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Core Radiology

Second Edition
Painting by Jacqueline Liu
Core Radiology
A Visual Approach to Diagnostic Imaging

Second Edition

Volume 1 and 2

Ellen X. Sun
Brigham & Women’s Hospital, Boston, MA

Junzi Shi
Brigham & Women’s Hospital, Boston, MA

Jacob C. Mandell
Brigham & Women’s Hospital, Boston, MA
University Printing House, Cambridge CB2 8BS, United Kingdom
One Liberty Plaza, 20th Floor, New York, NY 10006, USA
477 Williamstown Road, Port Melbourne, VIC 3207, Australia
314–321, 3rd Floor, Plot 3, Splendor Forum, Jasola District Centre, New Delhi – 110025, India
103 Penang Road, #05–06/07, Visioncrest Commercial, Singapore 238467

Cambridge University Press is part of the University of Cambridge.

It furthers the University’s mission by disseminating knowledge in the pursuit of
education, learning, and research at the highest international levels of excellence.

www.cambridge.org
Information on this title: www.cambridge.org/9781108965910
DOI: 9781108966450
© Ellen X. Sun, Junzi Shi, and Jacob C. Mandell 2021
This publication is in copyright. Subject to statutory exception
and to the provisions of relevant collective licensing agreements,
no reproduction of any part may take place without the written
permission of Cambridge University Press.
Second edition published 2021
First edition published 2013
Printed in Singapore by Markono Print Media Pte Ltd
A catalogue record for this publication is available from the British Library.
2 volume set: SET ISBN 9781108965910
Volume 1: ISBN 9781108984447
Volume 2: ISBN 9781108984454
Cambridge University Press has no responsibility for the persistence or accuracy
of URLs for external or third-party internet websites referred to in this publication
and does not guarantee that any content on such websites is, or will remain,
accurate or appropriate.

Every effort has been made in preparing this book to provide accurate and up-to-date information
that is in accord with accepted standards and practice at the time of publication. Although case
histories are drawn from actual cases, every effort has been made to disguise the identities of the
individuals involved. Nevertheless, the authors, editors, and publishers can make no warranties that
the information contained herein is totally free from error, not least because clinical standards are
constantly changing through research and regulation. The authors, editors, and publishers therefore
disclaim all liability for direct or consequential damages resulting from the use of material contained
in this book. Readers are strongly advised to pay careful attention to information provided by the
manufacturer of any drugs or equipment that they plan to use.
 CONTENTS
Volume 1

List of contributors vii

Acknowledgements x

1 THORACIC IMAGING 1
Khushboo Jhala, Junzi Shi, and Mark M. Hammer

2 GASTROINTESTINAL IMAGING 95
Cory Robinson-Weiss, Fiona E. Malone, Ellen X. Sun, Junzi Shi, Khushboo Jhala, and
Shanna A. Matalon

3 GENITOURINARY IMAGING 229

Cory Robinson-Weiss, Madhvi Deol, Fiona E. Malone, Khushboo Jhala, Junzi Shi, Ellen X. Sun,
Michael A. Buckner, Jose M. Lopez, Khanant M. Desai, and Daniel Souza

4 OBSTETRICAL IMAGING 324

Ellen X. Sun, Junzi Shi, Robin Perlmutter-Goldenson, and Mary C. Frates

5 BREAST IMAGING 368

Aaron Jen, Ellen X. Sun, and Christine M. Denison

6 NUCLEAR AND MOLECULAR IMAGING 444

Ellen X. Sun, Christopher G. Sakellis, and Hyewon Hyun

7 CARDIAC IMAGING 486

E llen X. Sun, Junzi Shi, Sharmila Dorbala, Ayaz Aghayev, and Michael L. Steigner

8 VASCULAR IMAGING 539

Junzi Shi, Ellen X. Sun, and Ayaz Aghayev

9 INTERVENTIONAL RADIOLOGY 588

Leigh Casadaban, Colette Martin Glaser, Junzi Shi, Ellen X. Sun, Steven Morales-Rivera,
Sharath Bhagavatula, Regina Maria Koch, and Timothy P. Killoran
 CONTENTS
Volume 2

10 NEUROIMAGING: BRAIN 650

Francis Deng, Shruti Mishra, Ellen X. Sun, and Raymond Y. Huang

11 NEUROIMAGING: HEAD AND NECK 753

Francis Deng, Shruti Mishra, Jeffrey P. Guenette, and Raymond Y. Huang

12 SPINE IMAGING 860

Francis Deng, Shruti Mishra, Nityanand Miskin, Ellen X. Sun, Raymond Y. Huang,
and Jacob Mandell

13 MUSCULOSKELETAL IMAGING 908

Yuntong Ma, and Jacob Mandell

14 PEDIATRIC IMAGING 1084

Ngoc-Anh T. Tran, Ellen X. Sun, Sanjay P. Prabhu, and Michael P. George

15 IMAGING PHYSICS 1195

Junzi Shi, Ellen X. Sun, and Jacob Mandell

Index 1222

 full list of references, resources and further reading can be found online at
A
www.cambridge.org/coreradiology
CONTRIBUTORS

Ayaz Aghayev, MD Sharmila Dorbala, MD

Staff Radiologist, Division of Director of Nuclear Cardiology,
Cardiovascular Imaging, Division of Cardiovascular Imaging,
Brigham and Women’s Hospital Brigham and Women’s Hospital
Instructor of Radiology, Associate Professor of Radiology,
Harvard Medical School Harvard Medical School
Sharath Bhagavatula, MD Mary C. Frates, MD
Staff Radiologist, Abdominal Assistant Director, Division of Ultrasound,
Imaging and Intervention, Brigham and Women’s Hospital
Brigham and Women’s Hospital Professor of Radiology,
Instructor of Radiology, Harvard Medical School
Harvard Medical School
Michael P. George, MD
Michael A. Buckner, MD Staff Pediatric Radiologist,
Resident in Radiology, Boston Children’s Hospital
Brigham and Women’s Hospital Instructor of Radiology,
Harvard Medical School Harvard Medical School
Leigh Casadaban, MD MS Colette Martin Glaser, MD
Clinical Fellow in Interventional Radiology, Resident in Radiology,
University of California, Los Brigham and Women’s Hospital
Angeles Medical Center Harvard Medical School
David Geffen School of Medicine
Robin Perlmutter-Goldenson, MD, MPH
Francis Deng, MD Staff Radiologist, Division of Ultrasound,
Resident in Radiology, Brigham and Women’s Hospital
Massachusetts General Hospital Assistant Professor of Radiology,
Harvard Medical School Harvard Medical School
Christine M. Denison, MD Jeffrey P. Guenette, MD
Staff Radiologist, Division of Breast Imaging, Director of Head and Neck Imaging,
Brigham and Women’s Hospital Division of Neuroradiology
Assistant Professor of Radiology, Associate Program Director, Diagnostic
Harvard Medical School Radiology Residency
Brigham and Women’s Hospital
Madhvi Deol, MD
Assistant Professor of Radiology,
Resident in Radiology,
Harvard Medical School
Brigham and Women’s Hospital
Harvard Medical School Mark M. Hammer, MD
Thoracic Imaging Fellowship Director,
Khanant M. Desai, MD
Brigham and Women’s Hospital
Clinical Fellow in Interventional Radiology,
Assistant Professor of Radiology,
University of Virginia Medical Center
Harvard Medical School
Raymond Y. Huang, MD, PhD Jacob Mandell, MD
Assistant Division Chief, Division of Neuroradiology Musculoskeletal Imaging and Intervention
Brigham and Women’s Hospital Fellowship Director,
Associate Professor of Radiology Brigham and Women’s Hospital
Harvard Medical School Assistant Professor of Radiology,
Harvard Medical School
Hyewon Hyun, MD
Program Director, Joint Program in Nuclear Shanna A. Matalon, MD
Medicine and Molecular Imaging, Staff Radiologist, Division of Abdominal
Brigham and Women’s Hospital Imaging and Intervention,
Assistant Professor of Radiology, Associate Program Director, Radiology Residency,
Harvard Medical School Brigham and Women’s Hospital
Assistant Professor of Radiology,
Aaron Jen, MD
Harvard Medical School
Resident in Radiology,
Brigham and Women’s Hospital Shruti Mishra, MD
Harvard Medical School Resident in Radiology,
Brigham and Women’s Hospital
Khushboo Jhala, MD
Harvard Medical School
Resident in Radiology,
Brigham and Women’s Hospital Nityanand Miskin, MD
Harvard Medical School Clinical Fellow in Neuroradiology,
Timothy P. Killoran, MD Massachusetts General Hospital
Integrated and Independent Interventional Harvard Medical School
Radiology Residency Director, Steven Morales-Rivera, MD
Brigham and Women’s Hospital Resident in Radiology,
Assistant Professor of Radiology, Brigham and Women’s Hospital
Harvard Medical School Harvard Medical School
Regina Maria Koch, MD Sanjay P. Prabhu, MBBS, DCH, FRCR
Staff Radiologist, Interventional Radiology, Staff Pediatric Neuroradiologist,
Brigham and Women’s Hospital Director, Advanced Image Analysis Lab,
Instructor of Radiology, Medical Director, Imaging Informatics
Harvard Medical School Boston Children’s Hospital
Jose M. Lopez, MD, MBA Assistant Professor of Radiology,
Resident in Radiology, Harvard Medical School
Brigham and Women’s Hospital Cory Robinson-Weiss, MD
Harvard Medical School Clinical Fellow in Abdominal Imaging,
Yuntong Ma, MD Massachusetts General Hospital
Resident in Radiology, Harvard Medical School
Brigham and Women’s Hospital
Christopher G. Sakellis, MD
Harvard Medical School
Staff Radiologist, Division of Nuclear
Fiona E. Malone, MD Medicine,
Resident in Radiology, Brigham and Women’s Hospital
Brigham and Women’s Hospital Assistant Professor of Radiology,
Harvard Medical School Harvard Medical School

List of contributors
Junzi Shi, MD Michael L. Steigner,
Clinical Fellow in Musculoskeletal Radiology, Staff Radiologist, Division of Cardiovascular
Brigham and Women’s Hospital Imaging,
Harvard Medical School Brigham and Women’s Hospital
Associate Professor of Radiology,
Daniel Souza, MD, MSc
Harvard Medical School
Fellowship Program Director, Abdominal Imaging
and Intervention, Ngoc-Anh T. Tran, MD
Brigham and Women’s Hospital Resident in Radiology,
Instructor of Radiology, Brigham and Women’s Hospital
Harvard Medical School Harvard Medical School
Ellen X. Sun, MD
Staff Radiologist, Division of Emergency Radiology,
Brigham and Women’s Hospital
Instructor of Radiology,
Harvard Medical School

List of contributors
ACKNOWLEDGEMENTS

Frontispiece painting by Jaqueline Liu

Chapter cover page cinematic renderings by Khushboo Jhala
 Khushboo Jhala, Junzi Shi, Mark M. Hammer

Thoracic Imaging

Introductory concepts ..............................2

Patterns of lung disease ............................8
Pulmonary infection ...............................21
Pulmonary edema and ICU imaging ........32
Lung cancer ............................................34
Pulmonary vascular disease....................46
Diffuse lung disease ................................54
Mediastinum ..........................................70
Airways ..................................................83
Pleura.....................................................92

Chest: 1
Introductory concepts
Anatomy
Lobar and segmental anatomy
apical apical
posterior anterior
posterior superior
lingula
right upper lobe
left upper lobe

anterior
inferior
lateral lingula

right middle lobe

bronchus
medial intermedius

e
superior
lob superior

lef
er

tl
w

ow
lo
ht

er
rig

lo
be
medial
basal medial
basal
posterior posterior
basal basal
lateral anterior anterior lateral
basal basal basal basal

Interlobar fissures
• The minor fissure separates the right upper lobe (RUL) from the right middle lobe (RML) and
is seen on both the frontal and lateral views as a fine horizontal line.
• The major (oblique) fissures are seen only on the lateral radiograph as oblique lines.
However, if they are fluid-filled, the major fissures can be seen on the frontal view as
concave curvilinear opacities in the lateral hemithorax.
On the right, the major fissure separates the RUL and RML from the right lower lobe.
On the left, the major fissure separates the left upper lobe (LUL) from the left lower lobe (LLL).
Accessory fissures
• The azygos fissure is an accessory fissure present in less than 1% of patients, seen in the
presence of an azygos lobe. An azygos lobe is an anatomic variant where a portion of the
apical right upper lobe is encased in its own parietal and visceral pleura.
• The superior accessory fissure is seen in approximately 5% of patients and separates the
superior and basal segments of the right lower lobe.
• The inferior accessory fissure is seen in approximately 12% of patients, more commonly in
the right lung, and divides the medial basal segment from the other basal segments.
• The left minor fissure is present in approximately 8% of patients and separates the lingula
from the left upper lobe.

