increase the clinical utility of CTA for
study with 320-detector technique found overall sensitivity evaluation of arteriovenous malformations and vasculitis.
of 96%, specificity of 100%, and accuracy of 95%. Many cen- Use of CTA in the setting of spontaneous parenchymal
ters have adopted immediate CTA in their protocol for the hemorrhage has become routine. Since the initial study
workup of spontaneous SAH (Fig. 1-23). If a ruptured aneu- of CTA in the setting of acute intracerebral hemorrhage
rysm is detected by this method, detail may be adequate for that demonstrated that tiny enhancing foci (extravasation)
treatment planning in certain situations. However, other in- within the hematoma (CTA spot sign) is an independent
vestigators have offered the opinion that the gold standard predictor of hematoma expansion, many other studies
of DSA (with 3D rotational angiography) provides greater have evaluated this sign.An underlying vascular lesion may
sensitivity and should not yet be replaced by CTA. This be found in up to 15% of patients with spontaneous ICH,
opinion is based on reports of a 10% false-negative rate of potentially affecting acute management. Some authors
CTA for aneurysm detection and the belief that the greater recommend spot sign evaluation during CTP imaging. In
spatial resolution of DSA is necessary to accurately deter- addition to its clinical predictive value, the spot sign will
mine proper triage to surgery versus endovascular coiling. continue to be of interest in trials of hemostatic therapy.
Both of these reasons support the use of DSA regardless of
a negative or positive result from CTA. Given its availability
and lack of invasive risks, CTA will probably continue to be CERVICOCEREBRAL ARTERIAL INJURIES
used as a diagnostic tool in this setting.
Spontaneous Cervical Dissection
In the setting of SAH, a negative result of a CTA or DSA
examination often requires a repeat examination, depend- Spontaneous cervical arterial dissection used to be con-
ing on the pattern of hemorrhage. DSA offers evaluation sidered a rarity, but since the 1980s, largely as a result
of cerebral hemodynamics, which is important for the of improvements in imaging, awareness of this cause of
diagnosis of brain and dural vascular malformations. This stroke has increased. It is estimated that up to 25% of
type of detail is still not available with most current CTA strokes in young and middle-aged adults occur on this
techniques, but because of continued technical improve- basis. Community-based studies have found that the an-
ments, time-resolved (multiphase, four-dimensional) CTA nual incidence of internal carotid artery dissection is
is expected to be commonly available in the near future. 3 per 100,000 per year, and that of vertebral artery dis-
On occasion, arteriovenous shunting may be inferred from section is 1.5 per 100,000 per year. A history of a trivial
precipitating event, such as minor movement of the neck, implementation of antithrombotic or other vascular treat-
is commonly reported. Chiropractic manipulation of the ments, the incidence of stroke will be reduced. Because
cervical spine has become recognized as a potential cause more subtle injuries will be detected with advances in CT
of dissection, but estimates of the rate of occurrence vary technology, outcomes research will be necessary to help
widely. Many different types of triggering events associat- determine the most appropriate therapy. It is well known
ed with hyperextension or rotation of the neck—includ- that a certain (small) percentage of patients will present
ing sport and recreational activities, painting of ceilings, with delayed formation and rupture of a posttraumatic
coughing, sneezing, and vomiting—have been reported. pseudoaneurysm, yet recommendations for and timing of
A higher incidence in the autumn suggests inflammation follow-up examination remain rather dubious (Fig. 1-24).
or an excess amount of sneezing and coughing related to Dissection of the internal carotid and vertebral arter-
upper respiratory tract infections as predisposing factors. ies may be the direct result of blunt trauma, with a re-
The effect of genetics has not yet been completely de- ported incidence of less than 1% in some series. As might
termined, but approximately half of patients show mild be expected, the risk of vascular injury in the setting of
ultrastructural connective tissue alterations similar to spine fracture is substantially higher. Another mechanism
Ehlers-Danlos syndrome. Traditional vascular risk factors of carotid injury is intraoral trauma, such as from a fall
have not been systematically studied, but atherosclerosis with a pencil in the mouth or from iatrogenic causes.
is generally not found in patients with spontaneous dis- Basilar skull fracture, especially involving the carotid ca-
sections. Migraine has been suggested as an independent nal, is also included in this category in most studies of
risk factor. traumatic dissection. The indications for CTA continue
to broaden. Because of the potential for devastating neu-
Traumatic Cervicocerebral Injuries rologic consequences of cerebrovascular injuries, some
trauma centers follow a liberalized screening approach—
The evaluation of vascular injuries of the neck and head including not only patients with symptoms referable to
has undergone a dramatic transformation as a result of vascular injury but also asymptomatic patients under-
the capabilities of helical and MDCT angiography. Since going CT for head and cervical spine trauma. In such a
