Professional Documents
Culture Documents
Ultrasound Teaching Manual
Ultrasound Teaching Manual
Ultrasound Teaching Manual
/"=\
-iN -/\
t
\/' \/
-Y ./
Y \.,,
I
I I I
UA, longitudinal(sagittal) LLQ, para-iliacoblique UA.transversesection
section
z\ n\
\-
Yl YI
RUQ,obliquesection RUQ,obliquesection RUQ,sagittalsection
(= extendedintercostalorientation) alongthe MCL
\A./\r \(
)^Y
"\ A
(r)
oj
l"l
ti ,l" I
\ Y)
Right intercostalflank section
IY
Y
\t I I
ntercosta
costal
rtalflr
/)
I
\-^-/ \--1 4\
l" \
"-'\
rYt
/
rYl
LUQ, transversesection suprapubic
transverse
-.. | ,-
Y'
LA,suprapubic
I
The most important organs and vesselsthat are seen in the (UA = upper abdomen; MA = mid-abdomen; MCL = mid-
various standard sonographic sections are listed here. In ad- clavicular line; LA = lower abdomen). Each imaging plane
dition to remembering the corresponding body landmarks, should be closely scrutinized using sweeping motions of the
the names of the sonographic sections should be memorized transducer.
Intercostal section of the left flank in the right lateral decubitus position.
Left kidney, left adrenal gland, left renal hilum, spleen (inferior portion ).
descending colon, diaphragm, lung: left costophrenic angle.
High intercostal section of the left flank in the right lateral decubitus posi-
tion.
Spleen (for measurements),left hepatic flexure, pancreatic tail and splenic
hilum, diaphragm, left adrenal gland, lung: left costophrenic angle.
MatthiasHofer,M.D.
Translated
by
PeterF.Winter,M.D.
486 lllustrations
T h ie m e
Stuttgart' New York 1999
Matthias Hofer, M.D.
Institute for Diagnostic Radiology List of Abbreviations
(Chairman: Prof. U. Modder, M.D.)
H. Heine University AC Abdominal circumference
Dtsseldorf, Germany ASD Atrial septaldefect
BPD Biparietaldiameter
Tatjana Reihs, M.D. CRL Crown-rumplength
Department of Obstetrics and Gynecology CT Computed tomography
H. Heine University doo Diameterof the aorta
Diisseldorf, Germany dvc Diameter of the inferior vena cava
EFW Estimated fetal weight
EP Ectopic pregnancy
Tianslated by ERCP Endoscopicretrogradecholangiopancreatography
Peter F. Winter, M.D. ESWL Extracorporealshockwave lithotripsy
Chlinical Professor of Radiology FHVI Frontal horn ventricular index
Boston University FL Femoral length
School of Medicine, FNH Focal nodular hyperplasia
Clinical Assistant Professor GI Gastrointestinaltract
University of Illinois GSD Gestationalsac(= sh6ri.nic cavity) diameter
College of Medicine at Peoria HC Head circumference
USA HCG Human chorionicgonadotropin
IUD Intrauterinedevice
IVF In vitro fertilization
MCL Midclavicular line
Library of Congress Cataloging-in-Publication Data
MR I Magneti cresonance i magi ng
Hofer, Matthias. NPO Nothing by mouth
[Sono Grundkurs. English] NT Nuchal translucency
Ultrasound Teaching Manual, The Basics of Performing and In- OFD Occipitofrontaldiameter
terpreting Ultrasound Scans/ Matthias Hofer : translated by Peter OHVI Occipitalhorn ventricularindex
F. Winter. PCOS Polycysticovarian syndrome
p. cm. PW Pulsedwave Doppler
Rev. translation of: Sono Grundkurs. 1997. RI Resistance index
Includes bibliographical references and index. SLE Systemiclupus erythematosus
rsBN 3-13-111041-4.- rSBN 0-86577-725-X(TNY) SMA Superiormesentericartery
1. Diagnosis. Ultrasonic. L Title. S/P Statuspost
[DNLM: 1. Ultrasonography, WN 208 H697s i999] TGA Tianspositionof the great arteries
RC78.7.U4H6413 1999 Volu6 Volume of the urinary bladder
616.07'543-dc2l VSD Ventricular septal defect
DNLMiDLC YSD Yolk sacdiameter
for Library of Congress 98-45748
CIP
fil@ X::lii:::::r:tt:i::iti:iii::r::iii:iii,:il:::::xixtir
,pcer Retrooeritoneum 11
-:.',er Retroperitoneum
in ObliqueSections:
Normal Stomach 51
: -: ngs 12 Colon 52
-:tic Ectasia and Aneurysms 13 SmallBowel 53
:e:'operitoneum: LymphNodes 14
:::.operitoneum: OtherClinical
Cases 15 F]lflfElilirHilllll i:::::i:::i:i:i:t:::::::::iiar:::l:iit:::::::::ii,:
NormalFindings,
VolumeMeasurements 54
Indwelling
Catheter,
Cystitis,
Sediment
*poerAbdomen:BasicAnatomy 17
*:cer Abdomen:NormalFindings 1B ffi::,.::::::::::,,,::i':i]',:::,:i,ii'::|
-ccer Abdomen:Pancreatitis
... 19
:=^creas:
Additional
Cases. 20 Prostate
Gland.Testicles
and Scrotum 56
-poerAbdomen:LymphNodes 21 UndescendedTesticle,
Orchitis/Epididymitis 57
l-zfor Self-Assessment... 22
--
ilEE[ .l:.t:t::::::i:ti:::il:l::irii::i::t
i:ii,iii:triiii:i:iriiitiiiirii::trit :
NormalFindings 58
:':-:a Hepatis:NormalFindings 23 Uterus 59
:':'ial Hypertension:LymphNodes 24 Tumorsof the Uterus 60
VeinConfluence and Hepatic .....
Congestion 25 Ovaries 61
-:Datic
Size,Gallbladder,NormalFindings 26
--=natic
rr'r"ndl Variants,FattyLiver 27 IIT+?t!fr+l?lE::::::x, ,::Xr::iiii:i::i::i
:::a FattyInfiltration 28
l:-=r FocalChanges 29 Diagnosisof EarlyPregnancy 63
-':ctrons.Parasite 30 BiometryIn the FirstTrimester 64
I'-.osis and Heoatocellular ..
Carcinoma 31 BiometryIn the SecondandThirdTrimester 65
-=:atic Metastases 32 Placental
Locationand FetalGender 66
l- z for Self-Assessment ... 33 Diagnosisof FetalMalformations. . . 67
QuizforSelf-Assessment... 73
,
fIt?JTlrElEf,ti ".
l' : estasis 34
f; ;ones and Polys 35 NormalFindings 74
1^: erystitisand Quizfor Self-Assessment 36 Dittuseand FocalChanoes 75
An echo reflected repeatedly back and forth (Fig.6.2) of about 1570 m/sec, it travels through fat with a lower speed
before it returns to the transducer has a travel time that is no of 1,476m/sec. The assumedmedium speed stored in the pro-
longer proportionate to the distance of its origin. The proces- cessor leads to small differences but no major distortion.
sor incorrectly assigns these ;ie"vffb#aii ;recl1oe* (51) to a If the propagation speed of adjacent tissue is vastly differ-
deeper level (Fig. 10.1). ent (bone: 3360 m/sec vs. air: 331 m/sec), total reflection
Additional distortion occurs through propagation speed takes place (Fig.6.1b along interface B) and acoustic
errors introduced by programming the processor based on shadowing ensues (45). For this reason a coupling gel is
the assumption that the propagation speed of sound in tissue needed to assuredirect contact between transducer and skin,
is constant, whereas in actual fact it is different for each type with no air trapped in between.
of tissue. While sound travels through the liver with a speed
'aq:-i:i1:,tY:*!1!#rr#.\dLijNtll*:jjr3l\l_9*{i'1!ifqif}1xtll+ll+tnn iutisi:Hr\r$rp$
\otes
Sonographic units used today can be operated with different shadowing (45) as caused by ribs can deteriorate the image
types of transducers (seebelow) and are mobile for use in the (Fig.8.2). In general, linear array transducers are not sui-
sonography suite as well as in the intensive care unit or emer- table for visualizing organs in the thorax or upper abdomen.
gency room (Fig.8.1). The transducers are generally stored
A j{dgj.gii iiiid$*F.giproduces a fan-like image that is nar-
on the storage shelf on the right side of the unit.
row near the transducer and increases in width with deeper
Precautions should be taken when moving the sonographic penetration (Fig.8.2, left). This diverging propagation of
unit. Avoid having a dangling transducer cable being caught sound can be achieved by moving the piezo elements me-
on a door knob, stretcher, etc., and do not drop a transducer chanically. This is the less expensive solution but has the in-
on the floor. Replacing a damaged transducer can be quite herent risk of wear and tear. The electronic version (phased
expensive! For the same reason, the transducer should never array) is more expensive but has become established pri-
be left unattended on the patient's abdomen when the exami- marily in cardiology with frequencies of 2.0-3.0 MHz. The in-
nation is interrupted, for instance by a phone call. Further- terference of the sound-reflecting ribs can be avoided by ap-
more, the transducer should be placed upside down to hang plying the transducer to the intercostal space and by takin-e
with the cable straightened and not pinched or kinked where advantage of the beam's divergency to a 60'- or 90"-sector
it enters the transducer (danger of breaking the wires in the with increasing depth (Fig.8.2). The disadvantagesof these
cable). types of transducer are poor near-field resolution, a decreas-
ing number of scan lines with depth (spatial resolution), and
Selection of the appropriate transducer:
handling difficulties.
Of the many types of transducers only the applications of the
three most important ones will be described here. .Curved o:r convex. arrali r{.ffi$ are predominantlv
used in abdominal sonography with frequencies from 2.5
rft" ibq"9.$ii,S.4+'a.f$*a,qi emits sound waves parallel to
MHz (obese patients) to 5.0 MHz (slim patients), with the
each other and produces a rectangular image. The width of
mean value around 3.5-3.75 MHz. As a compromise of both
the image and the number of scan lines are constant at all
preceding types, it offers a wide near and far zone and is
tissue levels (Fig. 8.2, center). An advantage of the linear
handled easier than a sector scan. F{owever, the density of
array transducers is good near-field resolution. They are pri-
the scan lines decreaseswith increasing distance from the
marily used with high frequencies (5.0-7.5 MHz) for evaluat-
transducer (Fig. 8.2, right). When scanningthe upper abdom-
ing soft tissues and the thyroid gland. The disadvantage of
inal organs, the transducer has to be carefully manipulated to
these transducers is their large contact surface, leading to ar-
avoid acoustic shadowing (45) of the lower ribs.
tifacts when applied to a curved body contour due to air gaps
between the skin and transducer. Furthermore, acoustic
Fig.8.1 Fig.8.2
L-urgnizanceof the physical properties of sound that can rather than falsely attribute it to focal sparing of fatty infiltra-
::rrnic pathologic findings is mandatory for the correct inter- tion (62) in the liver (9).