Chest: 2
Overview of atelectasis
• Atelectasis is loss of lung volume due to decreased aeration. Atelectasis is synonymous with
collapse. Atelectasis may be caused by bronchial obstruction, mucus plugging, or external
compression (e.g., by small lung volumes or pleural effusions).
• Direct signs of atelectasis are from lobar volume loss and include:
Displacement of the fissures. Vascular crowding.
Plate-like or triangular opacity from the collapsed
lung itself.
• Indirect signs of atelectasis are due to the effect of volume loss on adjacent structures and
include:
Elevation of the diaphragm. Overinflation of adjacent or contralateral lobes.
Rib crowding on the side with volume loss. Hilar displacement.
Mediastinal shift to the side with volume loss.
• Air bronchograms are not seen in atelectasis when the cause of the atelectasis is central
bronchial obstruction, but air bronchograms can be seen in atelectasis caused by external
compression.
Mechanisms of atelectasis
• Obstructive atelectasis occurs when alveolar gas is absorbed by blood circulating through
alveolar capillaries but is not replaced by inspired air due to bronchial obstruction.
Obstructive atelectasis can cause lobar atelectasis, which is complete collapse of a lobe, discussed on the
following pages.
Obstructive atelectasis occurs more quickly when the patient is breathing supplemental oxygen since
oxygen is absorbed from the alveoli more rapidly than nitrogen.
In children, airway obstruction is most often due to an aspirated foreign object. In contrast to adults, the
affected side becomes hyperexpanded in children due to a ball-valve effect.
Subsegmental atelectasis is a subtype of obstructive atelectasis commonly seen after surgery or general
illness, due to mucus obstruction of the small airways.
• Relaxation (passive) atelectasis is caused by relaxation of lung adjacent to an intrathoracic
lesion causing mass effect, such as a pleural effusion, pneumothorax, or pulmonary mass.
• Adhesive atelectasis is due to surfactant deficiency.
Adhesive atelectasis is seen most commonly in neonatal respiratory distress syndrome, but can also be
seen in acute respiratory distress syndrome (ARDS).
• Cicatricial atelectasis is volume loss from architectural distortion of lung parenchyma by
fibrosis.

Lobar atelectasis
• Lobar atelectasis is usually caused by central bronchial obstruction (obstructive atelectasis),
which may be secondary to mucus plugging or an obstructing neoplasm.
If the lobar atelectasis occurs acutely, mucus plugging is the most likely cause.
Mucus plugging is most common in the lower lobes, least common in the left upper lobe.
If lobar atelectasis is seen in an outpatient, an obstructing central tumor must be ruled out.
• Lobar atelectasis, or collapse of an entire lobe, has characteristic appearances depending on
which of the five lobes is collapsed, as discussed on the following pages.

Chest: 3
Patterns of lobar atelectasis

frontal schematic

RUL LUL

RML

LLL
RLL
right lung left lung

lateral schematic
RUL LUL

RML

RLL LLL
right lung left lung

Illustration showing direction of collapse for each of the five lobes.

Chest: 4
Left upper lobe atelectasis

Left upper lobe collapse and luftsichel sign: Frontal radiograph (left image) shows veil-like opacity with
obscured left cardiac margin, a characteristic finding of left upper lobe collapse on frontal view; note the
crescent of air lateral to the aortic arch representing the luftsichel sign (yellow arrow). The lateral view (right
image) shows the anterior displacement of the left major fissure and collapsed left upper lobe (red arrows).
• Key imaging findings include the veil-like opacity on frontal radiograph, anterior
displacement of major fissure and anterior collapsed lung on lateral radiograph.
• The luftsichel (air-sickle in German) sign is a crescent of air seen on the frontal radiograph,
which represents the interface between the aorta and the hyperexpanded superior segment
of the left lower lobe. However, this sign is not always present.
• It is important to recognize left upper lobe collapse and not mistake the left lung opacity for
pneumonia or pleural effusion, since a mass obstructing the airway may be the cause of the
lobar atelectasis.
Right upper lobe atelectasis

Right upper lobe collapse: Frontal radiograph (left image) shows a right upper lobe opacity with superior
displacement of the minor fissure (blue arrow) and a convex mass (Golden S sign; yellow arrow). Lateral
radiograph (right image) shows the wedge-shaped collapsed RUL projecting superiorly (red arrows).

• The reverse S sign of Golden is seen in right upper lobe collapse caused by an obstructing
mass. The central convex margins of the mass form a reverse S. Although the sign describes
a reverse S, it is also commonly known as the Golden S sign. Similar to left upper lobe
collapse, a right upper lobe collapse should raise concern for an underlying malignancy in
adults or mucus plugging, particularly common in children.
Chest: 5
 • The juxtaphrenic peak sign is a peridiaphragmatic triangular opacity caused by
diaphragmatic traction from an inferior accessory fissure or an inferior pulmonary ligament,
seen in upper lobe volume loss from any cause.
Left lower lobe atelectasis

Left lower lobe collapse: Frontal radiographs demonstrate a triangular retrocardiac opacity representing the
collapsed left lower lobe (yellow arrows). Lateral radiograph shows posterior hazy opacity (red arrows).

• Triangular retrocardiac opacity is the main imaging feature of left lower lobe collapse.
• The flat waist sign describes the flattening of the left heart border due to posterior shift of
hilar structures and resultant cardiac rotation.
Right lower lobe atelectasis

Right lower lobe collapse: Frontal radiograph shows a triangular opacity at the right lower zone with apex
pointing towards the right hilum and obscuration of the medial right hemidiaphragm (blue arrow). Note there
is preservation of the right heart border. Lateral radiograph shows a hazy posterior opacity of the collapsed
right lower lobe (red arrows).

• Right lower lobe atelectasis is the mirror-image of left lower lobe atelectasis. Lower lobe
collapse is not well-seen on lateral view since the lobes mostly collapse medially.
• The collapsed lower lobe appears as a triangular retrocardiac opacity.

Chest: 6
 Right middle lobe atelectasis

Right middle lobe atelectasis: Frontal chest radiograph shows an indistinct opacity in the right lung with
focal silhouetting of the right heart border (blue arrows). There is elevation of the right hemidiaphragm due
to volume loss. The lateral radiograph shows a triangular opacity (red arrow) projecting over the mid-heart
representing the collapsed right middle lobe.
• The findings of right middle lobe atelectasis can be subtle on the frontal radiograph.
Silhouetting of the right heart border by the collapsed medial segment of the middle lobe
may be the only clue. The lateral radiograph shows a triangular opacity anteriorly.
• Collapse of both right middle and lower lobes occurs from obstruction of the bronchus
intermedius, and it causes obscuration of both the right heart border and right
hemidiaphragm, with a linear superior margin directed towards the hilum.

Round atelectasis
• Round atelectasis is focal
atelectasis with a round
morphology that is always
associated with an adjacent pleural
abnormality (e.g., pleural effusion,
pleural thickening or plaque).
• Round atelectasis is most common
in the posterior lower lobes.
• All five of the following findings
must be present to diagnose round
atelectasis:
1) Adjacent pleura must be abnormal.
2) Opacity must be peripheral and in
contact with the pleura.
Round atelectasis: Noncontrast CT shows a rounded opacity in
3) Opacity must be round or elliptical. the medial right lower lobe (red arrows). This example meets
4) Volume loss must be present in the all five criteria for round atelectasis including adjacent pleural
affected lobe. abnormality (effusion), opacity in contact with the pleura, round
5) Pulmonary vessels and bronchi shape, volume loss in the affected lobe, and the comet tail sign
leading into the opacity must be (yellow arrows) representing curved vessels and bronchi leading
curved — this is the comet tail sign. to the focus of round atelectasis.

Chest: 7
Patterns of lung disease
Essential anatomy
Secondary pulmonary lobule (SPL)
acinus, not visible on CT
(approximately 12 per secondary lobule)
acinar artery and
respiratory bronchiole

centrilobular bronchus
and artery

1 cm

2 cm

3 cm

approximate
scale
pulmonary veins (and lymphatics, not pictured)
run in the interlobular septa

• The secondary pulmonary lobule (SPL) is the elemental unit of lung function.
• Each SPL contains a central artery (the aptly named centrilobular artery) and a central
bronchus, each branching many times to ultimately produce acinar arteries and respiratory
bronchioles.
On CT, the centrilobular artery is often visible as a faint dot. The centrilobular bronchus is not normally
visible.
The acinus is the basic unit of gas exchange, containing several generations of branching respiratory
bronchioles, alveolar ducts, and alveoli.
There are generally 12 or fewer acini per secondary lobule.
• Pulmonary veins and lymphatics collect in the periphery of each SPL.
• Connective tissue, called interlobular septa, encases each SPL.
Thickening of the interlobular septa can be seen on CT and suggests pathologic enlargement of either the
venous or lymphatic spaces, as discussed on subsequent pages.
• Each SPL is between 1 and 2.5 cm in diameter.

Chest: 8
Abnormalities of the secondary pulmonary lobule
Consolidation and ground glass
• Consolidation and ground glass opacification are two very commonly seen patterns of lung
disease caused by abnormal alveoli. The alveolar abnormality may represent either filling of
the alveoli with fluid or incomplete alveolar aeration.
• Consolidation can be described on either a chest radiograph or CT, while ground glass is
generally reserved for CT.
• Although consolidation often implies pneumonia, both consolidation and ground glass are
nonspecific findings with a broad differential depending on chronicity (acute versus chronic)
and distribution (focal versus patchy or diffuse).
Consolidation

Consolidation: Contrast-enhanced
CT shows bilateral consolidative
opacities, more densely
consolidated on the left. There
are bilateral air bronchograms.
Although these imaging findings
are nonspecific, this was a case
of multifocal consolidative
adenocarcinoma.

• Consolidation is histologically due to complete filling of affected alveoli (commonly

remembered as blood, pus, water, or cells).
• Pulmonary vessels are not visible through the consolidation on an unenhanced CT.
• Air bronchograms are often present if the airway is patent. An air bronchogram represents a
lucent air-filled bronchus (or bronchiole) seen within a consolidation.
• Consolidation causes silhouetting of adjacent structures on conventional radiography.
• Acute consolidation is most commonly due to pneumonia, but the differential includes:
Pneumonia (by far the most common cause of acute consolidation).
Aspiration, consolidation may appear heterogeneous from mucus plugging.
Pulmonary hemorrhage (primary pulmonary hemorrhage or aspiration of hemorrhage).
Adult respiratory distress syndrome (ARDS), which is noncardiogenic pulmonary edema seen in critically
ill patients and thought to be due to increased capillary permeability.
Pulmonary edema may cause consolidation if severe.
• The differential diagnosis of chronic consolidation includes:
Adenocarcinoma, previously bronchioloalveolar carcinoma
Lymphoma.
Organizing pneumonia, which is a nonspecific response to injury characterized by granulation polyps
which fill the distal airways, producing peripheral rounded and nodular consolidation.
Chronic eosinophilic pneumonia, an inflammatory process characterized by eosinophils causing alveolar
filling in an upper-lobe distribution.