2000, favorable results from the use of CTA in the setting study reported by Biffl and colleagues in 2006, 5.4% of
of penetrating trauma have supported its clinical applica- patients had blunt cerebrovascular injuries. In a 2-year
tion on a routine basis. High sensitivity and specificity for retrospective review of patients at our center, 8% of 106
the detection of vascular injuries have been reported in patients with fractures of the cervical spine and skull
a number of studies. CTA has essentially replaced DSA, base (involving the foramen transversarium or near the
which is still the gold standard, as the initial screening carotid canal) had vascular injuries detected by CTA. Of
modality of choice for penetrating neck injuries at many 161 trauma patients without fractures who also under-
institutions. In many cases it has been used as a comple- went CTA, 2% had vascular injuries detected. Therefore
mentary technique to surgical exploration of the neck, the presence of a fracture yielded an odds ratio for vas-
but more recently, a normal CTA may avert the need for cular injury of approximately 4 to 1 in this population.
surgical exploration. CTA has been applied to the set- False-positive and false-negative results are generally con-
ting of blunt trauma with similar results and has resulted sidered few, with the expectation that they will continue
in a decrease in the number of DSA examinations per- to decline as technology advances and experience with
formed. Abnormalities that may be detected include ste- the technique increases.
nosis, occlusion, dissection, pseudoaneurysm formation, Some authors propose mandatory imaging in the fol-
and contrast extravasation from vessel rupture. Vascular lowing instances: (1) arterial bleeding from the mouth,
evaluation is generally limited to the common carotid, nose, ears, or wound; (2) expanding cervical hematoma;
internal carotid, and vertebral and proximal branches (3) bruit in patients older than 50 years; (4) acute infarct;
of the external carotid arteries. With currently available (5) unexplained neurologic defect or TIA; and (6) Horn-
equipment, submillimeter, subsecond imaging is possible, er syndrome or neck or head pain. In one angiographic
and even minor abnormalities of the distal external ca- study of asymptomatic patients with skull base fractures,
rotid branches are now being diagnosed prospectively. up to 60% had abnormal angiogram findings. Other studies
Nondiagnostic examinations may occur as a result of have reported significantly lower rates of serious injury.
technical deficiencies such as extravascular contrast in- One recent series found a 4% incidence of traumatic
filtration from intravenous catheters or patient motion. carotid-cavernous fistula in patients with skull base f ractures.
Use of a contrast test bolus or bolus tracking techniques Although prompt diagnosis and treatment of carotid-
helps reduce the number of poor-quality scans due to ar- cavernous fistula are desirable, diagnosis at the time of
rhythmias or compromised cardiac output. Because an admission is not as critical as it is for dissection with its
intravenous contrast bolus may be impeded by transient inherent risk of stroke.
compression of the left brachiocephalic vein as a result Whether performed for screening or based on symp-
of pulsations of the great vessels, a right-sided antecubi- toms, the workup and treatment of dissection continue
tal injection site is preferred. Streak artifacts from den- to evolve. As with other vascular disorders, catheter angi-
tal fillings and hardware and beam-hardening effects also ography was once the only method available and is still
take their toll on image quality. Positive findings on CTA used for confirmation if other studies are equivocal. The
help guide therapeutic decisions toward medical, surgi- most common finding is a smoothly or mildly irregu-
cal, or endovascular intervention; however, well-defined lar tapered mid-cervical narrowing. Dissections that re-
pathways do not yet exist for most vascular injuries. It is sult in occlusion may show a “rat tail” or “flame-shaped”
the clinical expectation that with prompt diagnosis and lumen, which may help distinguish other causes such as
B
FIGURE 1-24 An arterial dissection resulting from blunt trauma. A, A volume-rendered image from a computed
tomography (CT) angiogram shows a comminuted mandibular fracture (arrows). The internal jugular vein ob-
scures the internal carotid artery. B, A 180-degree rotation and application of an anterior cutting plane reveal
tapered contour of the internal carotid artery (arrows) as a result of dissection. C, Multiplanar reconstruction from
a follow-up CT angiogram 1 week later shows development of a small pseudoaneurysm (arrow) with residual,
mild, distal stenosis.
thromboembolism or atherosclerotic disease from dissec- base.The most common sites of vertebral artery dissection
tion (Fig. 1-25). Saccular or fusiform aneurysmal dilatation are at the entry into the C6 foramen transversarium and at
(pseudoaneurysm) also may be identified.The presence of the C1-C2 level.
an intimal flap or a false or double lumen is unusual in the Ultrasound assessment of cervical internal carotid and
cervicocerebral vessels. In the internal carotid artery, the vertebral artery dissections is possible, but many pitfalls ex-
dissection is typically found a few centimeters beyond the ist.The pathognomonic finding is a membrane in the longi-
carotid bifurcation or a few centimeters below the skull tudinal and axial views. In addition to the findings that may
and is often performed immediately after or at the time of