::-tation of a sonographic image. The most important arti-
Relative distal acoustic enhancement (70) is found
:,;ris include so-called distal shadowing. An acoustic shadow
wherever sound waves travel for some distance through ho-
f{5) appears as a zone of reduced echogenicity (hypoechoic
mogeneous fluid. Because of decreased reflection in fluid,
- r lnechoic = black) and is found behind a strongly reflecting
the sound waves attenuate less and are of higher amplitude
>.:l.rcture,such as calcium-containing bone. Thus the visuali-
distally in comparison with adjacent sound waves. This pro-
:"tion of soft-tissue structures in the upper abdomen is
duces increased echogenicity that is seen as a bright band
--:peded by overlying ribs, and those of the lower pelvis by (70) behind the gallbladder (14) (Fig. 9.4),behind the urinary
-:e pubic symphysis.This effect, however, can be exploited to
bladder (38) (Figs.10.1-10.3), or even behind major vessels
,:,.'eal calcific gallstones (49) (Fig.9.21. renal stones (49)
such as the
Fisr. J2.1, 42.2), and atherosclerotic plaques (a9) @ig.9.3).
aorta (15)
Srmilar shadowing can be causedby air in the lungs or intesti-
(Fig.9.3).This
::l tract. Evaluating structures behind air-containing bowel
increased echo-
ups (46) is often precluded by acoustic shadowing (45) or
genicity is a
; ;:logenic comet-tail artifacts (Figs. 9.2-9.4).
physical phe-
The air artifacts interfere primarily with the evaluation of nomenon unre-
::rrLrperitoneal organs (pancreas,kidneys, and lymph nodes) lated to the true
:;hind air-containing stomach or bowel. Adequate visualiza- characteristicsof
---1n.however, is still possible by following the approach de- the underlying
.'.-:ibed on page 79. tissue. The
acoustic
-\nother characteristic finding is the so-called edge
enhancement,
(45) behind cysts (64), principally occurring be-
'hadowing however, can be
,;nd all round cavities that are tangentially hit by sound
r',:r es (Fig. 9.1). Edge shadowing is causedby scattering and applied to dis-
tinguish renal or
::iraction and can be seen behind the gallbladder (14).
hepatic cysts
Figure 9.4 requires careful analysis to attribute the acoustic
from hypoechoic
(45) to edge shadowing caused by the gallbladder,
'redow tumors. Fig.9.1
N
Fiig.9.2a, b Fig.9.3a,b Fig.9.4a,b
'r0
\ot all echoesthat originate at an acoustic interface return to from solid structures and are averaged by the processor.
the transducer u'ithout further reflection. If several strongly Consequently,the boundary betweensolid tissueand fluid is
reltrectingboundaries are encountered, the sound waves can seen as a low echogenicand indistinct structure. Section-
be reflected back and forth before they eventually return as thicknessartifacts can occasionallymimic sludge or layered
echo to the transducer. The resultant delay in registering material (concrements,blood clots) (52) in the urinary blad-
these echoes leads to reverberatiaa'echoes (51). These re- der (38) (Fig.10.3).
verberation echoes project as several parallel lines in the
anterior aspect (near the transducer) of the urinary bladder Strongly reflecting interfacescan causea scatteredreflec-
t Figs. 10.1 and 10.2) or gallbladder (Fig. 34.3), since the pro- tion of the echoeq spuriously displacingthe acousticinter-
cessorcalculatesthe site of the reflection solely from the reg- face laterally as a so-called a*e1.r$i!,i&#. For instance,the
istered time that has elapsedbetween emission and recording duodenal wall occasionallyprojects in the lumen of the
of the sound pulse by the transducer. neighboringgallbladder,or an air-containingbowel loop can
be seen within the urinary bladder (Fig.s7.a). Finally,
Section-thickress artifaets (S1) (Fig. 10.2) are caused 'm'iiror::artifaets are primarily produced Uy ttre diaphragm
s-hen the boundary between the wall of a cyst, gallbladder, or and visceralpleura, causingintrahepaticstructuresto be seen
urinarv bladder (77) and the containing fluid is not perpen- as a mirage on the pulmonary side of the diaphragm
dicular to the interrogating sound beam. The echoes within (Fig.27.2b).
the returning beam include echoes from liquid as well as
N
Fig.10.1b Fig.10.2b Fig.10.3b
1',I
Did vou already mark a cone coffee filter with the location of The irnage displays the superiorly located diaphragm (L3)
-he structures visualized on sagittal sections,as described on on the left and the more inferiorly located pancreas (33) and
:age 4? If not, please do so and compare your drawings with confluens (12) of the portal vein (11) on the right. The hypo-
-he results on page 78. Only thereafter should you proceed. echoic extensions of the diaphragm (the diaphragmatic
crura) (13) and the gastroesophageal junction (34) are shown
The transducer should be perpendicularly placed on the
anterior to the aorta and immediately below the diaphragm.
=p'ieastricregion along the linea alba and the sound beam
It is important to note where the left renal vein (25) crosses
:n'ept through the upper abdomen in a fan-like fashion
the aorta to reach the right-sided inferior vena cava. It travels
Fie. 11.1).For the time being, it should suffice to memorize
through the narrow space between aorta and SMA, immedi-
:tre appearance of the noilnal anatomy. With the transducer
ately caudal to the aortic origin of the SMA. If not well de-
-nclined to the patient's right side (Fig.11.2), aorta (15), monstrated, the uninitiated examiner might mistake this ves-
;eliac axis (32), and superior mesenteric artery (SMA) (L7)
sel for a hypoechoic lymph node. Comparison with the trans-
rre found paravertebrally on the left and dorsal to the liver
verse section at the same level clarifies this findins further
t9). Normally, all major vesselsare hypoechoic (dark) or an- (Fig.18.3).
;s-hoic (black).
Now the transducer is inclined to the patient's left side
(Fig.11.3) for the visualization of the right paravertebrally
situated inferior vena cava (16), including its continuation
into the right atrium. At the same level, the hepatic veins (10)
can be distinguished from intrahepatic branches of the portal
vein (11).
The presence of air prevents evaluation of the lungs (47).
The diameter of the inferior vena cava should not exceed
2.0 cm or, in young athletes,2.5 cm. The maximum diameter
of 2.5 cm also applies to the aortic lumen at this level. The
luminal diameter is always measured perpendicular to the
vessel'slongitudinal axis. The dao = 1.8 cm and dvc= 2.3 cm
in the casesillustrated here (Figs. 11.2,lL.3) are within the
normal range.
Fi9.11.1
The confluence of the external (22) and internal (23) iliac suresystemshowingeasycompressibility. On transversesec-
veins is a frequent site for regional nodal enlargement tion (Fig. 12.3'1,the iliac vesselscan be easily distinguished
(Fig.l2.2). The iliac artery (21) is anterior (i.e., superior on from hypoechoicfluid-filledintestinalloops $6) by the peri-
the image) to the vein. In unclear cases,the compression test stalsisof the intestinalwall.
can differentiate these structures,with the vein as a low pres-
//\
-\
tF
45
\
Fig.12.2a Fig.12.2b Fig.12.2c
5c
Fig.12.3a Fig.12.3b
%'
Fig.12.3c
t'
13
Localizeddilatations of the vascularlumen are generally size of the aneurysm and patients with an aortic aneurysm ex-
:ausedby atherosclerotic lesionsand local weakeningof the ceeding 5 cm in diameter should be assessedclinically for
uterial wall. They are rarely posttraumatic.A dilatation of surgical repair.
up to 3 cm is referred to as.eot$*ia,and can be found in addi-
If an aneurysm is detected, the sonographic examination
tion to an aneurysm(Fig.13.1).
should report its maximal length (Fig.13.2) and diameter
The dilatation can be fusiform or saccular.It can be com- (Fig.13.3) as well as any detected thrombi (52) and possible
plicated by dissection of the arterial wall {di dffib$ involvement of the renal and iliac arteries. Though most
aneurys ), or circumferential intraluminal clot formation i6*tie:t$$ i*i are infrarenal, their exact extent should be
[52)with possibleperipheral emboli. Risk factorsfor rupture established before surgical intervention. Any aneurysmal
rf an aorticaneurysmare a diameterof greaterthan 6 cm, an bleeding primarily occurs into the retroperitoneum but can
:xcentric lumen, and diverticulum-like bulging of the aortic extend into the peritoneal cavity in the presenceof high pres-
wall.As generalrule, the risk of a rupture increaseswith the sure.
a
a
a
Fig.13.1a Fig.13.1b
fjti]jJ-j]ri].l]]1]]:]:li.j.-l]jl:i.E'i]...1]:]j1lj:a]r]r.iif]!.]!|:i]!.:l!il]ri]*.rl8't+|i1fijil\s]:s
Lr:mph nodes (55) are generally hypoechoic and must be lymph nodes can often be encounteredalong the hepato-
differentiated from fluid-filled bowel loops (,16) by absent duodenal ligament (Fig. 2a.3) accompanyingviral hepatitis,
peristalsis and from veins by lack of compressibility. Comput- cholangitis,or pancreatitis(Fig. 19.3).
erized tomography (CT) is superior in evaluating throm- .lypp
In contrast,,roetagtatie nodgs.are more round than
bosed veins (non-compressible) or markedly obese patients,
oval, frequently of heterogeneousechogenicity,and indis-
but sonography is advantageous in very thin or cachectic
tinct in outline. They also have the tendencyto form aggre-
patients. Enlarged lymph nodes can be found with inflamma-
gates.The siteof the primary tumor canbe deducedfrom the
tion, malignant lymphoma (Hodgkin disease or non-Hodg-
known lymphatic pathways;para-aorticlymphadenopathyin
kin lymphoma), and metastatic deposits.
young men, for instance,suggestsa testicular tumor.