Chest: 9
Ground glass opacification (GGO)

Ground glass opacification:

Noncontrast CT shows diffuse
ground glass opacification (GGO).
The pulmonary architecture,
including vasculature and
bronchi, can be still seen,
which is characteristic for GGO.
Although these imaging findings
are nonspecific, this was a case
of acute respiratory distress
syndrome (ARDS).

• Ground glass opacification is histologically due to either partial filling of the alveoli
(by blood, pus, water, or cells), alveolar wall thickening, or reduced aeration of alveoli
(atelectasis).
• Ground glass is usually a term reserved for CT. CT shows a hazy, gauze-like opacity, through
which pulmonary vessels are still visible.
• Acute ground glass opacification has a similar differential to acute consolidation, since many
of the entities that initially cause partial airspace filling can progress to completely fill the
airspaces later in the disease. The differential of acute ground glass includes:
Pulmonary edema, which is usually central or dependent.
Pneumonia. Unlike consolidation, ground glass is more commonly seen in atypical pneumonia such as
viral or Pneumocystis jiroveci pneumonia.
Pulmonary hemorrhage, seen as pure ground glass in acute phase, but subacute phase shows peripheral
sparing and crazy paving.
Adult respiratory distress syndrome (ARDS).
• Chronic ground glass opacification has a similar but broader differential diagnosis compared
to chronic consolidation. In addition to all of the entities which may cause chronic
consolidation, the differential diagnosis of chronic ground glass also includes:
Lung adenocarcinoma, which can be focal or multifocal.
Organizing pneumonia, typically presenting as rounded, peripheral opacities.
Chronic eosinophilic pneumonia, usually with an upper-lobe predominance.
Interstitial lung disease, including desquamative interstitial pneumonia (DIP), nonspecific interstitial
pneumonia (NSIP), and hypersensitivity pneumonitis (HP).
Hypersensitivity pneumonitis (HP) is a type III hypersensitivity reaction to inhaled organic antigens. In
the subacute phase there is ground glass, centrilobular nodules, and mosaic attenuation.

Chest: 10
Peripheral ground glass or consolidation

Coronal schematic demonstrates peripheral Axial CT shows peripheral and subpleural ground glass
ground glass. attenuation. This was a case of organizing pneumonia.

• The differential diagnosis for peripheral consolidation or ground glass includes:

Organizing pneumonia.
Chronic eosinophilic pneumonia, typically with an upper lobe predominance.
Pulmonary infarction.

Interlobular septal thickening – smooth

Schematic demonstrates smooth Smooth interlobular septal thickening: CT demonstrates smooth

interlobular septal thickening. thickening of the interlobular septa (arrows) in pulmonary edema.
Courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• Conditions that dilate the pulmonary veins cause smooth interlobular septal thickening.
• By far the most common cause of smooth interlobular septal thickening is pulmonary
edema; however, the differential diagnosis for smooth interlobular septal thickening is:
Pulmonary edema.
Lymphangitis carcinomatosis.

Chest: 11
Interlobular septal thickening – nodular, irregular, or asymmetric

Schematic demonstrates irregular and Axial CT shows a diffuse nodular septal thickening (yellow arrows).
nodular interlobular septal thickening. This was a case of lymphangitic carcinomatosis.
• Nodular, irregular, or asymmetric septal thickening tends to be caused by processes that
infiltrate the peripheral lymphatics, most commonly by lymphangitic carcinomatosis and
sarcoidosis:
Lymphangitic carcinomatosis is tumor spread through the lymphatics.
Sarcoidosis rarely causes septal thickening.

Crazy paving

Schematic demonstrates interlobular Axial CT shows interlobular septal thickening in regions of ground
septal thickening and ground glass glass opacification, representing crazy paving. This was a case
opacification. of alveolar proteinosis, the entity in which crazy paving was first
described.
• Crazy paving describes interlobular septal thickening with superimposed ground glass
opacification, which is thought to resemble the appearance of a stone path.
• Although nonspecific, this pattern was first described for alveolar proteinosis, where the
ground glass opacification is caused by filling of alveoli by proteinaceous material and the
interlobular septal thickening is caused by lymphatics taking up the same material.

Chest: 12
 • The differential diagnosis for crazy paving includes:
Pulmonary edema, by far the most common cause.
Pulmonary hemorrhage.
Acute respiratory distress syndrome.
Pulmonary alveolar proteinosis (PAP), an idiopathic disease characterized by alveolar filling by a
proteinaceous substance. PAP is almost always seen with a crazy paving pattern.
Pneumocystis jiroveci pneumonia.
Adenocarcinoma, uncommon cause
Lipoid pneumonia, an inflammatory pneumonia caused by reaction to aspirated lipids, uncommon cause.

Approach to multiple micronodules

Tree-in-Bud
Centrilobular Perilymphatic Random
(Form of centrilobular)

Viral pneumonia Infectious bronchiolitis: Sarcoidosis Hematogenous metastases

Hypersensitivity pneumonitis Mycobacterial infections Pneumoconiosis Disseminated mycobacteria
Aspiration Viral infections Lymphangitic carcinomatosis Disseminated fungal infections
Pulmonary capillary hemangiomatosis Bacterial pneumonia
Metastatic calcification Aspiration

Occasionally, pulmonary edema Rarely, lymphangitic

carcinomatosis and vascular
abnormalities (endovascular
metastases and pulmonary
arterial aneurysms)

Table for Micronodular Patterns. KB pg14

Micronodules

No subpleural nodules Subpleural nodules

Peribronchial nodules, Uniform

non-uniform distribution distribution

Centrilobular Perilymphatic Random

aspiration sarcoid/silicosis metastases
inflammatory (HP, RB) lymphangitic carcinomatosis infection (miliary TB, fungal)
infection (viral, mycobacterial)

Chest: 13
Centrilobular nodules

Schematic demonstrates a centrilobular Axial CT demonstrates diffuse faint centrilobular opacities (arrows),
nodule, located at the center of the none of which extend to the pleural surface, which is typical of a
pulmonary lobule. centrilobular distribution. This was a case of pulmonary capillary
hemangiomatosis.
• Centrilobular nodules represent opacification of and around the centrilobular bronchiole (or
less commonly the centrilobular artery) at the center of each secondary pulmonary lobule.
• On CT, multiple small nodules are seen in the centers of secondary pulmonary lobules.
Centrilobular nodules never extend to the pleural surface. The nodules may be solid or of
ground glass attenuation, and range in size from tiny up to a centimeter.
• Centrilobular nodules may be caused by infectious or inflammatory conditions.
• Infectious causes of centrilobular nodules include viral pneumonias.
• The most common inflammatory cause of centrilobular nodules is hypersensitivity
pneumonitis (HP), an exposure-related lung disease.
HP is a type III hypersensitivity reaction to an inhaled organic antigen. The acute or subacute
presentation of HP is primarily characterized by centrilobular nodules.
Pulmonary capillary hemangiomatosis is a vascular pathology characterized by abnormal capillary
proliferation leading to pulmonary hypertension.
Viral pneumonias.
Aspiration is dependent.
Metastatic calcification most commonly occurs in the lung apices, typically in patients with renal failure.

Chest: 14
Perilymphatic nodules

Perilymphatic nodules: Schematic of the secondary pulmonary lobule (left image) demonstrates gray nodules
located along the bronchovascular bundle and white nodules located along the interlobular septa.
Axial CT (right image) demonstrates multiple subpleural nodules and nodules along the bronchovascular
bundles (arrows). This was a case of sarcoidosis.
• Perilymphatic nodules follow the anatomic locations of pulmonary lymphatics, which can be
seen in three locations in the lung:
1. Subpleural.
2. Peribronchovascular.
3. Septal (within the interlobular septa separating the secondary pulmonary lobules).
• Sarcoidosis is the most common cause of perilymphatic nodules, typically with an upper-
lobe distribution. The nodules may become confluent creating the galaxy sign in which
many tiny nodules surround a central lesion.

Pulmonary sarcoidosis with galaxy sign: Axial and coronal CT images demonstrate extensive upper-lobe
predominant confluent perilymphatic nodules. The galaxy sign is most apparent on the axial image, where the
confluent nodules appear like the confluence of stars forming a galaxy.

• The differential of perilymphatic nodules includes:

Sarcoidosis.
Pneumoconioses (silicosis and coal workers’ pneumoconiosis) are reactions to inorganic dust inhalation.
The imaging may look identical to sarcoidosis with perilymphatic nodules, but there is usually a history of
exposure (e.g., a sandblaster who develops silicosis).
Lymphangitic carcinomatosis.

Chest: 15
Random nodules

Random nodules:
Schematic of the secondary pulmonary lobule (top left image)
demonstrates nodules distributed randomly throughout the SPL.
Schematic of the lungs (bottom left image) demonstrates nodules
scattered randomly. Some of the nodules are in close contact with
the pleural surface.
Axial CT (top right image) demonstrates multiple random nodules.
Some of the nodules abut the pleural surface. This was a case of
metastatic colon cancer.

• Randomly distributed nodules usually occur via hematogenous spread. The differential of
random nodules includes:
Hematogenous metastases.
Disseminated mycobacteria.
Disseminated fungal infection.
• A miliary pattern is innumerable tiny random nodules the size of millet seeds.

Miliary nodules: Axial CT shows innumerable

tiny nodules distributed randomly throughout
both lungs in a miliary pattern. This was a case
of miliary tuberculosis.
Case courtesy Ritu R. Gill, MD, MPH, Brigham
and Women’s Hospital

Chest: 16
Tree-in-bud nodules

Schematic shows several nodules centered on an opacified small airway.

Tree-in-bud nodularity: Axial CT shows numerous small nodules (arrows) “budding” off of linear branching
structures in the right middle lobe. This case was secondary to atypical mycobacteria.

• Tree-in-bud nodules are multiple small nodules connected to linear branching structures,
which resemble a budding tree branch in springtime. The linear branching structures
represent mucus-impacted bronchioles, which are normally invisible on CT, and the nodules
represent impacted terminal bronchioles. Tree-in-bud nodules are due to mucus, pus, or
fluid impacting bronchioles and terminal bronchioles.
• Tree-in-bud nodules are almost always associated with small airways infection or
inflammation, such as endobronchial spread of tuberculosis.
• The differential of tree-in-bud nodules includes:
Mycobacterium tuberculosis and atypical mycobacteria.
Viral pneumonia.
Aspiration pneumonia.
Rarely, lymphangitic carcinomatosis and vascular abnormalities (endovascular metastases and
pulmonary arterial aneurysms).