imaging of the head and cervical spine.
CTA has also become the initial method for evaluation
of stable patients with penetrating trauma to the neck, face,
and head based on availability, efficiency, and similar pro-
files of sensitivity and specificity as in blunt trauma. The
high sensitivity of CT for the detection of small amounts of
contrast extravasation or air in the soft tissues helps to lo-
calize subtle injuries to major vessels that otherwise might
not be noticed. An understanding of the expected trajecto-
ry of bullets or knives based on skin entry and exit wounds
may increase the likelihood of the detection of injury. De-
tection of dissection, transection, pseudoaneurysm, and ar-
teriovenous fistula formation can help guide treatment—
that is, medical versus open surgical versus endovascular.
Posttraumatic vasospasm may lead to a false-positive diag-
nosis of dissection or transection, appearing normal on im-
mediate follow-up angiography. Definitive characterization
of an injury in cases of segmental arterial narrowing or oc-
clusion may be challenging in neck CTA, as well as in other
areas, given the overlap in imaging findings for traumatic
dissection, occlusion, and vasospasm. Retained bullets and
shrapnel often cause substantial artifacts that limit the diag-
FIGURE 1-25 Acute dissection. A digital subtraction angiogram nostic value of CTA. DSA can usually overcome this limita-
shows sharply tapered occlusion of the internal carotid artery as a tion through the use of multiple oblique projections.
result of spontaneous dissection.
Spontaneous Intracranial Dissection
be demonstrated by angiography, a thickened, hyperechoic Intracranial arteries lack an external elastic lamina and have
vessel and high-resistance spectral waveform or absence thinner media and adventitia compared with extracranial
of flow may be noted. However, Doppler analysis may be vessels, and thus intracranial dissections may behave dif-
normal in cases of low-grade carotid stenosis, and ultra- ferently. If the dissection occurs between the intima and
sound sensitivity of only 20% has been reported in such media, then luminal stenosis or occlusion may lead to isch-
cases. Ultrasound evaluation of vertebral artery dissection emia or infarct, similar to the extracranial setting. If the
is limited by the transverse processes of the cervical spine. dissection plane is between the media and adventitia, then
The combination of MRI and MRA is considered by (dissecting) pseudoaneurysm formation is likely. Because
many to be the preferred technique. MRA should be able of the thin media and adventitia, rupture and SAH may oc-
to demonstrate the morphologic features of the vessel in a cur. SAH is reported in approximately 20% of intracranial
fashion similar to DSA. In addition, MRI may demonstrate internal carotid dissections and more than 50% of intracra-
an eccentrically located narrowed lumen, a crescentic or nial vertebral dissections. The supraclinoid segment of the
circumferential intramural hematoma, and an increase in internal carotid artery and the segment of the vertebral
the external artery diameter. Fat-suppressed T1WIs are artery near the posterior inferior cerebellar artery (V4)
recommended to improve sensitivity for detection of the are the most common sites of intracranial dissection. The
intramural hematoma (Fig. 1-26). However, in the acute set- cause of intracranial dissection remains unknown, with
ting, the clot should not be expected to appear hyperin- some instances related to trauma or underlying connective
tense, because it may take a few days for conversion to tissue disorders (such as fibromuscular dysplasia, Marfan,
methemoglobin to take place. The reported sensitivity and Ehlers-Danlos types). It may not be possible to differ-
and specificity for detection of carotid dissection are very entiate traumatic stenosis or occlusion from atherosclero-
high—approximately 95% and 99%, respectively. Sensitiv- sis or thromboembolism by any imaging technique. The
ity is lower for vertebral dissection (approximately 60%) only truly diagnostic findings of dissection are the pres-
because of the smaller size of the native vessel and the rel- ence of a dissecting pseudoaneurysm and a double lumen.
atively high incidence of hypoplasia. One must remember Treatment options vary depending on stenosis versus
that lack of flow-related signal due to slow flow in a ves- pseudoaneurysm configuration and the presence of an in-
sel may simulate occlusion. These noninvasive techniques farct or SAH. Endovascular intervention with stent place-
are very useful for follow-up of dissection as a result of ment may be considered when medical therapy for stenosis
the lack of ionizing radiation or the need for injection of a has failed. Aneurysm coiling, proximal occlusion, and trap-
contrast agent. ping of an abnormal segment are other possible techniques.
CTA shares many of the advantages of MRA and pro-
vides higher spatial resolution. Another specific sign re- OTHER NONTRAUMATIC INTRACRANIAL
ported by CTA is the “target” sign, which is composed of a EMERGENCIES
thickened wall and a narrowed eccentric lumen surround-
ed by a thin rim of contrast enhancement. CTA is certainly As with ischemic stroke and spontaneous hemorrhage, the
the fastest way to screen patients in the emergency setting indication for workup of other nontraumatic emergencies
A B
C
FIGURE 1-26 Internal carotid artery dissection as seen on computed tomography (CT) and magnetic resonance
(MR) angiogram. A, A CT angiogram source image shows a narrowed upper cervical right internal carotid artery
lumen with an increase in the external caliber of the vessel (arrow). B, A fat-suppressed T1-weighted image shows
corresponding narrowed flow void with a hyperintense eccentric intramural hematoma (arrow). C, A time-of-flight
MR angiogram shows a narrowed segment of the right internal carotid artery (arrow).
affecting the brain will be based on an acute change in Hydrocephalus