The norma}..sl ,+f.g.bdp is given as
€gls1ge,l1fiqp-h nL.qdesrd$,maaife$,tetiotr:qf
mElignrurrlyrnr.
7-10 mm. Larger and still normal lymph nodes measuring up
to 20 mm in longitudinal diameter can be found in the ingui- ;B-trpiii+generally exhibit an ovoid form, smooth margins,
and more pronounced hypoechogenicitythan found in in-
nal region and along the distal external iliac artery (21)
flammatory or metastaticlymph nodes.In one third of cases,
(Fig.14.3). Important for all enlarged lymph nodes are fol-
the spleen shows concomitant focal or diffuse involvement
low-up examinations to determine any possible progression
(Fig. a8.1). Predominant involvement of the mesenteric
or regression-for instance, for the evaluation of chemother-
lymph nodes (55) (Figs.14.1,14.2)suggestsa non-Hodgkin
apy. Furthermore, any possible hepatomegaly or spleno-
lymphoma and not Hodgkin disease,which hasa predilection
megaly should be documented and quantified.
for thoracic and retroperitoneal lymph nodes. Malignant
I-ympl,nod6s,W,itft-igde maintaintheir
ehangg$, lymphomasindentor displaceadjacentvessels(Fig. 14.2)but
ovoid shape, have a distinct border, and exhibit two layers respectthe vascularwall and do not invade adjacentorgans
with a centrally increased echogenicity at the hilum (hilar fat (seealso p.2I).
sign) and peripheral liver-like echogenicity. Inflammatory
-i=-.-
,tt
/ l 4at (\\
l l l se
' oul lc@
K
\\\
3571 \
llt
ll
I\ \
r/lI\\\
i \\
ll
It 145
tl \'\
Fig.14.1b Fig.14.2b Fig.14.3b
t5
(t
Fi g.15.1b Fig.15.2b
/D.
Fig.15.3b
45
\
16
Before turning to the material of the following section, the swersto the figure of question7 canbe looked up on page76
following questions should be answered to test whether the after Ihe individual questions listed in the text have been
goal of the first lesson has been achieved. The answers to addressed.
questions 1 to 6 can be found on the preceding pages.The an-
Fig.16.'l
Fig.16.2
17
On these transverse sections,the examiner is confronted by writing the names of all the numbered structures in
-."ith a multitude of arteries, veins, biliary ducts, and lymph Figure 17.2 and 17.3below both figures and thereafter unfold
nodes, all confined to a small space and demanding differen- the back cover page to compare your list with the key. Re-
tiation from each other (all vesselsare hypoechoic, but so are view again the topography of pancreas, duodenum, and
lrmph nodes). Do you remember where the left renal vein spleen in relation to the major abdominal vessels as il-
,-rossesto the contralateral right side, or whether the right lustrated in Figure 17.3. To make the review easy,the three
renal artery is anterior or posterior to the inferior vena cava most important transverse sections of the upper abdomen
to the right kidney? Refresh your basic anatomic knowledge are described and illustrated on the next page.
Fig.17.2 Fig.17.3
18
First, the patient has to take a deep breath and hold it, so that more caudal sections (Fig. 1-8.3).A more cranial transverse
the inferiorly displacedliver can serve as an iil,fiil$ffi. visualizesthe celiac axis (32) together with
section (Fig. 1-8.1-)
whdsrv. for the pancreas and lesser sac, including the major the hepatic (18) and splenic (19) arteries.The gastric artery is
vesselstraversing it (seep. 79). Skin (1), subcutaneousfat (2), generally not visualized. The origin of the SMA (17) is more
and both rectus muscles (3) are directly beneath the trans- caudal by about 1.-2 cm (Fig. 18.2), as clearly illustrated on
ducer. The ligamentum teres (7) with the obliterated umbili- the sagittal images (Fig. 11.2).It should be noted that the dis-
cal vein can be delineated posterior to the linea alba (6), par- play inverts the position of the organs (which are shown as if
ticularly in obese patients. The lesser sac is seen as a small viewed from the patient's feet). The inferior vena cava (16),
cleft posterior to the liver (9) and, further posterior to it, the seen as an ovoid structure, is on the le.ft side of the image, and
pancreas (33). The tail of the pancreas is often obscured by the aorta (15), seen as a round structure, is on the right side
air shadows (45) arising from the stomach (26). The splenic anterior to the spine (35). The head of the pancreas (33)
vein (20) always runs directly along the posterior border of characteristically surrounds the confluens (12) of the portal
the pancreas.The renal vein (25), however, is more posterior vein (11), which is frequently obscured by duodenal air (46)
between the SMA (17) and aorta (15), and is only imaged on in the region of the lesser omentum.
The echogenicity of th" iffi changes with increasing creas,for instance anterior to the portal vein (11), can accom-
rge" In young and slim patients, the parenchyma is hypo- pany pancreatitis.
e;hoic in comparison with the surrounding tissue, including
The real contribution of sonography is not the early diag-
-:e hepatic parenchyma. The deposition of fat in the pan- nosis of acute pancreatitis. This can be better achieved by
reas (pancreatic lipomatosis) can be found in older or obese
laboratory tests or C! particularly in view of the markedly
p"atientsand causesthe parenchyma to increase its echogen-
increased bowel gas encountered with an acutely inflamed
icin. leading to a hyperechoic, i.e., brighter, appearance of
pancreasand interfering with
ile pancreas.The normal anteroposterior diameters of the
phy has the role of ,
f,ancreasare somewhat variable and should be less than 3 cm 't,
such as cholecystitis, choledocholithiasis, and aortic
:or its head and less than 2.5 cm for its body and tail. The
aneurysm. Furthermore, sonography can be used to follow
ratses of pancreatitis include biliary obstruction (cholesta-
the pancreatitis and to detect its complications, such as in-
sis) secondary to a stone lodged in the distal common bile
flammatory infiltration of the neighboring duodenal or
duct (biliary pancreatitis), increased viscosity of the bile sec-
gastric wall (46, 26) and thrombophlebitis of the adjacent
Ludary to parenteral nutrition and, above all, alcoholism (al-
splenic vein (20). It might be necessaryto add color Doppler
.-ohol pancreatitis), which is, among others, related to protein
sonography of the splenic vein if the conventional sono-
plugs obstructing the small pancreatic duct.
graphic evaluation of the spleen is normal. Moreover,
Acute.:l:il.$i$f. of the first degree can initially be necrotic paths in the retroperitoneum (grade II acute pan-
devoid of any sonomorphologic changes.The edema found in creatitis) and the development of pseudocystsshould be dis-
more advanced stages causesmarked hypoechogenicity, in- covered early, so that surgical intervention or puncture under
sreased thickness, and indistinctness of the pancreas (33). sonographic or CT guidance can be carried out, if indicated,
Cnro*e.giiii$4*ltiEl is ch aract eri zed by a he te ro gene ous f i - without undue delay. The inflammation does not always in-
brosis (Fig. 19.1), calcific deposits (53), and an undulated, ir- volve the entire pancreas,and segmental and "channel" pan-
regular outline of the pancreas (Figs. 19.1,19.2).Moreover, a creatitis confined to certain segments of the pancreas or
beaded or irregular dilatation of the pancreatic duct (75) can along its duodenal surface can be encountered. These
occur (Fig. 19.2). The normal pancreatic duct is smoothly manifestations cannot always be reliably differentiated from
outlined and measures up to 2 mm in diameter. Inflam- other localized space-occupying processes,such as a carci-
matory lymph nodes (Fig.19.3) in the vicinity of the pan- noma.
Looking at the normal echogenicity of the pancreas (33) on toneal carcinomatosis are responsible for the poor 5-year
loneitudinal (Fig. 11.2) or transversesections(Fig.18.3) re- survival rate, which is far below 10%.
veals no appreciable difference in comparison with the echo-
Endocrine pancreatic tumors are generally small at the
eenicitv of the liver. With increasing age or obesity, the echo-
senicin'increases as a manifestation of Aa,+.gqe*tig;$ip:b& time of diagnosis because of their systemic hormonal effects
$" and, as all. small pancreatic tumors, are best visualized by
sis (Fig. 20.1). This accentuates the contrast between oan-
creas and hypoechoic splenic vein (20). endosbnography (Fig.20.3). An annular transducer at the
tip of an endoscopeis positioned into the stomach or through
Tumors of the pancreas (54) are generally more hypo- the pylorus into the duodenum, surrounded by a water-filled
echoic than the remaining pancreas and are sometimes not balloon for acoustic coupling with the gastric or duodenal
easilv differentiated from adjacent bowel loops (by peristal- wall.
sis) or space-occupying lesions arising from peripancreatic
llrnph nodes (see p.2I). Pancreatic carcinomas have a poor Because of the short penetration needed to reach the tar-
prognosis and remain clinically silent for a long time. They get structure, a high frequency (5-10 MHz) can be selected,
are often only detected after they have metastasized,when resulting in improved resolution. The same principle is used
thev compress the common bile duct, or after they have led in transesophagealechocardiography that also has, because
to an otherwise unexplained weight loss. Early retroperi- of the use of high-frequency transducers, a markedly im-
toneal extension, nodal or hepatic metastases,and/or peri- proved image quality in comparison with transthoracic echo-
cardiography.
The criteria distinguishing inflammatory lymph nodes from mesenteric vessels.In such cases,representative lymph nodes
netastatic and lymphomatous lymph nodes were already dis- are identified and measured to assessany interval growth on
--ussedon page 14. Depending on the incidence angle, the subsequent studies. If intra,abd,ominal of retroperitaneal
upper abdominal vessels(15, 16) can be visualized as ovoid lyqph.tr''$o69s are encountered, the examination should
structures on transverse sections and must be distinguished proceed to measuring the size of the liver and spleen. Both
trom pathologic lymph nodes (Figs. 21.1, 21.2). Familiarity organs must also be searchedfor heterogeneousinfiltrations.
n'ith the normal vascular anatomy is therefore fundamental. Diffuse lymphomatous involvement of the splenic
\-ery hypoechoic lymph nodes that lack an echogenic hilus parenchyma does not always translate into sonomorphologic
and displace,but do not invade, adjacent veins are suggestive changes, and the infiltrated spleen can appear normal or
of the presence of a lymphoma, such as chronic lymphatic show only diffuse enlargement (Fig. a8.1). Additional lym-
leukemia (Fig. 21.2). The rpathologic:lyrnph,'node shown phadenopathy must be searched for in the inguinal, axillary
here is situated directly anterior and to the right of the bifur- and cervical regions. Paralytic fluid-filled intestinal loops are
cation of the celiac axis (32) into the common hepatic artery rarely mistaken for lymph nodes. An intestinal diverticulum
(18) and splenic artery (19). The resultant space-occupying (54) can mimic a tumor or enlarged lymph node, as shown in
effect obliterates the characteristic fluke-like confisuration Fig. 21.3. Eliciting peristaltic activity from a paralytic intesti-
of the celiac axis. nal loop by applying graded compression can clarify the
differential diasnosis.