Chest: 17
Cavitary and cystic lung disease
Solitary cavitary nodule/mass

Coronal schematic demonstrates a single cavitary Axial CT shows a single spiculated cavitary lesion in the
lesion. left upper lobe (arrow). This was a case of squamous cell
carcinoma.
• A cavitary lesion represents development of air within a pre-existing lesion (nodule, mass,
or consolidation). It typically has a thick, irregular wall, often with a solid mural component.
Although the findings of benign and malignant cavitary nodules overlap, a maximum wall
thickness of ≤4 mm is usually benign and a wall thickness >15 mm is usually malignant.
Spiculated margins also suggest malignancy.
• A solitary cavitary lesion is most likely cancer or infection.
Primary bronchogenic carcinoma. While both squamous cell and adenocarcinoma can cavitate,
squamous cell cavitates more frequently. Small cell carcinoma is never known to cavitate.
Tuberculosis classically produces an upper-lobe cavitary consolidation.
Fungal pneumonia.
Cavitary bacterial pneumonia.
Multiple cavitary nodules

Coronal schematic shows numerous cavitary Axial CT shows numerous cavitary and non-cavitary lesions
lesions bilaterally. bilaterally, in a random distribution. This was a case of
polysubstance abuse and septic emboli.
• The differential diagnosis for multiple cavitary lesions includes:
Septic emboli, typically peripheral.
Vasculitis, including granulomatosis with polyangiitis (GPA).
Metastases, classically squamous cell carcinoma but any metastatic lesion can cavitate.

Chest: 18
Cystic lung diseases

Coronal schematic shows numerous thin-walled Axial CT shows bilateral thin-walled cysts that are of
cystic lesions bilaterally. varying sizes but are predominantly regular in shape.
There is a small left pleural effusion. This was a case of
lymphangioleiomyomatosis.

• A cyst is an air-containing space with a thin wall. The differential diagnosis for multiple lung
cysts includes:
Lymphangioleiomyomatosis (LAM), a diffuse cystic lung disease due to smooth muscle proliferation of
the distal airways. LAM causes uniformly distributed, thin-walled cysts in a diffuse distribution. It may be
associated with chylous effusion, as demonstrated in the above right case.
Pulmonary Langerhans cell histiocytosis, which features irregular cysts and nodules predominantly in
the upper lungs.
Lymphoid interstitial pneumonia (LIP), a rare disease usually associated with Sjögren syndrome and
characterized by lymphocytic infiltrate and multiple cysts.
Amyloid which appears similar to LIP.
Birt-Hogg-Dube syndrome which is an autosomal dominant genetic disorder characterized by renal
tumors (most commonly chromophobe renal carcinoma and renal oncocytoma), and renal and
pulmonary cysts. Spontaneous pneumothoraxes can occur as a sequela of pulmonary cysts.
Pneumocystis jiroveci pneumonia, which features cysts in late-stage disease.
• Of note, it is important to distinguish cysts from emphysema. The latter typically does not
have walls and may have central vessels, whereas cysts classically do not have anything
inside.
• The differential for a single cyst includes:
Bulla. A bulla is an air-filled emphysematous space measuring >1 cm. A giant bulla occupies at least 30%
of the volume of the thorax.
Bleb. A bleb is an air-filled cystic structure contiguous with the pleura measuring <1 cm. Rupture of a
bleb is the most common cause of spontaneous pneumothorax.
Pneumatocele, which is an air-filled space caused by prior lung trauma or infection.

Chest: 19
Fibrotic changes
Lower lobe fibrotic changes

Coronal schematic shows basal-predominant Coronal CT shows bibasilar fibrosis and honeycombing
fibrotic changes. (arrows), with relative sparing of the upper lobes. This was
a case of idiopathic pulmonary fibrosis.

• The differential diagnosis of basal-predominant fibrotic change includes:

Usual interstitial pneumonia (UIP) pattern. Idiopathic pulmonary fibrosis (IPF) is a clinical syndrome of
progressive pulmonary fibrosis of unknown etiology and is the most common cause of basilar fibrosis. It
almost always features basilar honeycombing.
Other causes of UIP pattern, including rheumatoid arthritis and asbestosis.
Nonspecific interstitial pneumonia (NSIP) is a lung response to injury commonly associated with collagen
vascular disease and drug reaction. NSIP typically produces peribronchial reticulation and traction
bronchiectasis. Ground glass may be present.
Upper lobe fibrotic changes

Coronal schematic shows fibrotic changes in the Coronal CT shows upper-lobe predominant subpleural
upper lobes. fibrosis and traction bronchiectasis. A pathologic diagnosis
was not established in this case.
• Although IPF is the most common cause of pulmonary fibrosis, fibrosis primarily affecting
the upper lobes is typically caused by an alternative diagnosis, such as:
End-stage sarcoidosis. Sarcoidosis is a disease that primarily affects the upper lobes. The late stage of
sarcoidosis leads to upper-lobe predominant fibrosis.
Chronic hypersensitivity pneumonitis.
End-stage silicosis. The late stage of silicosis may lead to fibrosis with an upper lobe predominance.

Chest: 20
Pulmonary infection
Clinical classification of pneumonia
Community-acquired pneumonia (CAP)
• S. pneumoniae is the most common cause of community-acquired pneumonia (CAP).
• Atypical pneumonia, including Mycoplasma, viral, and Chlamydia, typically infects young
and otherwise healthy patients.
Mycoplasma has a varied appearance and can produce consolidation, areas of ground glass attenuation,
centrilobular nodules, and tree-in-bud nodules.
• Legionella most commonly occurs in elderly smokers. Infections tend to be severe.
• Infection by Klebsiella and other gram-negatives occurs in alcoholics and aspirators.
Klebsiella classically leads to voluminous inflammatory exudates causing the bulging fissure sign.
Hospital-acquired pneumonia (HAP)
• Hospital-acquired pneumonia (HAP) occurs in hospitalized patients and is due to aspiration
of colonized secretions. HAP is caused by a wide variety of organisms, but the most
important pathogens include MRSA and resistant gram-negatives including Pseudomonas.
Healthcare-associated pneumonia (HCAP)
• Healthcare-associated pneumonia is defined as pneumonia in a nursing home resident or in
a patient with a >2 day hospitalization over the past 90 days. Pathogens are similar to HAP.
Ventilator-associated pneumonia (VAP)
• Ventilator-associated pneumonia is caused by infectious agents not present at the time
mechanical ventilation was started. Most infections are polymicrobial and primarily involve
gram-negative rods such as Pseudomonas and Acinetobacter.
Pneumonia in the immunocompromised patient
• Any of the above pathogens, plus opportunistic infections including Pneumocystis, fungi
such as Aspergillus, Nocardia, CMV, etc., can be seen in immunocompromised patients.
• Different types of immunocompromise can lead to different infections. In particular,
neutropenia predisposes to fungal pneumonia.

Radiographic patterns of infection

Lobar pneumonia
• Lobar pneumonia is consolidation of a single lobe. It is usually bacterial in origin and is the
most common presentation of community-acquired pneumonia. The larger bronchi remain
patent, causing air bronchograms.
Bronchopneumonia
• Bronchopneumonia is patchy peribronchial consolidation with air-space opacities, usually
involving several lobes, and may be caused by both bacterial and viral pneumonias as well as
aspiration.
Interstitial pneumonia
• Interstitial pneumonia is a misnomer, a finding on CXR that usually corresponds to ground
glass on CT. Generally it can be caused by atypical (e.g., Mycoplasma, Chlamydia), viral, or
Pneumocystis pneumonia.
Round pneumonia
• Round pneumonia is an infectious mass-like opacity seen in children, most commonly due to
S. pneumoniae. Infection remains confined due to incomplete formation of pores of Kohn.

Chest: 21
Complications of pneumonia
Pulmonary abscess
• Pulmonary abscess is necrosis of the lung parenchyma typically due to Staphylococcus
aureus, Pseudomonas, or anaerobic bacteria.
• An air-fluid level is often present.
• An abscess is usually spherical, with equal dimensions on frontal and lateral views.
Empyema
• Empyema is infection within the pleural space.
• There are three stages in the development of an empyema:
1) Free-flowing exudative effusion: Can be treated with needle aspiration or simple drain.
2) Development of fibrous strands: Requires large-bore chest tube and fibrinolytic therapy.
3) Fluid becomes solid and jelly-like: Usually requires surgery.
• Although pneumonia is often associated with a parapneumonic effusion, most pleural
effusions associated with pneumonia are not empyema, but are instead a sterile effusion
caused by increased capillary permeability.
• An empyema conforms to the shape of the pleural space, causing a longer air-fluid level on
the lateral radiograph. This is in contrast to an abscess, discussed above, which typically is
spherical and has the same dimensions on the frontal and lateral radiographs.
• The split pleura sign describes enhancing parietal and visceral pleura of an empyema seen
on contrast-enhanced study.
Split pleura sign: Contrast-enhanced CT shows
enhancement of the thickened visceral and
parietal pleural layers (arrows), which encase a
pleural fluid collection.
The split pleura sign is seen in the majority of
exudative effusions, although it is not specific.
Similar findings can be seen in malignant effusion,
mesothelioma, fibrothorax, and after talc
pleurodesis.
Case courtesy Ritu R. Gill, MD, MPH, Brigham and
Women’s Hospital.

Empyema necessitans
• Empyema necessitans is extension of an empyema to the chest wall, most commonly
secondary to tuberculosis. Other causative organisms include Actinomyces.
Pneumatocele
• A pneumatocele is a thin-walled, gas-filled cyst that may be post-traumatic or develop as a
sequela of pneumonia, typically from Staphylococcus aureus or Pneumocystis.
Bronchopleural fistula (BPF)
• Bronchopleural fistula (BPF) is an abnormal communication between the airway and the
pleural space. It is caused by rupture of the visceral pleura. By far the most common cause
of BPF is surgery; however, other etiologies include lung abscess, empyema, and trauma.
• On imaging, new or increasing gas is present in a pleural effusion. A connection between the
bronchial tree and the pleura is not always apparent, but is helpful when seen.
• The treatment of BPF is controversial and highly individualized.

Chest: 22
Tuberculosis (TB)
• Tuberculosis (TB), caused by Mycobacterium tuberculosis, remains an important disease
despite remarkable progress in public health and antituberculous therapy over the past
century. Tuberculosis remains a significant problem in developing countries. In the United
States, TB is seen primarily in immigrant, institutionalized, and immunocompromised
individuals.
• Initial exposure to TB can lead to two clinical outcomes:
1) Contained disease (90%) results in calcified granulomas and/or calcified hilar lymph nodes. In a patient
with normal immunity, the tuberculous bacilli are sequestered with a caseating granulomatous response.
2) Primary tuberculosis results when the host cannot contain the organism. Primary tuberculosis is seen
more commonly in children and immunocompromised patients.
• Reactivation (post-primary) TB is reactivation of a previously latent infection.
Primary tuberculosis

Primary TB: Chest radiograph (left image) shows a vague right upper lung opacity (arrow). CT shows a patchy
opacification (arrow) in the lower portion of the right upper lobe with adjacent tree-in-bud nodularity. The
patient's sputum grew Mycobacterium tuberculosis.
Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.
• Primary TB represents infection from the first exposure to TB. Primary TB may involve the
pulmonary parenchyma, the airways, and the pleura. Primary TB often causes adenopathy.
• As many as 15% of patients infected with primary TB have no radiographic changes and the
imaging appearance of primary TB is nonspecific.
• The typical imaging manifestation of primary TB is lobar consolidation +/- pleural effusion
and lymphadenopathy, although not all of these need to be present. Primary TB may occur
in any lobe. Both primary and reactivation TB can also present as isolated pleural disease or
miliary disease, see next section on miliary TB.
• Classic imaging findings are not always seen, but include:
Ghon focus: Initial focus of parenchymal infection, usually located in the upper part of the lower lobe or
the lower part of the upper lobe.
Ranke complex: Ghon focus and lymphadenopathy.
• Cavitation is rare in primary TB, in contrast to reactivation TB.

Chest: 23
 • Adenopathy is common in primary TB, typically featuring central low-attenuation and
peripheral enhancement, especially in children.