mental status or onset of headache, seizure, or a focal neu-
rologic deficit. Delirium, or acute confusional state, is a Disturbance of the usual pattern of CSF flow or produc-
common indication for brain imaging in concert with a tion/absorption may result in dilatation of the ventricu-
search for other causes such as hypoxia, cerebral hypo- lar system. Hydrocephalus may occur acutely or may be
perfusion, systemic or regional infection, intoxication, and of chronic duration, and the distinction between the
other metabolic causes. Noncontrast head CT offers rapid two forms may not be entirely clear based on imaging
noninvasive detection of lesions producing mass effect alone. Hypodensities/T2-weighted hyperintensities in
or brain edema. Spontaneous and subacute hemorrhages the periventricular white matter of the frontal and peri-
have been addressed in previous sections of this chapter. atrial regions may be a sign of interstitial edema—often
Other causes run the gamut of infection, inflammation, tu- described as transependymal flow of CSF—and may be
mors, and other causes of encephalopathy. The following seen with acute hydrocephalus. Chronically compen-
sections illustrate a few of the more commonly seen enti- sated hydrocephalus is less likely to demonstrate this
ties from these categories. finding.Terminology can be confusing; obstruction at the
sinus thrombosis or stenosis. The incidence is highest

in obese females of child-bearing age, and it may pres-
ent with headache and visual loss due to papilledema.
Although intracranial pressure may be severely elevated
in this disorder, the ventricular system is generally small.
Progressive visual loss may be an indication for emergent,
fluoroscopic-guided, diagnostic, and therapeutic lumbar
puncture. As described in the section on cerebral sinus
thrombosis, CT or MR venography is commonly requested
in this setting.
Colpocephaly is the term applied to enlarged occipital
horns of the lateral ventricles as a result of a developmen-
tal structural abnormality of the brain, and it sometimes
may be mistaken for acute hydrocephalus. Other congeni-
tal abnormalities such as agenesis of the corpus callosum
will also present with abnormal ventricular configuration
and should be recognized as one of the expected constel-
lation of findings. Benign external hydrocephalus or be-
nign extracerebral fluid collections are two of the terms
commonly applied to the pattern of mild ventriculomegaly
and generous subarachnoid spaces in neonates and infants.
It is associated with macrocephaly and usually resolves
spontaneously by 1 to 2 years of age.
FIGURE 1-27 Hydrocephalus as a result of shunt malfunction. Se- Infections