Occasionally, large 'ncdal'aggiegates (Fig.21.1) can be
seen around and virtually "encasing" the retroperitoneal or
Fig.21.1a F tg .2 1 .2 a Fig.21.3a
After this session the standard sagittal and transverse sec- subsequentquestionscorrectlyis a prerequisitefor the next
tions are supplemented by oblique sections, clarifying the session.The answerto question4 is found on page76.
soatial orientation of individual structures. Answerins the
4 Otr this image, name every vessel and all other structures.
Which vessel appears distended/congested?What can be
the cause? Is this finding pathologic?
Fig.22.1
:i\il.-+r!l*. jj-t'riiM.Ur!:tqfiltii!4liit+:ri-\:\4iitlr:t-!itgllil!rrli!a-::!l
Notes
23
- ::s sessionleaves the transverseplane and moves to a sono- The common bile duct can be so narrow that it might be
.- -,phic plane that visualizes the major structures in the barely visible along the adjacent artery. Its normal diameter
-esseromentum. Again, the patient has to be asked to take a should be less than 6 mm. After cholecystectomy it assumes
-;=p breath and hold it so that liver and porta hepatis move some reservoir function and can dilate up to 9 mm without
:ieriorly from under the acoustic shadow of the lung and pathologic significance. A borderline dilated common bile
-.-s. The transducer is turned from the previous transverse duct (obstructive cholestasis)can no longer be differentiated
:r-ntation until the sound beam is parallel to the portal vein from adjacent vesselsby its luminal diameter but only by its
-,ushly parallel to left costal arch) (Fig. 23,1a). Sometimes, location anterior to the portal vein. Visualizing the duct's en-
,- transducer has to be angled craniad (Fig.23.1b) to follow tire length is important to exclude intraductal gallstones (see
.r- course of the portal vein (11) from the porta hepatis to p 35). By moving the transducer, an attempt should be made
. .; confluens of the splenic vein and superior mesenteric to follow all three tubular structures upward to the porta he-
..rn (12) (Fig.23.2\. patis. Distally, the common bile duct should be followed to
the duodenal ampulla at the pancreatic head, the hepatic
Three hypoechoic layers can be delineated in the minor
artery to the celiac axis, and the portal vein to the porto-
;rlentum. The normal position of the portal vein (11) is im-
splenic confluence or the splenic vein.
-;diately anterior to the obliquely sectioned inferior vena
:,ra (16), with the common bile duct (not visualized in The normal lurninal'w.idth of the: portal vein is less than
Fig. 23.2) and hepatic artery proper (18) situated more ante- 13 mm when its main branch is measured perpendicular to its
:-L-rr.Good visualization without intervening duodenal air longitudinal axis. Dilatation should only be suspected with
-,.st'rallows delineation of the pancreatic head, aorta (15), measurements exceeding 15 mm. A dilated portal vein alone
,:d SMA (1-7) on the right side of the display (i.e., on the is an uncertain criterion for the presence of portal hyperten-
:itient's left side). sion. The highest accuracy is achieved by the definitive de-
monstration of portocaval collaterals,which are described on
The major'branches of the,hepatic afiery (18) divide at
the next page.
,r. porta hepatis, with one branch seen in cross-sectionon
-r- sonographic orientation under discussion here. This
-:irss-section should not be mistaken for preaortic lymph-
::enopathy (Fig. 23.2b).
Normal values:
:T:;
Portal vein
Common bile duct
Common bile duct,
S/P cholecystectomy
Fig.23.1a
2t J JLiver
The most common cause of increased pressure in the portal and ligamentum teres from the porta hepatis to the umbilical
r ein is impaired drainage secondary to cirrhosis. Direct com- vein, recanalizes(Cruveilhier-Baumgarten syndrome). In its
pression of the portal vein by adjacent tumor is found less advanced stage, this collateral circrrtation (Fig.24.2) can
frequently. A pancreatic tumor can involve the splenic vein produce dilated and markedly tortuous subcutaneous peri-
or superior mesenteric vein, without affecting the portal vein. umbilical veins referred to as caput medusae.In questionable
Dilatatio* cf the portal vein (11) to more than 13 mm cases, color Doppler sonography can be used to detect a
should be considered suspicious for portal hypertension decreasedor reversed (hepatofugal) portal blood flow.
lFig.24.l). The luminal diameter of the portal vein is
measured perpendicular to the vessel's longitudinal axis, Evaluation of the lesser omentum should not only assess
s'hich is usually obliquely oriented in relation to the sono- the luminal diameter of the portal vein but also exclude
graphic image. The vascular wall is not included in the (ss) (Fig.24.3),which
'ssliiigi.4,:,p-e"{qii.b$a1:'r.;i*q$
frequently accompany viral hepatitis, cholecystitis, or pan-
measurement. It should be kept in mind that splenomegaly of
any other causecan lead to an increased luminal diameter of creatitis. They are caused by inflammatory changes and
the splenic vein or portal vein, without the presenceof portal should be repeatedly checked for resolution and exclusion of
hypertension. malignant lymphoma.
il\"r*
,$
46\
Aner the porta hepatis has been evaluated, the liver itself is If the inferior vena cava is borderline in diameter and the
nethodically visualized on transverse images uttd ffi.,ffi$ maneuver to test the caval collapse with forced inspiration is
obtiq:re:.if$di# parallel to the right costal arch. What is unsuccessful(see p. 15) or inconclusive,the luminal diameter
ilrong with the position of the transducer shown in Fig. 25.1? of the hepatic veins is best measured at this level. The maxi-
The answer can be found in the left lower corner of this page. mal diameter of a peripheral hepatic vein should not exceed
6 mm (Fig.25.2). Measuring the hepatic veins at the con-
The right subcostal oblique image (Fig.25.2a) is particu-
fluence with the inferior vena cava has the disadvantage of
-arlr suiLblefor fffi-ffiztne ih€ Eepati*c
vdfs#* $.?*fi€W wide anatomic variations and corresponding false measure-
110) and their confluence with the obliquely visualized infe-
ments. For instance, the hepatic veins of the patient with no
ior vena cava (L6).
cardiac problems shown in Fig.25.2 measure 10 mm directly
anterior to the vena cava while the peripheral hepatic veins
measure only 3-5 mm. With venous congestion proximal to
the right atrium secondary to right-sided heart failure, the he-
patic veins are dilated (Fig.25.3) and lack any respiratory
chanqes.
This section also allows the exclusion of a iiiii*ft
, which appears as echo-free fluid between
the diaphragm (13) and the acoustic shadow of the lung (47).
Vascular rarefaction along the periphery of the liver can be a
signof advanced
cirrhosis.
!$,{ffif#ffi
ffi,#H canbediagnosed on theobliquesubcostal
image with color Doppler sonography,which can determine
velocity, profile, and direction of the intravascular blood
Fig.25.1 flow.
\ormal values:
Hepaticveins (peripheral): ( 6 mm
After the liver (9) has been scrutinized on transverse and Th"ffi by measuring the antero-
subcostal image sections, it is further evaluated iffi, posterior (sagittal) and the superoinferior diameters in the
also in deep inspiration (Fig. 26.1a).It is important to keep right MCL (Fi9.26.2a, Fig.26.3a). To encompass an en-
the patient cooperative by allowing adequate time intervals larged liver, the transducer has to be angled superiorly and
for normal breathing. The best method seems to be a two- inferiorly (Fig.26.1b). Measurements are taken in inspira-
stage evaluation with a slow, continuous sweeping of the tion. The normal craniocaudal diameter should be less than
transducer. First, the left hepatic lobe is screenedto the level 13 or 15 cm, depending on the patient's body habitus. It is im-
of the inferior vena cava, followed by a break for normal portant to watch for the acute angle formed by the inferior
breathing while the transducer is moved from the midline to margin of the right hepatic lobe. In hepatic congestion or he-
the right MCL. The patient takes another deep breath and patomegaly,this angle exceeds45'and becomesblunted. The
the right hepatic lobe is now methodically screenedapplying normal lateral margin of the left hepatic lobe also should
the same sweeping motion (Fig.26.1a) to the transducer. form an acute angle measuring less than 30".
Fig.26.1a Fig.26.1b
-l
In athletic persons, hyperechoic struc-
iures (J) that appear to arise from the
,'oncave diaphragmatic surface (13)
Jan indent the hepatic dome (9)
r Fig.27.1). These structuresare only a
feiv millimeters in width and are im-
:rints caused by thickened muscular
bundles that run from the central
tendon to the costal insertion of the
Jiaphragm. They have no clinical sig-
nificance and should not be mistaken
for pathologic processes.A similar dia-
phragmatic muscular bundle can also Fig.27.1a Fig.27.2a
re seen as a mirror artifact along the
pulmonary side of the diaphragm
\Fis.27.2\.