Tuberculous adenopathy: Contrast-enhanced neck CT

shows marked right-sided adenopathy (arrows) with
peripheral enhancement and central necrosis.
Case courtesy Ritu R. Gill, MD, MPH, Brigham and
Women’s Hospital.

Reactivation (post-primary) tuberculosis

• Reactivation TB, also called post-primary TB, usually occurs in adolescents and adults and is
caused by reactivation of a dormant infection acquired earlier in life. Clinical manifestations
of reactivation TB include chronic cough, low-grade fever, hemoptysis, and night sweats.
• Reactivation TB most commonly occurs in the upper lobe apical and posterior segments and
superior segments of the lower lobes.

Reactivation TB: Frontal chest radiograph (left image) shows a cavitary lesion in the left upper lobe (arrow),
confirmed by CT (arrow). There was no significant mediastinal adenopathy. The differential diagnosis of this
appearance would include cavitary primary lung cancer, which would be expected to feature a thicker wall.
Case courtesy Michael Hanley, MD, University of Virginia Health System.
• In an immunocompetent patient, the imaging hallmarks of reactivation TB are upper-lobe
predominant consolidation with cavitation. Tree-in-bud nodules are common and suggest
active endobronchial spread.
• Low-attenuation adenopathy is a common additional finding, seen more often in
immunocompromised patients.
• A tuberculoma is a well-defined rounded opacity consisting of an encapsulating fibrous wall
with central caseation, usually in the upper lobes.

Chest: 24
Healed tuberculosis

Healed TB: Radiograph shows scarring, volume loss, and superior hilar retraction (arrows). CT shows apical
scarring. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• Healed TB is evident on radiography as apical scarring, usually with upper lobe volume loss
and superior hilar retraction.
• Calcified granulomas may be present as well, which indicate containment of the initial
infection by a delayed hypersensitivity response.
Miliary tuberculosis

Miliary TB: Radiograph and CT show innumerable tiny nodules in a random pattern, reflecting hematogenous
seeding of TB. Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.

• Miliary TB is a diffuse random distribution of tiny nodules seen in hematogenously

disseminated TB.
• Miliary TB can occur in primary or reactivation TB.

Chest: 25
Atypical mycobacteria
Atypical mycobacteria infection

Mycobacterium avium intracellulare infection: Coronal (left image) and axial CT show right upper lobe and
lingular tree-in-bud opacities and bronchiectasis, with more focal consolidation in the lingula (arrow).

• There are three types of atypical mycobacterial infection:

(1) “Classic” or nodular cavitary form that simulates TB; typically seen in patients with chronic lung
disease.
(2) Non-classic or bronchiectatic form (more common).
(3) Disseminated form, typically lymphadenopathy in immunocompromised patients (usually AIDS).
• The presentation of bronchiectatic atypical mycobacteria is an elderly woman with cough,
low-grade fever, and weight loss, called Lady Windermere syndrome. Mycobacterium avium
intracellulare and M. kansasii are the two most common organisms.
Radiographic findings are bronchiectasis and tree-in-bud nodules, most common in the right middle lobe
and lingula.
“Hot-tub” lung
• “Hot-tub” lung is a hypersensitivity pneumonitis in response to atypical mycobacteria, which
are often found in hot tubs. There is no active infection and the typical patient is otherwise
healthy. Imaging is similar to other causes of hypersensitivity pneumonitis, featuring
centrilobular nodules.

Endemic fungi
• Endemic fungi can cause pneumonia in normal individuals, with each subtype having a
specific geographic distribution.
Histoplasma capsulatum
• Histoplasma capsulatum is localized to the Ohio and Mississippi river valleys, in soil
contaminated with bat or bird guano.
• Acute infection usually produces nodules and lymphadenopathy.
• Chronic sequela of infection is a calcified granuloma. A less common radiologic
manifestation is a pulmonary nodule (histoplasmoma), which can mimic a neoplasm.
• Fibrosing mediastinitis is a rare complication of Histoplasma infection of mediastinal lymph
nodes leading to pulmonary venous obstruction, bronchial stenosis, and pulmonary artery
stenosis. Affected lymph nodes tend to calcify.

Chest: 26
 Coccidioides immitis and Blastomyces dermatitidis
• Coccidioides immitis is found in the southwestern United States and has a variety of
radiologic appearances, including multifocal consolidation, multiple pulmonary nodules, and
miliary nodules.
• Blastomyces dermatitidis is found in the central and southeastern United States. Infection
is usually asymptomatic, but may present as flu-like illness that can progress to multifocal
consolidation, ARDS, or miliary disease.

Viral pneumonia
• In general, viral pneumonias have a large overlap with bacterial pneumonias in imaging
appearance.
• Classic imaging findings on CT include centrilobular or tree-in-bud nodules, patchy ground
glass opacities, and bronchopneumonia (peribronchial consolidations).
Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)
• Severe acute respiratory syndrome coronavirus 2 SARS-CoV-2 (i.e., COVID-19) is a respiratory
viral disease that became a pandemic in early 2020.
• Imaging findings are nonspecific, however bilateral, dependent, lower-lobe predominant
ground glass opacities or consolidations are classic features.
• Pleural effusions, centrilobular nodules, and tree-in-bud nodules are typically not
associated.

COVID-19 infection: Chest radiograph (left image) shows bilateral peripheral opacities (arrows). Chest CT (right)
in a different patient shows peripheral ground glass and consolidations in both lungs (arrows).

Chest: 27
Infections in the immunocompromised
• Immunosuppressed patients are susceptible to the same organisms that infect
immunocompetent patients; however, one must be aware of several additional
opportunistic organisms that may present in the immunocompromised.
• An immunocompromised patient with a focal air space opacity is most likely to have a
bacterial pneumonia (most commonly pneumococcus), but TB should also be considered if
the CD4 count is low.
• In contrast, multifocal opacities have a wider differential diagnosis including Pneumocystis
pneumonia and opportunistic fungal infection such as Cryptococcus or Aspergillus.
Pneumocystis jiroveci pneumonia
• Pneumocystis jiroveci (previously called Pneumocystis carinii) is an opportunistic fungus that
may cause pneumonia in individuals with CD4 counts <200 cells/cc or other T-cell deficiency
(e.g., status post bone marrow transplant or solid organ transplant). The incidence of
Pneumocystis pneumonia is decreasing due to routine antibiotic prophylaxis.

Pneumocystis pneumonia: Radiograph (top left

image) shows multiple upper-lobe predominant
airspace opacities. CT (top image) shows crazy paving
(arrows), with confluent ground glass attenuation in
the upper lobes.

Axial CT in a different patient with Pneumocystis

pneumonia (bottom left image) shows asymmetric
ground glass opacification, with thin-walled cysts.
Cases courtesy Ritu R. Gill, MD, MPH, Brigham and
Women’s Hospital.

• Chest radiograph findings can be normal but a classic finding of Pneumocystis pneumonia is
bilateral perihilar (central) airspace opacities with peripheral sparing.
• The classic CT appearance is ground glass opacification, sometimes with crazy paving
(ground glass and thickening of the interlobular septa).
• A normal CT rules out Pneumocystis pneumonia; however, the disease can hide in a normal
chest radiograph.
• Pneumocystis pneumonia has a propensity to cause upper lobe pneumatoceles particularly
if untreated, which may predispose to pneumothorax or pneumomediastinum.

Chest: 28
 Cryptococcus neoformans
• Cryptococcus is an opportunistic organism and is the most common fungal infection in AIDS
patients. Pulmonary infection usually coexists with cryptococcal meningitis.
Typically CD4 count is less than 100 cells/cc in affected individuals.
• In the immunosuppressed, Cryptococcus can have a wide range of appearances ranging from
ground glass attenuation to focal consolidation to cavitary nodules. Cryptococcus can also
present as miliary disease, often associated with lymphadenopathy or effusions.

Aspergillus
Overview of Aspergillus

Spectrum of pulmonary Aspergillus

increased/inappropriate immune response

finger-in-glove sign:
Asthma or CF? mucoid impaction of
ABPA bronchiectasis

abnormal lungs or abnormal host

Preexisting cavity?
e.g., sarcoid, TB mobile mycetoma
Aspergilloma/Mycetoma
Monod sign:
air surrounding mycetoma

Chronic lung disease

like emphysema? chronic consolidation
Semi-invasive (chronic necrotizing)
cavitation

invasive disease seen in the immunocompromised

bronchopneumonia
Airway invasive centrilobular nodules
Neutropenic or
immunocompromised? tree-in-bud nodules

halo sign: acute infection

Angioinvasive peripheral ground glass
air crescent sign:
crescentic air in a cavity

• Aspergillus is a ubiquitous soil fungus that manifests as five distinct categories of pulmonary
disease. Aspergillus only affects those with abnormal immunity or preexisting pulmonary
disease. Depending on the manifestation, the predisposing abnormality may include
asthma, immunocompromised state, prior infection, or structural/congenital abnormality.

Chest: 29
Allergic bronchopulmonary aspergillosis (ABPA)

Finger-in-glove sign of ABPA: Chest radiograph shows upper-lobe predominant bronchiectasis with branching
perihilar opacities. CT shows dense bronchial mucoid impaction representing the finger-in-glove sign (arrow).
Case courtesy Ritu R. Gill, MD, MPH, Brigham and Women’s Hospital.
• Allergic bronchopulmonary aspergillosis (ABPA) is a hypersensitivity reaction to aspergillus
seen most commonly in patients with long-standing asthma. ABPA is not an infection.
• Patients present clinically with recurrent wheezing, low-grade fever, cough, and sputum
production containing fragments of aspergillus hyphae. The diagnosis may be made using
serum testing for aspergillus IgE.
• The key finding on CT is central bronchiectasis and mucoid impaction, which can be high
attenuation or even calcified. This combination of mucoid impaction within bronchiectatic
airways represents the finger-in-glove sign.
The finger-in-glove sign is not specific to ABPA, however high attenuation mucus is a specific finding.
Saprophytic aspergillosis (aspergilloma)
• An aspergilloma is a conglomeration of
intertwined aspergillus fungal hyphae and
cellular debris (a mycetoma or “fungus ball”)
in a preexisting pulmonary cavity.
The aspergilloma is mobile and will shift position
when the patient is imaged in a different position.
• The most common causes of a preexisting
cavity are prior TB and sarcoidosis.
Less common causes include congenital anomalies
such as bronchogenic cyst or sequestration, and
post-infectious/post-traumatic pneumatocele.
Aspergilloma and Monod sign: CT shows an irregular
• If an aspergilloma is symptomatic, hemoptysis opacity (arrows) resting dependent within a left
is the most common symptom. Treatment upper lobe cavity, representing an aspergilloma
is embolization or resection rather than (arrows). The Monod sign is the curvilinear air
surrounding the aspergilloma. This patient has prior
antifungal medication.
TB with biapical scarring and left apical cavity.
• When a crescent of air is seen outlining the Case courtesy Ritu R. Gill, MD, MPH, Brigham and
mycetoma against the wall of the cavity, the Women’s Hospital.
correct term is Monod sign. The air crescent
sign is reserved for angioinvasive aspergillus.
Chest: 30
Semi-invasive (chronic necrotizing) aspergillosis
• Semi-invasive aspergillosis is a necrotizing granulomatous inflammation (analogous in
pathology to reactivation TB) in response to chronic aspergillus infection. Semi-invasive
aspergillosis is seen in debilitated, diabetic, alcoholic, and COPD patients.
• Clinical symptoms include cough, chronic fever, and less commonly hemoptysis.
• On CT, there are segmental areas of consolidation, often with cavitation and pleural
thickening, which progress slowly over months or years.
Airway-invasive aspergillosis
• Airway-invasive aspergillosis is aspergillus infection deep to the airway epithelial cells. It is
seen only in the immunocompromised, including neutropenic and AIDS patients.
• The spectrum of clinical disease ranges from bronchiolitis to bronchopneumonia.
• The main CT findings of airway-invasive aspergillosis are centrilobular and tree-in-
bud nodules. When bronchopneumonia is present, radiograph and CT findings are
indistinguishable from other causes of bronchopneumonia, such as Staph. aureus.
Angioinvasive aspergillosis
• Angioinvasive aspergillosis is an aggressive infection characterized by invasion and occlusion
of arterioles and smaller pulmonary arteries by fungal hyphae. Angioinvasive aspergillosis is
seen almost exclusively in neutropenic patients.
• The CT halo sign represents a halo of ground glass attenuation surrounding a consolidation.
The ground glass corresponds to hemorrhage.
Halo sign: CT shows a left upper lobe mass
with peripheral ground glass (yellow arrow),
representing pulmonary hemorrhage.
Case courtesy Michael Hanley, MD,
University of Virginia Health System.