vere hydrocephalus is shown. Portions of the bilateral ventriculo- Meningitis
peritoneal shunts are visible. Abdominal computed tomography
(not shown) demonstrated a pseudocyst as a cause of the mal- Suspected meningitis is a very common cause for im-
function. aging, not necessarily for diagnosis, but as a precaution
prior to performance of a lumbar puncture. In adults
with suspected meningitis, clinical features can be used
level of the foramen of Monro, cerebral aqueduct of Syl- to identify those who are unlikely to have abnormal find-
vius, or foramina of Magendie and Luschka is considered ings on CT of the head. However, many practitioners still
noncommunicating hydrocephalus, whereas obstruction rely on CT prior to lumbar puncture to exclude unsus-
at the level of the arachnoid granulations is considered pected mass effect and lesions that might result in rapid
communicating hydrocephalus. One should always re- increases in intracranial pressure; this is especially true
member the value of prior examinations, because long- for patients who are immunocompromised or older
standing, compensated hydrocephalus is generally not a than 60 years. Findings of the majority of examinations
cause for alarm even if encountered in the emergency are normal, but the detection of findings such as brain
setting. Ventricular obstruction may develop as a result edema possibly leading to herniation, hydrocephalus, or
of SAH, IVH, intraventricular mass, aqueductal steno- other complications will alter management. On FLAIR
sis, and any lesion that may cause extrinsic mass effect. images, sulci may appear hyperintense as a result of pro-
Analysis should include evaluation of basal cisterns and teinaceous exudates; however, SAH or a high concentra-
a search for possible complications that may result from tion of inspired oxygen also may cause the same appear-
herniation. Ideally, treatment of hydrocephalus will pre- ance. In the vast majority of cases, meningitis is aseptic
vent such complications. Recurrence of symptoms due (generally of viral origin, commonly enteroviruses) and is
to ventricular shunt malfunction is a common problem self-limited. Bacterial meningitis is more likely to result
that may result from catheter/tubing obstruction (intrin- in severe disease, and in some cases the source of men-
sic or in the peritoneal cavity), disconnection, or migra- ingitis may be evident on imaging, such as a sinus or ear
tion (Fig. 1-27). infection. On intravenous contrast-enhanced CT and MR
Classification is complicated further by normal pres- examinations, diffuse enhancement within the sulci (lep-
sure hydrocephalus. The cause of this disorder in which tomeningeal) may be detected. Imaging is also indicated
intracranial pressure is not elevated is unknown. In the for patients who do not respond to antibiotic treatment
setting of ventriculomegaly out of proportion to sulcal in the hope of detecting a drainable source, such as a
prominence, the presence of the classic triad of demen- subdural empyema or parenchymal abscess. Gadolinium-
tia, abnormal gait, and urinary incontinence can help enhanced MR is generally preferred to CT because of its
to make this diagnosis. However, by the time the clas- relatively higher soft tissue contrast. Neonatal meningitis
sic symptoms are evident, treatment may be ineffective. due to Citrobacter species is another indication for im-
The fourth ventricle may be relatively spared, and peri- aging because brain abscess develops in 80% to 90% of
ventricular edema may be absent in normal pressure cases. Meningoencephalitis (encephalomeningitis) is the
hydrocephalus. term applied to brain parenchymal infection in associa-
A related disorder is IIH (pseudotumor cerebri), which tion with meningitis. Other complications of meningitis
may be due to poor CSF absorption such as from venous include infarcts, venous thrombosis, subdural empyema
A B
C
FIGURE 1-28 Meningitis caused by group B streptococcus in a 4-year-old. A, A postgadolinium T1-weighted im-
age shows mild diffuse leptomeningeal enhancement and abnormal enhancement of the bilateral cranial nerve
III (black arrows). B, A magnetic resonance angiogram shows the bilateral internal carotid artery terminus and
anterior cerebral artery and middle cerebral artery origin stenoses (white arrows). C, A diffusion-weighted image
shows resultant infarcts.
or hygroma, and obstructive or communicating hydro- Diffuse thickened enhancement of the dura is a sign of
cephalus (Fig. 1-28). Subdural empyema and epidural pachymeningitis, which can be due to carcinomatous, gran-
abscess are illustrated in the section on head and neck ulomatous, and noninfectious causes, including idiopathic
imaging. intracranial hypotension (Fig. 1-29). Tuberculosis has a pre-
Many other infectious agents may cause meningitis, dilection for causing basal meningitis with resultant stroke
including Lyme disease (Borrelia) and, especially in the due to involvement of arteries at the base of the brain.
immunocompromised setting, human immunodeficien-
cy virus (HIV), toxoplasmosis, cryptococcosis, tubercu- Brain Parenchymal Infection
losis, syphilis, cytomegalovirus, and a variety of fungi The term encephalitis refers to inflammation of the brain
(see Fig. 1-12). and is usually applied in the setting of viral infection.
FIGURE 1-29 Pachymeningitis. A postgadolinium T1-weighted