/t
l\
trl
fft
Fig.27.1b
I
Fig.27.2b
Fig.27.3b Fig.27.ab
Fatty Infiltration
28
Fig.28.3b Fig.28.4b
3 29
Fig.29.1b
Fig.29.2b Fig.29.3b
2/t
Fig.29.4b
3 i Li v e r Infections,Parasites
-\nother important group of focal hepaticchangescomprises The most common parasitic involvement of the liver is
inflammatory and parasitic changes.The primary causesof a cystic echinococcal disease (Echinococcus cysticus), which
focal inflammation are cholangitis, fungal disease, and he_ characteristically produces several daughter cysts within a
matoqenous seeding, particularly in immunosuppressed large cyst. Such hydatid cysts should not be aspirated since
patlents. this might lead to peritoneal seeding of the larvae. Echino-
Hepatic abscesses (58) can produce a rather variable coccal diseasecan be treated medically with mebendazole or
sonomorphology. including an anechoic center due to lique_ surgically by excision. Alveolar echinococcal disease
faction (Fig.30.2), heterogeneousfoci surrounded by a rim (Echinococcus alveolaris) poses more sonographic difficul-
of decreasedechogenicity, and echogenic lesions (Fig.30.l). ties. A lesion with a mixed solid, liquid, and cystic pattern,
The effectivenessof inserted drainage catheters (59) can be traversed by several septa, is typically found (54) (Fig.30.3).
easily monitored by follow-up sonographic examinations Differentiating this finding from a primary hepatocellular
(Fig. 30.1).If compressionof adjacentbiliary ducts has led to carcinoma, metastasis(compare Fig. 32.3), abscess,or old he-
obstruction (cholestasis),bile can be drained by internal matoma is virtually impossible.
stents into the duodenum or percutaneous transhepatic
catheters into a collection bag. Checklist of Criteria for Establishing a Cyst:
ln addition to chronic alcoholism, the possible causes of the transducerover the liver), and an enlarged and rounded
cirrhosis include viral hepatitis, metabolic disorders, and left lobe or caudate lobe suggestcirrhosis.
exposure to toxic environmental substances.Latent cirrhosis
The complications of cirrhosis include portal hyperten-
ri'ith hepatic decompensationcan be present without sono-
sion and its sequelae (see p.24), ascites (68), and hepato-
vraphically detectable changes,and sonography is not suit-
cellular carcinomas (54) that arise from long standing cirrho-
able for excluding a cirrhosis. More advanced stagesproduce
sis (Fig. 31.2). Therefore, a cirrhotic liver must be carefully
several sonographic changes that can serve as criteria
and thoroughly (l) scrutinized for pathologic lesions. Only
for the presence of a cirrhosis.
the late stage of cirrhosis produces a shrunken liver
While the normal liver (9) exhibits a thin echogenic cap- (Fig. 31.2). The hepatocellular carcinomas (54) can be iso-
sule along its border (Fig. 26.3). the cirrhotic liver has an ir- echoic in relation to the remaining hepatic parenchyma (9)
regular surface (small undulations and bumps), which causes and might only be detectable by the convex displacement of
increased sound scattering with loss of the normal capsular adjacent hepatic veins (9) (Fig.31.3).
reflection. This results in absent or only patchy capsular visu-
alization. The absence of a capsular line is best appreciated
*hen the liver is surrounded by ascites (68) (Fig.31.1). Checklist of Criteria for Establishing Hepatic Cinhosis:
Furthermore the peripheral vasculature becomes rarefied in
o Absence of thin, hyperechoic capsular line
cirrhosis (Fig.31.1), with the remaining visualized vessels
o P auci tyof peri pheralhepati cvessel s
,showinga variable diameter and an increased angle, at their
o Obtuse angulation of the hepatic veins ) 45'
confluence(> 45').Normal hepaticveins (10) have a straight
r Accentuated echogenic wal1 of the portal vein
course,join eachother at an acute angle and are visible to the
o Abrupt caliber chinges of the branches of the portal
hepatic periphery (Fig. 25.2). In cirrhosis, the portal vein
vei n
branchesclose to the porta hepatis show thickening of their
o R egenerati ngnodul es w i th di spl acementof adjacent
[1'psrreflective walls and sudden changesin caliber ("pruned
vessel s
portal tree"). Regeneratingnodules are of normal echogen-
o Nodular liver contour (advanced stage only)
icitv and recognized only indirectly by displaced adjacent
o C ontractedl i ver (advancedstageonl y)
vessels.Finally. a deformed and biconvex hepatic configura-
e Signs of portal hypertension
tion. decreasedpliability (as revealed when pressing down
/74\
Wr
)\ \
/\45
\.
Before you proceed from the sonographic examination of the only after all the questions have been answered so that the
liver to the evaluation of the gallbladder, you should try to suspensedoes not disappear too early! (You would otherwise
work through the following questions. The required drawings inadvertently read the answersto the second and third image
should be done on a piece of paper. The answersto the ques- questions, that are listed next to each other on page 76.)
tions 6a-c can be found on page76, but check the answers
L fty to draw from memory the body marker that shows the
section of the porta hepatis. Then make a drawing in the
shape of a cone coffee filter and systematically enter from
front to back all lines, organs, and vesselsthat can be ex-
pected to appear in this sonographic section. Compare
your drawing (but only after completion) with the find-
ings in Figures 23.2b and c. Did you place all major struc-
tures in the lesser omentum at the correct depth? If not,
repeat this exerciseuntil you succeedwithout making any
mistakes.
The biie duct (66), comprising the common hepatic duct above the cystic duct in-
sertion and the common bile duct below it, normally measures up to 6 mm at the
level of the minor omentum, but luminal diameters between '7 and 9 mm are still
within the range of normal (Fig. 34.1),particularly after cholecystectomy.A dilated
duct (exceeding 9 mm in diameter) invariably becomes visible anteroiaterally to
the portal vein (11) (compare p.23). Even when the distal segment of the common
bile duct is obscured by duodenal air (compare Fig.17.3), a proximal intrahepatic
obstruction (e.g.. hepatic metastasis) can be sonographically distinguished from a
distal obstruction (e.g.,stone lodged at the papilti,lymphaienopathy in the lesser
omentum, or carcinoma of the pancreas). The proximal obstruction distends
neither gallbladder (14) nor common bile duct.
The small rist?e*l$.p. ,bi$H,*{$&ils, ur" parallel to the portal vein branches (11)
and are normally invisible. They become visible along the portal veins when biliary Fig.34.1a
obstruction has dilated the ducts, resulting in the double-barreled shot-gun sign
(Fig.35.3). Sonography is successfulin up to 90o/oof cases in distinguisling bi-
tween obstructive (ductal dilatation) and hepatocellular (no ductal dilataiion)
jaundice. characteristically, a severe biliary obstruction (Fig.3a.2) produces a
tortuous dilatation of the intrahepatic biliary ducts (66) that can assume the ap-
pearance of a towering antler. Cholestasiscan increase the viscosity of the bile thit
can lead to the precipitation of cholesterol or calcium crystals (Fig. 34.3). This so-
called "sludge" (67) can also be seen after prolonged fasting without biliary ob-
struction. Before diagnosing sludge, a thickness artifact (p. 10) should be excluded
by obtaining additional sectionsand by turning and shaking the patient. The ERCp
can drain a biliary obstruction by inserting a biliary stent (59). Alternatively, biliary
drainage can be achieved with a percutaneous transheoatic catheter.
Fig.34.1b
\\\\
\\\
Flg.3a.2b Fig.34.3b Fig.34.4b
Gallstones
and Polyps ?q
>,trnesare formed in the gallbladder (gallstones) becauseof this case(Fig. 35.2) should be followed for signs of growth to
.,: altered composition of the excreted bile. Depending on exclude any malignant process.
reir composition, gallstones (49) can transmit sound almost
Intrahepatic cholestasis (Fig. 34.2) is not always a mani-
: ,mpletely (Fig.35.3), float within the gallbladder
festation of malignancy and can be caused by obstructing
-rolesterol stones) or, if high in calcium content, reflect stones (49) in the intrahepatic ducts (66) (Fig.35.3). The
'rund to the degree that only the surface is visualized
prevalence of cholelithiasis is about 15%, whereby older
Fie.35.1). A stone is establishedif an echogenicstructure
women are affected more often. Since 80% of the patients
,.n be dislodged from the gallbladder wall (80) by moving
with gallstones are asymptomatic, detected gallstones are
patient, in contradistinction to a polyp (65)
':d turning the only consequential in context with their complications
F ig .3 5 .2 ).
(cholecystitis, cholangitis, colics, biliary obstruction). If re-
Some stones remain fixed at the gallbladder wall because moval is indicated, this can be achieved by percutaneous or
, inflammatory processes,or become lodged in the infun- open cholecystectomy or, alternatively, by ESWL (extracor-
::buium, rendering the differentiation between stones and poreal shock wave lithotripsy) or ERCP. Furthermore, the
: -rlvpsdifficult. Acoustic shadowing (45) distal to such a le- composition of the bile can be altered by medication and
:.rrn (Figs.35.1,35.3) indicatesa stone.An edge effect of the some stones regress following nutritional changes.
.,,llbladder wall (45) (Fig.35.2) must be carefully distin-
Note the thin, single-layered, echogenic wall (80) of both
..rished from stone-induced acoustic shadowing (compare
gallbladders (14) shown in Figures 35.1 and 35.2. There is no
Fig.9.a) to avoid any misinterpretation.The polyp shown in
inflammatory thickening of the gallbladder wall. Compare
this finding to the one on the images on the next page.
/o
\
lv
\=)
Choioe$Sli is invariably caused by stones (49). Early can become indistinct in outline where it abuts the hepatic
cholecystitis only causes the gallbladder (14) to be tender, parenchyma (9). An increased diameter of the gallbladder of
but inflammatory edema of the gallbladder wall (80) soon more than 4 cm is a sign of hydrops, but even more charac-
develops and the wall becomes thickened and multilayered teristic for hydrops is the associated altered configuration
(Fi g. 36. 1) . from a pear-shaped to a more biconvex and spherical struc-
ture.