The halo sign is not specific to angioinvasive aspergillosis, and can also be seen in viral infection,
granulomatosis with polyangiitis (GPA), Kaposi sarcoma, hemorrhagic metastasis, and others.
• The air crescent sign represents a crescent of air from retraction of infarcted lung and occurs
with recovery of neutrophil counts. It a good prognostic sign as it indicates that the patient
is in the recovery phase.

Air crescent sign: Noncontrast CT shows a

lesion in the left lower lobe with a crescent-
shaped air collection anteriorly (arrows).

Chest: 31
Pulmonary edema and ICU imaging
Pulmonary edema
Overview of pulmonary edema

Mild pulmonary edema: Radiograph demonstrates moderate enlargement of the cardiac silhouette and
sternotomy wires. There are increased interstitial markings with Kerley B lines (arrows). Chest CT shows
smooth interlobular septal thickening (arrows), corresponding to the Kerley B lines seen on radiography. Mild
geographic ground glass attenuation likely corresponds to early alveolar filling.

• The radiographic severity of pulmonary edema typically progresses through three stages,
corresponding to progressively increased pulmonary venous pressures.
• Vascular redistribution is the first radiographic sign of increased pulmonary venous
pressure. Imaging shows increased caliber of the upper lobe vessels compared to the lower
lobe vessels.
• Interstitial edema is caused by increased fluid within the pulmonary veins, which surround
the periphery of each secondary pulmonary lobule. On radiography, there are increased
interstitial markings, indistinctness of the pulmonary vasculature, peribronchial cuffing, and
Kerley B lines.
Kerley B lines are seen at the peripheral lung and represent thickened interlobular septa.
• Alveolar edema is caused by filling of the alveoli with fluid. Edema typically has a perihilar
(central) distribution. Pleural effusions and cardiomegaly are often present.
• CT findings of pulmonary edema include dependent or central ground glass opacification
and interlobular septal thickening.
• Pulmonary edema is usually symmetric and dependent. A classic cause of asymmetric
pulmonary edema is isolated right upper lobe pulmonary edema, caused by acute mitral
regurgitation secondary to myocardial infarction and papillary muscle rupture.
• A complication of aggressive thoracentesis is reexpansion pulmonary edema, caused by
rapid reexpansion of a lung in a state of collapse for more than three days.

Chest: 32
Support devices
Endotracheal tube
• The endotracheal tube tip should
be approximately 4–6 cm above
the carina with the neck in neutral
alignment. However, in situations
with low pulmonary compliance (e.g.,
ARDS), a tip position closer to the
carina may reduce barotrauma.
• Direct intubation of either the
right or left mainstem bronchus
(right mainstem bronchus far more
common) is an emergent finding that
can cause complete atelectasis of the
un-intubated lung.

Right mainstem bronchus intubation: Chest radiograph

shows the endotracheal tube terminating in the right
mainstem bronchus (yellow arrow), a few centimeters distal
to the carina (red arrow).
Central venous catheters

Peripherally inserted central catheter (PICC) in the azygous vein: Frontal radiograph shows a left-sided PICC
coursing medially at the confluence of the brachiocephalic vein and the SVC (arrow). Lateral radiograph shows
the PICC curves anteriorly before heading inferiorly and posteriorly into the azygous vein (arrow).
Case courtesy Beatrice Trotman-Dickenson, MD, Brigham and Women's Hospital.

• The tip of a central venous catheter, including a PICC should be in lower SVC or the
cavoatrial junction. Azygous malposition is seen in approximately 1% of bedside-placed
PICCs. Azygous malposition is associated with increased risk of venous perforation and
catheter-associated thrombosis, and repositioning is recommended.
• A dialysis catheter should be located in the right atrium.

Chest: 33
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Title: Mehiläinen 1840

Editor: Elias Lönnrot

Release date: March 23, 2024 [eBook #73242]

Language: Finnish

Original publication: Helsinki: G. O. Wasenius, 1840

Credits: Jari Koivisto

*** START OF THE PROJECT GUTENBERG EBOOK MEHILÄINEN

1840 ***
MEHILÄINEN 1840

Toim.

Elias Lönnrot

Helsingissä, Präntätty G. O. Waseniuksen tykönä, 1840.

Imprimatur: H. Widenius.

MEHILÄINEN. W. 1840.
Tammikuulta.
MUUALTA LÄHETETTY.

Uusia Wirsiä, Kirkossa ja kotona veisattavia. Joita ensin Suomen

Papit, Ignatius, Frosterus, Helenius, Pesonius, Achrenius, ja muut
ovat kirjoittaneet; mutta sitten yhdistänyt, uudistanut, ja lisännyt
Arkki-Pispa vainaja Jak. Tengström, ja nyt Wirsi-Kirjan-Seurasto
pränttiin antanut. Ensimmäinen ja jälkimmäinen osa. Turusa, vuonna
1836 Frenckellin ja Pojan Kirja-painosa.

Kauvan on Suomalaiset olleet täydellisemmän Wirsi-Kirjan

puutteessa, joko, ei ainoastansa, selkeemmällä puheenparrella, kuin
nykynen Wirsi-Kirjamme, ilmoittais Evangeliumin puhdasta oppia,
mutta jossa myös olis Wirsiä muista tarpeellisista aineista kuin
nykysessä vanhassa Wirsikirjassamme löytään; täma puute on
huomattu, ja se on myös ollut Jumalan sanaa, ja yhteistä hengellista
parasta rakastavaisten Sielunpaimenten sydämmellä; heitin
yhteisestä toimesta ja työstänsä on nämät mainitut Wirret, präntin
kautta, annettu kunkin erinäiseksi, ja kaikkein Suomalaisten
yhteiseksi hengelliseksi hyödyksi. Ne on myös erinomattain
täysinäisen kielensä vuoksi parhaita, tähänasti painetuista
Suomalaisista Wirsistä. Mutta ne monet takaperoset sanat, jotka
näyttää ehdolla, vaston kielen luontoo ja tavallista puhetta olevan
kirjotettu takaperosiksi, on niin oudot korvalle, että, jos ei ne juuri
öksytä lukiaansa, niin ovat ne kumminkin häneltä työlläästi
ymmärrettävät, ja ainakin on ne oikeinpäin, luonnollisessa
järjestyksessänsä, paremmat, jonkatähden tähän pannaan
muutamia esimerkiksi, ja niitten selitys, niille tiedoksi, jotka ei
senlaiseen takaperoseen puheen luontoon (Renkoon) tottuneet ole.

N:o 552 v. 1 luetaan: "Hän Isän lyöpi vitsalla" olis paremmin

ymmarrettävä, sanojen luonnollisessa järjestyksessä, ja versyn-
rakennusta (meter) vahingoittamatta, sanottuna: Hän lyöpi Isän
vitsalla. N:o 1 v. 1 "Maan, Taivaan noskoot Luojalle," oikein päin:
Noskoot maan, Taivaan luojalle. N:o 2 v. 2. "Äänes kuulen jylinän",
oikein päin: Kuulen äänes jylinän.

Erilaita on niitten takaperosten sanojen, joita versyn juoksu, eli

laatu, vaatii semmoisiksi; esimerkiksi: viimmeksi mainitun virren
kolmann. versyssä seisoo: "Käskee teille Taivahan", ja N:o 4 v. 2
"Pukus säteet auringon", rikkois versyn luonnon, jos niitä oikeinpäin
sanottaisiin: Käskee Taivahan tielle, ja Pukus auringon säteet. Mutta
näistä edellä nimitetyistä, niinkun seuraavistakin takaperosista
sanoista, ei ole ollut versyn-rakennuksen apua, vaan pikemmin
pahennusta, ja ainakin ovat luonnottomat, niinkun jo sanottu on. N:o
162 on jambista versyn lajia, mutta ensimmäisessä versyssä 3:mas
rati alkaa daktylillä ja takaperosesti: "Kuoleman pääsi vallasta", jos
tässa olis kielen luontoo seurattu, niin olis versyllä oma jambinen
luontonsa, esimerk. Hän pääsi kuollon vallasta. N:o 34 alkaa
"Jumalan Herran ainoan kunnia olkoon aina"; tässä sanotaan
Jumalalla olevan Herra, mutta ei toivoteta: Jumalalle (taikka) Herralle
ainoalle kunnia olkoon aina. N:o 56 alkaa "Tuntos äänen koskas
kuulet", oikeinpäin: Koskas tuntos äänen kuulet. N:o 146 v. 6.
"Haudan nousit kammiosta", oikeinp. Nousit haudan kammiosta. N:o
149 v. 2 "Kuoleman vapaat vaarasta". oikeinp.: Wapaat kuoleman
vaarasta. 156 v. 2. "Heille vaan se omaksi". oikeinp. Waan se heille
omaksi. N:o 161 v. 2 "Jesuksen etsein ruumista", oikeinp. Etsein
Jesuksen ruumista. N:o 162 v. 6 "Hän suuren voitti kunnian", oikeinp.
Hän voitti suuren kunnian. N:o 166 v. 3 "Usiamman päätin kerran",
oikeinp. Päätin usiamman kerran. N:o 167 v. 1 "Uuteen nousit
elämään", oikeinp. Nousit uuteen elämään. N:o 180 v. 3 "Elämän
ruokkii leivälla", oikeinp. Ruokkii Elämän leivällä. N:o 317 v. 3 "JoS
epä-usko armos estää valon", oikeinp.: Jos epä-usko estää armos
valon. N:o 371 v. 2 "Surun näännyn vallasa", oikeinp.: Näännyn
surun vallasa. N:o 393 v. 5 "Isä suo rakas", oikeinp.: Suo Isä rakas.
N:o 442 v. 3 "Sen heille hyvyys Herran suo" oikeinp.: Sen heille
Herran hyvyys suo. N:o 474 v. 2 "Kansansa asuu seasa", oikeinp.
olis: Asuu kansansa seassa. N:o 476 v. 3 "Niin Taivaan voitan
palmun", oikeinp.: Niin voitan Taivaan palmun. N:o 512 v. 1 "Elämän
käymään teitä", oikeinp.: Käymään elämän teitä. N:o 513 v. 1 "Sun
käskyis käymään teitä", oikeinp.: Käymaän sun käskyis teitä. N:o
590 v. 4 "Isäs tunnet rakkauden", oikeinp.: Tunnet Isäs rakkauden.
N:o 64l v. 1 "Monen hän kerran", oikeinp.: Hän monen kerran. N:o
677 v. 3 "Ja teitä synnin seurataan", oikeinp.: Ja synnin teitä
seurataan. N:o 684 v. 1 "Taivaan nähdä kotomaan", oikeinp.: Nähdä
Taivaan kotomaan.[1] Nro 710 v. 1 "Ei kuollon päästä kädestä",
oikeinp.: Ei päästä kuollon kädestä ja paljo muita senkaltasia.