image shows diffuse, pachymeningeal, thickened enhancement
due to neurosarcoidosis.
Cerebritis is often used interchangeably; however, it should

be reserved for the cerebrum with cerebellitis added B
when necessary. Usually the findings are nonspecific, with FIGURE 1-30 Herpes encephalitis. Diffusion-weighted (A) and
simultaneous involvement of various structures. A certain fluid-attenuated inversion recovery (B) images show correspond-
pattern may suggest a particular organism, such as the clas- ing hyperintensities in the left temporal lobe and insula as a result
sic findings of T2WI hyperintensity, restricted diffusion, of herpes simplex virus type I infection. Note the motion artifact
and minimal enhancement within the temporal lobe(s) so commonly encountered in patients evaluated for a change in
and limbic system as a result of herpes simplex type 1 in- mental status.
fection (Fig. 1-30). Nonspecific patchy T2 hyperintensities,
variable diffusion, and enhancement characteristics may
lead to a differential diagnosis including infarction, infil- subacute infarct, and subacute hematoma. In the setting
trating neoplasm, status epilepticus, and toxic/metabolic of immune suppression, a fungal abscess should be con-
causes. Rather than identify the exact agent, imaging find- sidered. In the setting of acquired immunodeficiency
ings may be able to suggest infection and exclude other syndrome (AIDS), the differential diagnosis for single or
possibilities. multiple ring-enhancing lesions includes toxoplasmosis
versus lymphoma (Fig. 1-32). Also prevalent in the AIDS
Abscess population are Mycobacterium tuberculosis and Cryp-
An abscess is a focal parenchymal infection due to bacte- tococcus, which can present as either meningitis or fo-
ria, fungi, or parasites. The imaging characteristics reflect cal parenchymal lesions. To further complicate matters,
the phase of the infection as it evolves from early cerebri- another classic presentation of cryptococcosis is that of
tis to late cerebritis, then to early and finally late encapsu- nonenhancing, gelatinous pseudocysts that distend the
lated stages. If diagnosed early, it often appears as a low- perivascular spaces.
density (on CT), T2-weighted hyperintense region with Single or multiple abscesses may develop from septic
faint enhancement and a mild amount of surrounding emboli as a result of endocarditis. Initially, these abscess-
edema. Once in the capsule stage, a typical fluid collec- es appear similar to other cardioembolic infarcts but in
tion with a thin rim of enhancement and larger amount time develop relatively more surrounding edema and
of edema becomes evident (Fig. 1-31). Over time (with enhancement as a result of the inflammatory response
treatment), the lesion may decrease in size and develop (Fig. 1-33). If cardiac valve replacement is considered,
a thicker rim of enhancement, and surrounding edema screening for mycotic aneurysms may be requested pri-
will wane.The rim is typically T2 hypointense and thinner or to surgery.
along the deep margin, which may predispose cerebral Neurocysticercosis is an intracranial infection by the
lesions to rupture into the ventricular system, leading to pork tapeworm, Taenia solium, which is endemic in many
ventriculitis and a dramatic clinical decline. A bacterial parts of the world. It is the leading cause of seizures world-
abscess typically shows diffusion-weighted hyperinten- wide and has a unique life cycle and imaging characteris-
sity, which may help to distinguish a bacterial abscess tics. After ingestion of contaminated food or water, larvae
from a necrotic tumor. Lesions in the differential diag- migrate from the gastrointestinal tract to the brain and
nosis other than neoplasm might include demyelination, skeletal muscle. Once intracranial, the larvae develop into
A B
C
FIGURE 1-31 A pyogenic abscess. A, A T2-weighted image shows hyperintense fluid collection in the right
frontal lobe with a hypointense rim and extensive surrounding edema. B, Corresponding hyperintensity on a
diffusion-weighted image. C, A postgadolinium T1-weighted image shows a relatively thin rim along the deeper
portion of the abscess adjacent to the lateral ventricle.
cysticerci, and these cysts may be located in the subarach- other brain abscess. Next is the granular nodular stage in
noid spaces, brain parenchyma, or ventricular system. The which the cyst involutes, the wall thickens, the lesion be-
cysts then progress through four stages with distinct im- gins to calcify, and edema decreases. In the final nodular
aging features based on the lesion and the host response. calcified stage, only a small calcification persists and the
In the vesicular stage, the lesions appear as thin-walled, edema resolves completely. Because lesions may progress
fluid-filled cysts, possibly with mild rim enhancement, at different rates, it is not uncommon to find more than
but without surrounding edema. Lesions are generally one type of lesion. Identification of cysts in different com-
small (less than 1 cm), and often an eccentric scolex of a partments (parenchymal, subarachnoid, and intraventricu-
few millimeters can be detected. In the colloidal vesicular), the presence of a scolex, variable amounts of edema,
lar stage, in which the larva starts degenerating, a thicker and small calcifications in the same patient offer great
rim of enhancement and surrounding edema develop. It is sensitivity and specificity. It is not often that the radiolo-
in this stage that the appearance is similar to that of any gist can show such confidence in diagnosis, and therefore
A B
C
FIGURE 1-32 Toxoplasmosis. A, A fluid-attenuated inversion recovery image shows isointense lesions in the right
basal ganglia and left parietal lobe with surrounding edema. B, A postgadolinium T1-weighted image shows faint
rim enhancement of right basal ganglia lesion. C, A postgadolinium T1-weighted image shows a typical “target”
sign in a left frontal lobe lesion.
neurocysticercosis deserves special recognition (Fig. 1-34). chapter it is possible to provide only a limited framework
One might not expect this infection to be common in the and describe some of the more common lesions.
United States; however, because of travel and immigration, Metastases account for approximately half of all intra-
it presents fairly commonly in patients presenting to U.S. cranial neoplasms in adults. They may present as multiple
EDs with new or recurrent seizures. small enhancing lesions at the gray–white junction or as
a single large lesion with extensive surrounding edema.
Lesions are usually found in the cerebral hemispheres
Tumors
and may be solid, cystic, calcified, or hemorrhagic, and ap-
As with infection, it is not possible to review all of the proximately 50% will present as a solitary lesion.The most
myriad entities in this category. Within the scope of this common primary tumors are lung, breast, and melanoma.
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EMERGENCY RADIOLOGY:THE REQUISITES, SECOND EDITION ISBN: 978-0-323-37640-2