The preprandial gallbladder wall normally measures less
than 4 mm. Thickening of the iggl,hldg-4#":ffiEl does not have Recognizing air within the lumen of the gallbladder or in
to be a sign of inflammation since it can be found in many its wall (mural emphysema) is crucial since an infection with
conditions, including ascites (68) (Fig.36.2), hypoalbu- gas-forming organisms implies a poor prognosis and is as-
minemia, or right-sided cardiac insuffiency. sociated with a high risk of perforation. iie i.,! $, 1
indicative of an acute inflammation r$S$t*fi*lcan lead to a contracted gallbladder or a porcelain
gallbladder with mural calcifications.Both conditions cannot
(68), which in some
easily be differentiated by sonography and have to be eval-
casescan be confined to Morrison's pouch between the infe-
uated together with the clinical findings.
rior hepatic border and right kidney. Finally, the gallbladder
Fig.36.1a Fig.36.1b
::.::-lr:!!,.Frnaj$1!ltii'ni+;/at'Fs'+jM.fi1+i+*i!!iiltjji,.li,:itnffl:i,,lrifi-riirrr-*+t*FFi:.r
Fig.36.2a Fig.36.2b
The kidneys are generally best shown in the lateral decubitus parenchymal width and pelv,ic\yidth (= PP-index) decreases
position. he .Iofi$tu4:inatrs€bfio,ti.sf, kidniiyl is visualized with age (compare normal values bglqw). In the typicallongi-
by placing the transducer on the extended intercostal line of tudinal section (Fig.37.2). the hypoechoic medullary py-
the flank. With deep inspiration, the kidney moves inferiorly ramids (30) are seen like a string of pearls between the
away from the obscuring costal acoustic shadows and ap- parenchymal cortex and the centrally situated echogenic col-
pears in its longitudinal dimension (Fig.37.1a) for evalua- lecting system(renal pelvis, 31). They should not be mistaken
tion. As is essential for a complete evaluation of any organ, for tumors or cysts. an ie*l*gd*L$-Aa;$4Ligl4dd should Ue
the kidney must also be delineated in a second plane, as dem- searchedfor within the perirenal fat above the upper pole ot
onstrated in Figure 37.1b for tfre ,le$at:{rtiOiit. Ltttlet,.:i-t the kidney (27), where it can appear as a hypoechoic mass
verselplan$.l1ottt'ti!,rlB..*,r (rightlateraldecubitusposi- within the echogenic perirenal fat. The renal hilum, together
tion). with the renal vein (25), is generally well seen on the trans-
verse section (Fig. 37.3). Because of their thin diameter, the
Normal .genalij$afiiichpna (29) is slightly decreased or
ureter and renal artery are often identified only with great
equal in echogenicity relative to the splenic or hepatic
difficulty. Why is the position of the transducer depicted in
parenchyma (9). The width of the parenchyma should
Figure 37.3a not completely compatible with the images
measure at least 1.3 cm (the measurements in Fig.37,2 are
shown in Figures 37.3b and c?
1.5 cm and 2.4 cm, respectively). The ratio between
1ffifi""j;?:
::$f#:r '*+iiii,tr
Fig.37.1a Fig.37.1b
Fig.37.2a Fig.37.2b
f i.:iii*a:- li!\r ii\- :q.* I
a_
r- 10-
The ,noru.S,i1$q$,$ig*t{+& $.-1 {Jig.37.2) can show differentiation from a true renal tumor might occasionally be
several findings that can be traced to its embryologic difficult.
development. Hyperplastic columns of Bertin can protrude
from the parenchyma (29) into the renal pelvis (31) and do ..&B&#;$+XE:(64) are echo-free and produce, as shown in
Figure 38.2,distal acoustic enhancement (70). Additional cri-
not differ in echogenicity from the remaining renal
teria for the diagnosisof a cyst are the same as for the diagno-
parenchyma. An equally iso-echogenic parenchymal bridge
sis of hepatic cysts (see p.29). Cysts can be separated into
can completely divide the collecting system. A partial or
peripheral cysts along the renal surface, parenchymal cysts,
complete parenchymal gap at the same location indicates a
or peripelvic cysts,with the latter to be differentiated from an
renal duplication (Fig. 38.1) with separate ureters and blood
obstructed and dilated renal pelvis (Big. aL\. The evalua-
supply for each moiety. The prevertebral parenchymal bridge
tion of a cyst should include measuring its diameter as well as
of horseshoe kidneys might even be mistaken at first sight
stating its approximate location (upper, middle, or lower
for preaortic lymphadenopathy or a thrombosed aortic
third of the kidney).
aneurysm. A lobulated renal contour can be seen in children
and young adults as manifestation of persistent fetal lobula- Finding a few renal cysts is clinically inconsequential,
tion, characterized by an otherwise smooth renal surface that though re-evaluation at regular intervals is advisable.In con-
is indented between the individual medullary pyramids. (Fig.38.3)
trast,the adultformor :pe$.qtb$l[Si#,ffi{ii#6-!"ffi
These changes have to be differentiated from renal infarcts presents with innumerable cysts (64) that progressively in-
(Fig.423) that can be found in old patients with athero- creasein size.Since the cystscan reach a considerablesize,the
sclerotic stenosis of the renal artery. patients can complain of fullness and pressurein the upper ab-
domen. Furthermore, polyeyslic iqnql diieffis leads to renal
Localizedparenchymal thickening along the lateral border
atrophy by displacing and thinning the renal parenchyma, re-
of the left kidney, usually just below the inferior pole of the
sulting in renal insufficiency in early adulthood and eventu-
spleen,is found in about 10% of patients. This is an anatomic
ally requiring dialysis or a renal transplant. Other causes of
variant, generally referred to as i,f1.ffiSffi and its
renal atrophy will be discussedon the next page.
The kidney reacts to the i-*W In addition to causing peripheral infarcts (Fig. a23), dAt'
with similar sonographic changes.It can be entirely normal in :art€r iis*eaCIttg,can induce a generalized decrease in renal
early pyelonephritis or glomerulonephritis. Later, edema size (Fig.39.1), which, however, can also be a manifestation
causes an enlargement and interstitial infiltration an in- of recurrent or chronic inflammation. The marked thinning
creased parenchymal echogenicity with accentuated demar- of the parenchyma (29) found in end-stage chronic nephritis
cation of the parenchyma (29) relative to the hypoechoic py- leads to renal atrophy (Fig. 39.2), which is frequently accom-
ramids (30) (Fig. 39.3). This is referred to as "punched-out panied by degenerative calcifications (53) or concrements
medullary pyramids." In comparison with the adjacent he- (49) with their corresponding acoustic shadows (45). The
patic or splenic parenchyma (9), the renal parenchyma ap- atrophic kidney can be so small that it eludes sonographic de-
pears more echogenic (Fig. 39.3) than the parenchyma of the tection. The associated loss of excretory function can be
normal kidney (Fig. 38.2). Interstitial nephritis can be caused made up by compensatory hypertrophy of the contralateral
by chronic glomerulonephritis, diabetic nephropathy, urate kidney. In a unilaterally small kidney, the PP index (see p. 37)
nephropathy (hyperuricemia as manifestation of gout or in- should be determined. If this index is normal, a developmen-
creased nucleic acid turnover), amyloidosis or autoimmune tally hypoplastic kidney might be present.
disease, but the etiology cannot be deduced from the in-
While sonography does not contribute to the differential
creased parenchymal echogenicity.
renal disease, it is of value in
Another s an inflammationis the $iffi{S.t! h: during therapy, in ex-
cluding any complications (e.g., acute obstruction) and in
guiding any percutaneousneedlebiopsy.
fhe l*9l&iffi is seen as a central complex of strong Sonography cannot reveal all the
echoes that are only traversed by small thin vascular struc- #.ffiWj Since the midureter is obscured by overlying aii in
tures (Fig. 37.2). With increased diuresis after fluid intake, the majority of cases,a ureteral stone is generally not visual-
the renal pelvis (31) can distend and be visualized as a more ized unless it is lodged at the ureteropelvic junction or in the
echo-free structure (87) (Fig. 40.1): The same finding can prevesical ureter. Less frequent causes of ureteral obstruc-
represent the developmental variant of an extrarenal pelvis. tion are a tumor of the bladder or uterus and aggregated
In both conditions, the dilation does not involve the calices lymph nodes as well as retroperitoneal fibrosis after radia-
and infundibula. tion, or idiopathic as a manifestation of Ormond disease.A
latent obstruction can develop during pregnancy, caused by
It can be difficult to te this findins from a first
ureteral atony, and during infection. Furthermore, an over-
degree (mild) (Fig.40.2),which also
distended bladder as manifestation of a neurogenic bladder
causes a dilated renal pelvis but without infundibular exten-
or secondary to prostatic hypertrophy can cause ureteral ob-
sion and detectable parenchymal thinning. A second degree
struction, and the sonographic evaluation must include the
(moderate) obstructive dilatation causes increasing fullness
bladder and a search for an enlarged prostate gland in men
of the infundibula and calices as well as the onset of
(compare Figs. 56.1,56.2).For assessingthe postvoid residual
parenchymal thinning (Fig. a03). The bright central echo
see page 54.
complex (31) becones rarefied and eventually disappears.
The third degree (severe) obstructive dilatation is character- The obstruction causingthe dilatation of the collecting sys-
izedby severe pressure atrophy of the parenchyma (no case tem can be relieved by cystoscopicallyplaced ureteral stents
illustrated). (compare Figs.45.3, 45.4) or by sonographically guided per-
cutaneous nephrostomy.
41
Not everyt$ffffi (31)is indicariveof obstruc- represent blood vesselscontaining rapidly flowing blood or
tive uropathy. The developmental variant of an extrarenal the collecting system filled with essentially stationary urine.
pelvis was already mentioned on the preceding page. Blood vessels are seen as color-coded structures with the
Furthermore, the renal hilum can show prominent vessels color depending on the direction and velocity of blood flow,
(25) (Fig. 41.1) that can be followed to the hypoechoic medul- while the barely moving urine in the collecting system re-
lary pyramids (30) and might be mistaken for structures of mains black. The same principle of difference in relative flow
the collecting system. These vesselsgenerally appear rather can be employed to differentiate pelvic or peripelvic cysts
delicate and lack the characteristic fullness found with an ob- (64), which do not require any therapy, from an obstructively
structed and dilated collecting system (compare Fig.40.2). dilated renal pelvis (87), which has to be expectantly ob-
served or treated. Both conditions can, of course, concur
.,tt.. llg --findings are inconclusive,Liffi iffi (Fig. aL2).
sci$ffiffi.\i can easilydeterminewhetherthesestructures
Fig.41.1a Fig.41.2a
NS
?,
35
Fig.41.1b Fig.41.2b
Notes
RenalStonesandlnfar
42
Detecting concrements in the kidney f{Wl it after phenacetin abuse. Large staghorn calculi are difficult to
more difficult than detecting stones in the gallbladder since diagnose if the distal acoustic shadowing is weak and its
the echogenic renal stones (49) are often located within the echogenicity mistaken for the central echogenic complex.
equally echogenic collecting system (31) (Fig. 42.1) and
If renal concrements dislodge and migrate from the in-
might not elicit any echogenicity that is discernible from its
trarenal collecting system into the ureter, they can, depend-
surrounding structures. Concrements in a dilated collecting
ing on their size, pass into the bladder without symptoms or
system are a notable exception since they are easily revealed
with colics,or become lodged and causeureteral obstruction.
as echogenic structures within the echo-free urine. In the ab-
In addition to detecting obstructive uropathy, sonographv
sence of any dilatation, it is of utmost importance to look for
can exclude other causes of abdominal pain, such as pan-
acoustic shadowing (45) caused by concrements or calcifica-
creatitis. colitis. and free fluid in the cul-de-sac.
tions, such as is found in hyperparathyroidism.