N:o 642 Sanotaan veisattavan kuin: O Jesu Kriste sä autuuden, ja

68 samalla nuotilla; mutta näitten virsien rakennus on peräti
erinlainen: Ensiksi mainittu virsi (642) on Daktylinen, 10 ja 9 tavausta
versyen ratisa; toinen (N:o 68) on Jambinen, 8 ja 7 tavausta ratisa.
Eikö olis luonnikkaampi, että kaikki yhdellä nuotilla veisattavat virret
olis yhtä versyn laija?
 N:o 734 4:sä ja 5:sä versyssä on, ainoastansa, 8 ratia, mutta
edellisissä on 12; tietämätön on mistä näihin viimeisiin versyin
saadaan 4 puuttuvaista ratia?

N:o 148 v. 4 ja viidennestä radista puuttuu 1 tavaus ja N:o 258 v. 2

ensimm. rati samalla lailla; mutta seuraavaissa on yksi tavaus liiaksi.
N:o 122 v. 4 2 rati. N:o 255 7 v. 7 rati. N:o 586 4 v. 1 r. ja 601 3 v. 7
radisa.

Puolia, eli katkastuita sanoja on tyystin ja taiten kartettu; niitä ei

ole myös muuta kuin harvassa paikka joku sana ("Nuorna"),
esimerkiksi virsissä N:o 582 v. 1, 583 v. 5, 584 v. 4, 589 v, 4, 592 v.
1, 599 v. 8, 615 v. 1, ja 707 v. 3. Paitti näitä on koko kirja,
ylistettävästi, täydellistä ja selkeetä Raamatun Suomee,[2] ja
niinmuodon Suomen-maan joka paikkakunnissa, suomalaisilta
ymmärrettävä. Mutta, kaikki ei näytä hyväksyvän niin täydellistä
kieltä, ja puhdasta puheenpartta virsissä,[3] vaan pitäävat katkaistut
sanat niin tarpeellisina, ettei he ilman niitä sano saavan versyä
luonnistumaan, siitä syystä, että Suomen kielessä on vähän lyhkösiä
ja yksi tavaus sanoja. Mutta jos tätä asiaa tarkemmin tutkitaan, niin
huomataan piankin ettei katkastuista sanoista ole versylle apua, eikä
sitä luonnikkaammaksi auta; Roschierin ja Heleniuksen
Ruottinkielestä Suomentamat Wirsi-kirjat todistaapi tämän; sillä ne
on melkeen koottu katkaistuista sanoista, ja sentään taajemmassa
versyn-rakennuksen vikoja, kuin Wirsi-Kirjan-Seuraston virsissä.
Tähän otan esimerkiksi Roschierin "Psalmi-kirjan", ainoastansa,
ensimmäisestä Psalmista (virrestä); sillä ne seuraavaiset on kaikki
samallaisia, ja Heleniuksen on myös yhtäläinen: "Juur', häneen,
heill', tääl', niins, kaikk'." Kukin ajatteleva lukia näkee tässä, jos
nämät tavaukset on lyhkösiä, jotka lyhköseksi merkitty on. Sillä
nämät katkaistut sanat: Juuri, heille, täällä, kaikki, ja muut
senkaltaiset, ovat Trocheukset, niissä on pitkä ja lyhy tavaus; jos
niistä jätetään pois viimmonen tavaus, joka on lyhy, niin jääpi
kumminkin ensimmäinen tavaus, joka on pitkä, sanottavaksi, eikä
sovi lyhkösen siaan pantaa, niinkuin sanan-katkasiat on tehneet, ja
luulleet sen sillä lyhköseksi muuttuneen, kuin he viimmesen
tavauksen on pois jättäneet.

Senlaiset lyhennetyt sanat kuin: "Mulle, Sulle" joita löytään

Wirsikirjan-Seuraston Wirsissä ovat hyvät ja käpöset, jos ei niitä
enää lyhennetä niinkuin Rosch. ja Hel. on tehnyt 'Mull', ja Sull'.

Mitä Ruottalaisten uuden Wirsi-kirjan ja Suomalaisten Runojen

sanojen katkasemiseen tulee, niin löytyy niitä näissä molemmissa,
sangen harvassa paikkaa; tuskin on koko ensinmainitussa kirjassa
usiampia kuin R. ja H. joka virressä. Kullakin kielellä on oma
luontonsa ja vaatimuksensa, meitin ei tule suoria kieltämme muitten
kielien mukaan, vaan seurata sen omia vaatimuksia ja luontoo.
Waikka Suomalaisissa Runoissa onkin, harvassa paikkaa,
katkastuita sanoja jossa ei niitä myös tarvittaisi niin tiedämme ne
olevan Talonpoikasten tekemiä, joilta ei sovi parempaa vaatiakkaan;
mutta Oppineilta, joilla on taitoo ja aikaa tutkia kielen laatua ja
luontoo, on senlaiset, katkaistut sanat, kuin jo nimitetty on suuri
rikos.

Merkittävä on myös, että katkaistuilla sanoilla sanotaan virsi

saatavan hengellisestä hartaudesta rikkaammaksi kuin täysillä, joilla
sanotaan virsi tulevan kankeemmaksi ja hengettömäksi; mutta eikö
syy tähän luuloon lienee ainoastansa se, että Hengelliset virtemme
on tähänasti ollut katkaistuilla sanoilla kirjoitetut suureksi vahingoksi
kielellemme ja että korvat on niihin jo niin tottuneet, ettei
Hengellisempiäkän virsiä enää pidetä arvossansa, jos ei niissä
katkastuita sanoja löytä. Samalla lailla oli muinaan: koska
Paavilaisuuden aikana pidettiin Jumalanpalvelukset Latinan kielellä,
jota ei oppimaton seurakunta ollenkaan ymmärtänyt, ja kuin sitte,
Lutheruksen-Opin mukaan, ruvettiin maakunnan omalla kielellä
Jumalanpalvelusta pitämään, niin ei Seurakunta (ensimmältä) pitänyt
sitä enää siinä arvossa kuin ennen; juuri kuin Jumalan sana olis
senkautta pyhyydensä kadottanut, että sitä Seurakunnan omalla
kielellä juliistettiin, eikä latinan kielellä, jonka he luuli ainoastansa
olevan Jumalan sanalla pyhitetyn.

Jälkimaine. Waikkei kyllä tässä edellä luettava tutkinto olekkaan

täydellinen, joka vaan vaatisikin pidempätä kirjoitusta, niin panemma
mielellämme sen anomusta myöten Mehiläiseen, toivoen, että
usiampiaki löytyisi, jotka ilmoittaisivat ajatuksensa mainitusta uusien
virsien kokouksesta. Mitä Mehiläisessä löytyy tilaa, annamma
ainakin kernaasti semmoisiin tutkintoihin, koska tunnemma niiden
suuren arvon nykyaikana. Mitä tähän nykyiseen tutkintoon koskee,
niin olemma muutamin paikoin vähän eriajatuksesta tutkijan kanssa,
jonka vaan nimitämmä, hyvin tieten, itsekullaki löytyvän omansa.

Mehiläisen toimittaja.

[1] Sana, Koto-maa, näyttää olevan paremmin Suomenkielen

luontonen kuin "Isän-maa", jota nimee on paikottain tässä kirjassa
pruukattu, esimerkiksi: Wirsiä "Isän-maan rakkaudesta" j.n.e.

[2] Liiaksi näyttää, kuitenkin, tässä kielessä olevan ne, ei

ainoastansa joka virressä vaan myös melkeen joka versyssä löytyvät
kertomus sanat (pronomina). Esimerkin otan ainoastansa yhdestä
virrestä: N:o 36 v. 1 "Sun kiitostas me aina veisaamme" v. 2. "Ja
uhrimme Me sulle kannamme." Jos näistä versyista jätettäisiin pois
kertomus sanat "Sun ja Me", niin olis kieli luonnikkaampi, ja saatasiin
niitten siaan sovittaa tarpeellisempia sanoja.

[3] Tämä näkyy Turun ruottalaisista Sanomista nimeltä Åbo

Tidningar N:o 19 ja 20 1838. Jollenka vastaukseksi seuraava on
kitjoiettu.

KAIKENLAISIA.
Pilvien suuruudesta.

Moni pilvi liiatenki syntyessänsä ei ole, kun muutaman kyynärän

suuruinen; toiset päälle penikuormanki ja välistä on koko näkyvä
taivas yltä pilvessä. Pilvien suuruus on helposti arvattava varjosta
(kuvasesta), jonka allansa maalla tekevät. Korkioilla vuorilla, joiden
kukkurat pistäksen ylemmäksi pilviä (katso: Mehil. Elokuulta 1837),
taitaan pilvien paksuuski mitata. Eräät ovat ohuita hennukoita, toiset
satoja ja tuhansiaki kyynäriä paksut.

Maanviljeliöille.

Usiassa paikassa Franskan maalla kylvetään alkukesässä toukoja,

joista sitte 2 ja 3:ki kertaa niitetään karjanruokaa ja ehästään sillä
keinon tähkään pääsemästä. Wasta seuraavana vuonna annetaan
saman touon rauhassa kasvaa, joka joutuu ja valmistuu tavallisena
aikana leikattavaksi. Tästä viljelyskeinosta oli edellisenä vuotena
saatu karjanruoka melkein sulaa voittoa. Mahtaisko Suomessaki niin
menestyä?

Sateen paljoudesta.

Ilmasta alasputoava vuotinen vedenpaljous on suurin maan

keskiseuduilla ja vähenee sitä myöten, kun siitä tullaan likemmä
maan pohjais- eli eteläpäätä, s.t.s. lämpimämmillä maaseuduilla
alasputoaä vuosittain enempi vettä, kun kylmemmillä. Mutta peräti
vastahakaan on sade'päivien luku sitä suurempi, mitä kylmempi
maaseutu. Hispaniassa, Italiassa, Greikan maalla. Persiassa,
Arabiassa, Palestiinassa j.n.e. luetaan vuosittain keskikohtasesti 100
sade'päivää; Franskan maalla, Etelä-Saksassa, Hungariassa,
Pohjas-Turkissa j.n.e. 130 päivää; Englannissa, Pohjas-Saksassa,
Preusissa, Puolassa, Keski-Wenäjässä j.n.e. 160 päivää; Ruotsissa,
Suomessa, Pohjais-Wenäjässä, Lapissa j.n.e. vieläki usiampaa
sadepäivää. Ylisumman on kesäs-aikana alastulo suurempi, kun
talvis-aikana, vaikka luetaanki syys- ja talvis aikana enempi
sadepäiviä. Jos lumiki, mikä talvella sataa, sulattaisi vedeksi, niin
siitä kevät- ja syys-sadetten kanssa yhteenlukein ei kuitenkaan tulisi
paljo enempi vettä, kun mikä kesällä kolmena kuukautena (Kesä-,
Heinäja Elokuussa) yksinään sataa. Päiväs-aikana sataa aina paljo
enempi, kun yöllä, ja rakeita ei juuri muistella koskaan yöllä
sataneen. Muuten sataa vaaramailla (vuorisilla seuduilla) enempi,
kun tasasilla eli alhasilla mailla; ja jos yhdessä kohtiki asetetaan
yhtäsuuret astiat, toinen korkialle katolle, toinen pihalle, niin
kokoutuu katolla olevaan astiaan enempi vettä.
 Tuulten kulusta.