Copyright © 2017 by Elsevier, Inc. All rights reserved.

Previous edition copyright © 2009 by Mosby, Inc., an affiliate of Elsevier, Inc.

Library of Congress Cataloging-in-Publication Data

Soto, Jorge A., editor.

Executive Content Strategist: Robin Carter

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

Margaret N. Chapman, MD Sarah S. Milla, MD

Osamu Sakai, MD, PhD Joshua W. Stuhlfaut, MD

TABLE 1-1 Usual Magnetic Resonance Signal Characteristics of Hemorrhage

Hyperacute (0-12 h) Oxyhemoglobin Isointense Hyperintense

INTRAAXIAL HEMORRHAGE Contusion

impact) types. On CT, a contusion typically appears as an Diffuse Axonal Injury

65 years. The 20% mortality rate is surpassed only by car-

Approximately 10% to 15% of strokes present with an

Diffusion-weighted hyperintensity generally begins to Magnetic Resonance Angiography

A B CBV CBF MTT

infarct core), and infarct core lesion volume less than 70

the common variants is necessary to avoid diagnostic pit-

ANEURYSMS, VASCULAR MALFORMATIONS,

FIGURE 1-23 Subarachnoid hemorrhage due to a ruptured aneu-

and is often performed immediately after or at the time of

affecting the brain will be based on an acute change in Hydrocephalus

sinus thrombosis or stenosis. The incidence is highest

FIGURE 1-27 Hydrocephalus as a result of shunt malfunction. Se- Infections

FIGURE 1-29 Pachymeningitis. A postgadolinium T1-weighted

Cerebritis is often used interchangeably; however, it should

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EMERGENCY RADIOLOGY:THE REQUISITES, SECOND EDITION ISBN: 978-0-323-37640-2