Renal emboli or renal arterial stenosiscan cause 0
Depending on its composition, a renal stone (49) can be
lffiti (71), which, conforming to the vascular
either completely sound transmitting (as seen in Fig. 42.1) or
distribution, are broad-based at the renal surface and
so reflective that only its near surface is seen as echogenic cap
tapered toward the renal hilus. Sonographically, they are
(.Jig.a2.2).Th" i$ffim$.$gtffi.$$St includesthe arcuate
seen as triangular defects (Fig. 42.3) in the renal parenchyma
arteries between the renal cortex and medullary pyramids
(29). The resultant scars are as echogenic as renal calculi but
(bright echoes without shadowing), vascular calcifications in
should not be mistaken for concrements on the basis of their
diabetic patients, and calcified fibrotic residues following
form and localization.
renal tuberculosis. Finally, papillary calcifications can occur
43
N \45
\\
Fig.43.-1b Fig.43.2b Fig.43.3b
44 5 | KidneYs
Fig.44.1a Fig.44.1b
It is crucialto detectu igrp,Ji{,$1ffi tion (Fig. 44,3) to avoid missing on subsequent studies any
early (compare p.45). It is normal for a renal transplant to progression that might require therapeutic intervention.
show an often permanent increase in size by up to 20o/o after
surgery.In comparison with the native kidneys, its cortex (29) The renal transplant should be further evaluated for the
appears wider (Fig. 44.2) and the parenchymal echogenicity distinctness of its outline and its interface between the
can increase so that the medullary pyramids (30) become bet- parenchyma (29) and collecting system (31). An indistinct
ter demarcated. Progressive inflammatory infiltration must PP-interface or a slight increase in volume can be warning
be excluded by serial sonographic studies, which should be signs of the onset of rejection. To allow a valid comparison,
obtained at short intervals during the immediate postopera- reproducible longitudinal and transverse diameters should
tive period. A prominent renal pelvis or a slightly distended be selected for measurements and documentation (compare
(first degree) collecting system (compare Figs. 40.1, 40.2) p. 45). After transplantation, the immunosuppressive medi-
might be observed without requiring intervention becauseof cations can gradually be reduced and the intervals between
functional impairment of the renal transplant. The urinary the sonographic studies extended.
distention should be documented and measured in cross sec-
m
Fig.214.3
a Fig.4a3b Fig.44.3c
45
For an iqiF$t$.1i$ii#$eB. e}'! , the renal transplant lated volume (simplified volume formula: vol = A x B x C x
has to be visualized longitudinally first (Fig. a5.1b) and the 0.5) on follow-up examinations.
position of the transducer then adjusted until the maximal
(73) can developas a ,eot#fi*eifiCi1l*{**t:
length comes into view. The diagram (Fig. 45.1a) illustrates a -A'.lypphocele
jffi$, -usuatty
line too far lateral (dotted line) that would measure a iii .}l surgery(Fig.a5.2) and is rounA
between the lower pole of the renal transplant and the uri-
spuriously short distance.To get to the "true" longitudinal di-
nary bladder (38), but can be anywhere adjacent to the trans-
mension (d1) the transducer has to be tilted along the straight
plant. Urinary obstruction (87) is an equally frequent compli-
arrows.
cation and, depending on its severity, might require tem-
Thereafter, the transducer is slightly turned (Fig.45.1c) porary stent drainage (59) (Figs. 45.3, 45.4) to prevent dam-
until there is no longer angulation along the curved arrow age of the renal parenchyma (29). Measuring the RI of the
(Fig.45.1a). This two-step approach to guiding the trans- supplying renal vesselby Doppler sonography provides addi-
ducer should assure that the length documented is not too tional information concernins the condition of the renal
short, which could lead to a spurious increase in the calcu- transplant.
It is the goal of this workbook to provide factual knowledge become faster and better oriented with the three-dimen-
and to facilitate memorization by means of most effective sional abdominal space if they are able to sketch the few
teaching strategies. This should facilitate immediate and standard orientations from memory. Do not get annoyed at
rapid recall from memory whenever necessaryat a later time. the following questions: there are no better teaching
Empirically, it has been shown that beginners in sonography methods that relate new material in a shorter period of time.
Ftg.46.1 Fi1.46.2
47
Fig.47.1
t\\
-){
-
, rr\
\
Fig.47.2a Fig.47.2b Fig.47.2c
:::?ia'.i+itrf+*!i{tjrllslnPJrr!!qr{!r.r!fqs.,+.Jfillad$rrjjrijrr.Flf]*r;nEttr:ir!::rilit!:l
Fig.47.3b Fig.47.4b
48 6l sPleen
Manyconditionsareassociated
*irh ffi.$ffii&,.l#ffi
tffi of (Fig.48.1) are generally located at the splenic hilum or adja-
the spleen, and the differential diagnosis does not only in- cent to the lower splenic pole and cannot always be differen-
clude portal hypertension (Fig. a8.2) secondary to hepatic tiated from enlarged lymph nodes (55) (Fig. a8.3).
cirrhosis but also viral infections, such as mononucleosis.
Suggestions: If the sonographic examination of the abdo-
Furthermore, all diseasescausing an.increased turnover of
men reveals a splenomegaly, a systemic hematologic condi-
erythrocytes, such as hemolytic anemia and polycythemia
vera, can produce a splenomegaly (Fig.48.3). tion must be considered and
(see
tV; pp. 14 and 21). Furthermore, portal hypertension should be
, suchasacuteor chronicleukemia(Fig.aS.1 excluded by measuring the luminal diameter of the splenic
in CLL), but can be found in rheumatic, immunologic, and vein (20), portal vein, and superior mesenteric vein and by
storage diseases.Not every splenomegaly is of pathologic rel- searching for portocaval collaterals. The size of the spleen
evance since many diseasesheal by leaving behind a mild to should be measured accurately. Only by having a baseline
moderate splenomegaly,for instance mononucleosis.The en- measurement of the splenic size can subsequent examina-
largement of the spleen (37) begins with a rounding of its tions determine any interval growth. Questions that sub-
normal crescentic configuration (Fig. 47.2) and can progress sequent examinations might address,such as possible inter-
to the so-called "giant spleen." The massively enlarged val growth during therapy, should already be kept in mind
spleen can touch the left hepatic lobe and this is referred to as during the initial examination. Neither size nor echogenicity
"kissing phenomenon." Occasionally, an of the spleen allows any inference as to the nature of the un-
can reach a considerable size. Accessory spleens (86) derlvins condition.
Areas that are hypoechoic in relation to the remainins trauma, and it is advisable during this interval at least to per_
splenic parenchyma include as possible causes all focd- form serial follow-up studies.
tynapfrnm#nrur*fidinmtions. ln non-Hodgkin lymphoma.
these lymphomatous infiltrations can be localized as well as Finally,the spleencanexhibitffiffi$.F,ffiffi. Theycould
diffuse throughout the spleen giving it a heterogeneous ap- represent splenic hemangiomas, which are rare, or calcified
pearance. Congenital (dysontogenetic) splenic cysts are granulomas, which are rather common and usually found
rather uncommon and do not differ sonographically from he- with tuberculosis or histoplasmosis.Splenic calcifications can
patic cysts (6a) @ig.29.1), thus they are not illustrated again also accompany cirrhosis. A spleen harboring multiple echo_
here. Acquired splenic cystsfrequently develop after trauma genic foci (53) has been called the ,,star-sky spleen.,
or infarcts. As is true for hepatic cysts, internal septations (Fig. 49.3). Splenic abscessesand splenic metastases,which
suggest a parasitic origin (compare Fig.30.3). are rare, can have a rather varied sonomorphology, in part
depending on their duration and underlying cause.There are
Recognizing
u mightbe dif-
ff..{i1*.ffi16ig.a9.z) no simple reliable differential diagnostic criteria, and consul_
ficult since a fresh hemorrhage can be iso-echoic with the sur- tation of reference textbooks is recommended. Solenic in_
rounding splenic parenchyma (37). In general, the echogen- farcts (71) can be observed in splenomesalv with com_
icity of the extravasated blood decreaseswithin a few days, promised vascular supply (Fig. a9Ji.
and subacute or old hematomas (50) are usually well visual-
ized as hypoechoic space-occupyinglesions. A parenchymal Suggestion: Patients with acute abdominal and thoracic
laceration without a capsular tear can produce an initially un- trauma should be searchedfor free fluid in the cul-de-sacand
recognized subcapsularhematoma. The risk of such a hema- below the diaphragm (13) as well as around the spleen and
toma is a delayed tear of the splenic capsule,which releases liver. Carefully scrutinize the spleen for a double contour
the tamponaded hematoma and causesfree bleedins into the along its capsule (subcapsularhematoma?) and for a hetero_
abdominal cavity. More than 50% of these io-called geneous echo pattern of its parenchyma, to avoid overlook_
"delayed" splenic ruptures occur within 1 week after the ing a possible splenic rupture.
7/ .= .{ t .;.
/ oS J" ^ q 3o'
h
'6 o o
z qa_ o
"6f.@ g O
*--
---'/
The material about the spleen presented in the preceding tained in the text, and the answer to question 5 is found on
three pages should have prepared you to answer the follow- page 77.
ing questions. The answers to questions 7 to 4 are con-
Fig.50.1
\ ote s
51
Fig.51.1
Ir
/l'
Fig.51.3b Fig.51.4b Fig.51.5b
52
fhe *sg.g+digsrreelg.nr can be seen in the lateral sagittal sec- upper abdomen) is shown in Figures 52.1b and c. This con-
tion (Fig. 52.1a\.In most cases,air in the colon precludes vi- trasts with the thickened wall (74) found in ulcerative colitis
sualization of its lumen. Large amounts of retained fecal mat- or ischemia (e.g. due to mesenteric artery infarction or
ter (coprostasis)can occasionallybe found in the colon of old mesenteric vein thrombosis), as seen in a case of colitis
patients. A transverse colon (43) without any evidence of in- (Fig.52.2) in which the descending colon exhibits strikingly
flammatory mural thickening (transverse section of the thickened haustral indentations.