Kevyt, vaivon havattava tuuli, kulkee tiimassa puolentoista

Wenäjän virstan paikoilla; kohtalainen tuuli penikuorman; rajutuuli
kolmesta niin kuuteenki penikuormaan; myrsky kahdeksan
penikuormaa, ja tuulispää, semmoinen, joka kukistaa huoneita ja
tempaa maasta puita juurineen matkaansa, kulkee kaksitoista
penikuormaa tiimassa. Ilmalaivoilla kulkiat ovat havanneet, että
korkiammalla ilmassa useinki tuuli puhaltaa vastoin sitä tuulta, joka
alempana käypi. Jäämerellä ajelehtii halki kesän suuria
suunnattomia jäätönkäleitä ja purjehtiat kertovat niistäki moniaiden
kiireesti vaston tuulta kulkevan, koska toiset liikkuvat tuulen mukaan.
Syy tähän kummitukseen sanotaan olevan se, että kun
vedenpinnassa aalto käypi tuulta myöten, syvemmässä vesi taas
virtoisi jälelleen vaston tuulta täyttämään sitä lomaa vedessä, jonka
poisaaltoava vesi jälkeensä jätti. Tämä syvemmässä käyvä virta
kuljettaisi myötänsä ja vaston tuulta niitä jäätönkäleitä eli jäävuoria,
jotka painonsa suhteen ovat syvemmässä ja toiset, jotka eivät painu
niin syvään, menisivät tuulen mukaan. Tätä oppineilta mietittyä
selityslaatua emme kuitenkaan pidä tyydyttäväisenä. Sillä kun tuuli
kuljettaisi muutamia, alusvirta toisia jäävuoria, niin pitäisi
välttämättömästi niiden välillä löytyä eräitä, jotka pyörisivät ympärite
paikaltaan liikkumatta. Mutta onko semmoisia? — Myös pitäisi
samaa selityslaatua myöten pienempien jäävuorien kulkea tuulen
mukaan, suurempien vaston tuulta; mutta tapahtuuko sillä tavalla?
— Kaikissa virroissa erotetaan pääväylää alasjuokseva ukonvirta
sen vieriltä ylösjuoksevasta ämmänvirrasta. Eikö liene sama syy
jäävuorienki kahtalaiseen kulkuun Jäämerellä, kun vedenki virroissa
kahtalaiseen, toinen toistansa vastahakaseen juoksentaan? — Ja
olkoonpa kuinka tahansa, niin ainaki sanovat olevan hyvin oudon ja
kummittavaisen Jäämerellä katsella, kuinka jäävuorista yhdet
juoksevat peräsukaa sinne, toiset rientävät tänne aivan vastahakaan
niiden vieressä kulkevien suuntaa ja retkeä.

Liikkuvista pyhistä vuodessa.

Uusissa almanakoissa katsotaan ainaki ensimmäiseksi, mihen

aikaan ne liikkuvat pyhät, Laskiainen, Pääsiäinen ja Heluntai
lankeavat. Kun kellä ei ole almanakkaa, niin useinki täytyy mennä
muilta kysymään näiden pyhien aikaa ja tulevista vuosista on työläs
kysymälläkään tietoa saada. Waan kun yhdenkään näistä liikkuvista
pyhistä tietää, niin huokiasti saa niistä toisistaki tiedon, koska niin
Laskiaisen ja Pääsiäisen, kun Pääsiäisen ja Heluntain väliä on täysi
seitsemän viikkoa. — Joksiki hyväksi lukioillemme panemma tähän
kahdenkymmenen seuraavan vuoden Pääsiäiset. Tänä vuonna
(1840) on Pääsiäispäivä 19 päivä Huhtik. ja siitä lähtein:

1841 se 11 Huhtikuussa. 1842 — 27 Maaliskuussa. 1843 — 16

Huhtikuussa. 1844 — 7 Huhtikuussa. 1845 — 23 Maaliskuussa.
1846 — 12 Huhtikuussa. 1847 — 4 Huhtikuussa. 1848 — 23
Huhtikuussa. 1849 — 8 Huhtikuussi. 1850 — 31 Maaliskuussa.
1851 — 20 Huhtikuussa. 1852 — 1l Huhtikuussa. 1853 — 27
Maaliskuussa. 1854 — 16 Huhtikuussa. 1855 — 8 Huhtikuussa.
1856 — 23 Maaliskuussa. 1857 — 12 Huhtikuussa. 1858 — 4
Huhtikuussa. 1859 — 24 Huhtikuussa. 1860 — 8 Huhtikuussa.

Niillen, jotka halunnevat tietää minkä vuoden Pääsiäisen tahansa

ja osaavat ne neljä tavallisinta laskukeinoa (k. Mehil. m.v.
Maaliskuulta), saamma neuoksi antaa, että Pääsiäispäivä kunaki
vuonna helposti löytään seuraavalla tavalla: ala jakaa itse saman
vuoden
 Wuosiluku jakimella 19, merki viimeksi ylijääpä a.
Sama luku — 4, — — — b.
Sama luku — 7, — — — c.
19 x a + M — 30, — — — d.
2xb+4xc+6xd+N — 7, — — — e.

Niin on Pääsiäispäivä sinä päivänä Maaliskuussa, joka saadaan,

kun ne luvut, mitä d ja e merkitsivät, ja luku 22 luotetaan yhteen.
Mutta jos Summa näistä Luotoksista kasvaa suuremmaksi, kun 31,
niin otetaan Summasta pois 3l ja Jääpä merkitsee, minä päivävä
Huhtikuussa Pääsiäisväivä tulee. Muistettava on, että tässä laskussa
M ja N merkitsevät lukuja, joilla on seuraava arvo: kaikissa
vuosiluvuissa siitä ajasta asti, jona Uusi Luku keksittiin, taikka

Alkain 1582 lopettain 1699 merkitsee M 22, N 3. — 1700 —

1799 — M 23, N 3. — 1800 — 1899 — M 23, N 4. — 1900 —
1999 — M 24, N 5. — 2000 — 2099 — M 24, N 5.

Myös on muistettava, että jos Pääsiäinen tätä laskua myöten tulisi

olemaan sinä 25 eli 26 päivänä Huhtikuuta, niin muuttuu se 7 päivää
ylemmäksi, taikka siksi 18 ja 19 päiväksi samaa kuuta. Wielä seki on
muistettava, että Ruotsissa ja Suomessa vastoin tätä muussa Uuden
Luvun seuraajassa Euroopassa tavallista laskua. Pääsiäinen
vuosina 1845, 1869, 1900 tulee yhtä viikkoa myöhemmin
vietettäväksi, taikka se 30 Maalisk., 4 Huhtik., 22 Huhtik. sen siaan,
kun muualla se 23 Maalisk., 28 Maalisk. ja 15 Huhtikuuta.

Jos nyt tahdot tietää Pääsiäispäivän v. 1840, niin jakaa

esinnä 1840 jakimella 19 ja kirjota jääpä a s.o. 16.

— 1840 — 4 — — — b — 0.
— 1840 — 7 — — — c — 6.
 19x16+23 s.o. 327 30 — — — d — 27.
2x0+4x6+6x27+4 190 7 — — — e — 1.

Sitte luota yhteen d + e 22 s.o. 27 + 1 + 22, josta saat Summan

50, josta 3l pitää pois ottaa, että jääpi 19, joka merkitsee Pääsiäisen
lankeavaksi sinä 19 p. Huhtikuuta. Jos summa 50:nen siasta olisi
tullut 31 eli joku vähempi luku, niin olisi se suorastaan Maaliskuun
päivän merkinnyt, jona Pääsiäinen siinä tilassa olisi ollut vietettävä.

Wenäjän ja muun vanhan luvun seuraaja Pääsiäinen saadaan

samalla tavalla tietä, kuu vaan muistetaan, että siinä M aina
merkitsee 15 ja N aina 6. Muut pyhät niinkun Joulu, Uusivuosi,
Maaria, Juhannus j.n.e. ovat seisovia, ettemme niistä huoli mitään
kirjottaa.
TYTTÖIN LAULUJA.

Inka.

Ei oo sia surunen meiän majassamme;

Päivät kuluu kunnialla, illat aitassamme.
Pojat käyvät kulkemahan illan pimiällä.
Laulellen ja rallatellen ilovirsiänsä.
Illan tullen näille maille pojat kylihin kulkee;
Likat menee aittahansa, oven kiini sulkee.
Käykää pojat kylissä, vaan elkää menkö saunaan;
Pienet piiat pirtissä paljo teille nauraa.

Elsa.

Puhun minä poikasille, eipä houkutella

Nuoria likkoja tarvitseisi, eikä viekotella.
Leskiä saapi liikutella, ei se haittaa mitään;
Ei saa tyttöhin koskea; hävetä poikiin pitää.
Eipä tämä tyttö lähe hylkypojan viereen;
Hylkypoika viettelee ja saattaa mierontielle.
Poika rahat menettävi olvehen ja viinaan,
Tytöt ei pane rahojaan, kun silkkihin ja liinaan.
 Kyllä sinäki tyttöjä saisit, saisit vaika kenen,
Kun olis viina loppunut jo viittä vuotta ennen.

Kaisa.

Laulaisinpa taitaisinpa kun palkka maksettaisi;

Emmä paljo pyytäiskään, kun markan sanasta saisin.
Ei ole tyttöin ikävä pimeillä öillä.
Pojat käyvät kyliä myöten tyttöin tinkitöillä.
Tuli poltti Turun linnan, vesi vei sen sillan.
Pojat itkee ikävissään päivän sekä illan.
Likka käypi kankahalla, niinkun kaunis kukka,
Poika juoksee jälestä, niinkun vanha hukka.
Likka astuu ahoa pitkin, pumpuliliivit liuhkaa,
Poika ryömii jälessä, tuohivirsut viuhkaa.
Likka istuu linnassansa, kulta rippuu rinnassa;
Tänä vuonn' on huonot pojat huokiassa hinnassa.

Anni.

Woi minä polo likka, kun ma olen yksin!

Olen tullut kaikilta hyljätyksi.
Muut tytöt toimittivat asiansa ennen,
Minä olen heitetty ikävihin tänne.
Enkä tieä miten minä hylyksi nyt tulin,
Joka ennen kaikkien kukkana kulin.
Olin minä ennen, kun enkeliskukka
Kehnojen päällen en katsonu'kaan.
Parahinten parvessa kävin minä kirkkoon,
Jo nyt olen joutunut koiarien joukkoon.
 Waan mitä entisistä ajoistani huolin? —
Noitapa muistaissa syämeni kuoli.
Syän ompi kylmä kun syksyinen jää,
Ei sitä rakkauskaan lämmitä.

Leena.

Minä olen kainu, kun syvän salmen siika,

Murehella täytetty pienonen piika.
En vielä muistane kovin monta vuotta,
Walitella täytyy jo kuitenki totta.
Maailman meri se on vaarallinen aivan,
Pian myrsky särkevi pienosen laivan.
Ei aina käynti ole kukkien päällä,
Toisin ajoin ompi orjantappuria tiellä.
Wälistä se näyttää, kun ilonen ois' olla,
Usiammin taitavi mure'pilvi tulla.
Niin on koko elomme ja koko olo täällä,
Lehenkanta katkeava syksysellä säällä.
Omp' on elo ihmisten, kun aaltosien veellä,
Yksi tulee jälessä ja toinen meni eellä.
Nuoruuteni aika ja ilopäivä kulkee
Jopa noista vaivoista väsymyski tullee.
Waan kun olen nuori ja ruumihilta raitis,
Mahan olla luojoani kiittämähän valmis.
Luojoansa kiittävi varpusetki pienet;
Enkö toki varpusia parempi mä liene.

Sanna.