Fig.52.3a F i g . 52.3
Fig. 5 2 .3 b Fi g.52.3c
Because of air in the intestinal lumen, the sonographic eval- ascitic fluid (Fig. 53.3) that is devoid of internal echoes ex-
uation iq&,$il$.$ft (46) is often limited or not cept for reverberation artifacts from the anterior abdominal
possible"f at all. F{owever, the intraluminal air frequently wall (2,3) (compare p 10). Lymphomatous infiltration of the
decreaseswhen it is surrounded by inflammatory wall thick- small bowel often leads to long segmentsof hypoechoic wall
ening or can be reduced by graded (!) compression applied to thickening and is primarily observed in immunocom-
the transducer. promised patients.
'g$$Sii ,ffii..e frequently presentsas terminal ileitis i$'t*i*{:lW (> 5 MHz) can add informa-
(Fig.53.1). The edematous wall thickening (74) confined to tion in selected casesif used, for instance,intraoperatively to
this segment is easily separable from adjacent uninvolved exclude mesenteric lymphadenopathy. If a tender appendix
loops (46). In more advanced stages(Fig. 53.2), the intestinal shows no peristalsis,has reduced or no compressibility, and
wall (74) becomes massively thickened and can resemble the measures more than 6 mm in diameter, it fulfills the criteria
sonographic findings of intestinal invagination. On cross sec- of acute appendicitis. Sonography has the advantage of al-
tions, the thickened, edematous walls of intestinal loops can lowing real time evaluation of intestinal peristalsis,easily re-
be compared to a concentric lamellation of a "target." The vealing aperistalsis (atony) or prestenotic hyperperistalsis.
examiner should always look for adjacent fistular tracts or Though it is often necessaryto proceed with other imaging
abscessesas well as for free abdominal fluid in the cul-de-sac. modalities (endoscopy, endosonography, conventional radi-
ology, CT) because of acoustic shadowing (a5) by intestinal
rn",&bp,iffi $ t of individualsmallbowelloopsare air that limits the sonographic evaluation of the small bowel,
normally not identified, but can be delineated in the presence
sonography can still make a contribution if properly targeted
of extensive lymphadenopathy or massive ascites (68). The
in selected cases.
small bowel loop seen in cross section (46) floats within
b*
45
The longitudinal section delineates the bladder more as a measure the craniocaudal diameter (horizontally displayed
triangle (Fig.54.3), with the prostate gland (42) and vagina, on the image) without interfering acoustic shadowing (45) of
respectively,seen below the bladder (compare Fig. 58.1). the pubic symphysis (a8) Gig.54.3b).
rr$.p,i."it$br or pros- Using the;imp-lifled volume formula (voluo= A x B x C x
tatic hypertrophy(Figs.56.2,56.3)are suspected,
the post- (ml) can be calculated bv dividins
void residual should be calculated by measuring the maxi- the product of the three diameters by two.
mum transverse and sagittal diameters of the bladder after
the patient has voided (Fig. 54.2b). Thereafter, the trans- Find out which diameter in the caseshown in Figure 54.3b
has been incidentally measured twice?
ducer is turned 90' and angled inferiorly (Fig.54.3a) to
//t
45 1
it.'\\
Fig.54.3a Fig.54.3b Fig. 54.3c
UrinaryBladder IndwellinECatheter,Cystitis,Sediment
55
The wall (77) and lumen (38) of the urinary bladder can wall (Fig. 55.3) are seen in the bladder (38) anteriorly, or sec-
only be adequately evaluated when the bladder is full. An tion thickness artifacts posteriorly, simulating intraluminal
indwelling catheter (76) usually results in an empty bladder matter (compare p. 10). These artifacts have to be differen-
(Fig.55.1), precluding any reliable evaluation.The catheter tiated from the real sedimentations of blood clots (52) or
therefore should be clamped for an extended period to concrements (49) along the floor of the urinary bladder
achieve filling of the bladder (38). When the edema of the (Fig.55.3). By rapidly changing the pressureapplied to the
bladder wall (77) is rather advanced, cystiris (Fig.55.2) can transducer, intraluminal matter can be mechanically dis-
also be recognized with the bladder empty. turbed and made to float within the lumen. A section thick-
The wall thickness of the distended bladder should not ness artifact or wall-based tumor lack any response to this
exceed 4 mm. After voiding, the wall is irregularly thickened maneuver.
and measures up to 8 mm in width. Wall-based tumors or As an incidental finding, a forceful jet of urine can be pro-
polyps can no longer be detected. Wall thickening can be pelled from the ureteral ostium into the bladder lumen. This
causedby inflammatory edema, increasedtrabeculations due jet phenomenon is physiologic. If transabdominal sonog-
to prostatic hypertrophy with bladder outlet obstruction, or a raphy is inconclusive, transrectal or vaginal transducers
space-occupyinglesion. should be used. These endocavitary transducers generally
have a better resolution because a higher frequency can be
Even the heallhy bladder is never entirely echo-free.
Often, reverberation artifacts (51) of the anterior abdominal used due to the shorter distance to the target organ. These
special examinations require additional expertise and train-
ing.
@\
N\
Fig.55.1b Fig.55.2b Fig.55.3b
55
Transabdominal sonography of the genital organs requires a with voiding and can lead to a trabeculatedbladder (com-
filled urinary bladder (38), which displaces the air-contain- pare Fig.55.2).
ing intestinal loops (46) cranially and laterally to avoid their
interfering shadows (45) and serves as an acoustic window.
rh" iffiffi#Fd$$S$#H#4 (42) erevates
the bladder
floor (38), but the urinary bladder remains outlined by a
The prostate gland (42) is located on the floor of the bladder
wall that is seen as a smooth line (Fig. 56.2). Advanced pros-
anterior to the rectum (43) and is visualized on the supra-
tatic hypertrophy stenosesthe urethra, causing hypertrophy
pubic transverse section and on the sagittal longitudinal sec-
of the bladder wall, that beomes visible as a thick rim (77)
iion (Fig.56.1).rhe i$$i*#.{|i Effig_ shoutdnot around the bladder (Fig.56.3). The carcinoma of the pros-
exceed the approximate size of 3 x 3 x 5 cm or the approxi-
tate gland (54) usually arises in the periphery of the gland,
mate volume of 25 ml. In older men, an enlarged prostate
can infiltrate the bladder wall and extend as a lobulated
eland is frequently encountered (Fig. 56.2), which interferes
mass into the lumen of the bladder (Fig.56.3).
'.-,
/,/e
/-\W N \
\
I
Fig.56.1b Fig.56.2b Fig.56.3b
Fig.56.4a Fig.55.4b
Testicle,OrchitisfEpididymitis
Undescended
If both testicles are not found in the scrotum after the age of 3 months, the question of localizing the or ectopic
'uiii&sceaded
must
4b.li,$sldgt be addressed. Frequently, the testicle (9S) is found in the inguinal canal near the anterior abdominal wall (2. 5).
as seen in Figure 57.1. An unsuccessfulsonographic detection of an undescendedor ectopic testicle, which is at risk of malie-
nant transformation, should be supplemented by an MR examination.
The sudden onset of severe scrotal pain radiating into the groin demands differ-
ential diagnostic clarification between ffiamrnatiOo *O- torg,ii# since the
ischemic tolerance of testicular tissue before irreversible necrosisis only 6 hours. In
inflammation, perfusion is maintained, and can be seen by (color) Doppler sono-
graphy as a characteristic arterial flow profile (", ) in the testicular tissue (Fig. 57.2),
frequently increased on the affected side. Torsion, in contrast, shows decreased
perfusion in relation to the other side or lacks perfusion entirely.
Fig.57.1a
Fig.57.1a Fig.57.1 b Fig.57.2
i$.$$ bv
iid.ljl;ffitsf,4ffiiq is usuallv accompanied is established by the Valsalva maneuver or color-
edematous thickening of the testicle (98) or epididymis (99) coded Doppler sonography. Occasionally, herniated borvel
(Fig. 57.3). If the findings are inconclusive, comparing both loops (46), a hydrocele (64), and the ipsilateral testicle (98)
sides to determine their relative size can be helpful. A can be visualized together on one sonographic section
thickened and partially multilayered scrotal wall (100) can be (Fig. 57.5). A hydrocele can accompany a testicular malis-
seen as manifestation of an accompanying edematous reac- nancy. Most, but not all, i.idstf$i+t#i. cause a hetero-
tion. geneous parenchymal pattern. A well-differentiated semi-
A homogeneous anechoic fluid collection (64) invariably noma can be homogeneous and present as an unremarkable
represents a ,!6adto'erdlq(Fig.57.a). The diagnosis of a 'v sonographic pattern.
-,
Tovisualize
th" ffi (f9) andffiili$## (91),transabdominal achieve the necessary depth penetration, low frequencies
sonographic imaging of the lesserpelvis requires a distended (3.5-3.75 MHz) with the corresponding decreasedspatial res-
urinary bladder (38) as acoustic window (Figs.58.1a-c). To olution have to be selected (refer to p. 8).
'.7t62 r\
. - {r \
Fig.58.1a Fig.58.1b
n
Fig.58.1c
\\\\
\ \\
Fig.58.2a
Fig. 58.2 b
In comparison to transabdominal images, the images are and the anterior abdominal wall (1-3) at the upper border on
acquired from below and the endovaginal images are seen coronal images,far away from the probe. On sagittal sections
"upside down." The sound waves propagate from the probe (Fig.58.3), the urinary bladder is on the right side of the
(located inferiorly in the body and at the inferior border of image if viewed from the right side of the patient. Some.ex-
the images) upward (superiorly). fhir f,*}i , to which aminers prefer the images as viewed from the left side, with
the novice is unaccustomed, shows the urinary bladder (38) the anterior structures then seen on the left side of the imase.
The width of the :dhdsdiFtfiffi (78) varies wirh the men- an echogenicrim (z) (Fig. 59.2). After ovulation, the midline
strual cycle: immediately after menstruation, a thin, echo- echo (r) gradually disappearsin the secretory endometrium
genic, linear echo is seen (Fig. 59.1). At the time of ovulation, (Fig. 59.3) until only an echogenic endometrium is recoq-
the endometrium is separated from the myometrium (39) by nized.
The normal uterus is demarcated by an echogenic serosaand cavity can easily mistaken for endometrial polyps (65). Fi-
exhibits a homogeneously hypoechoic myometrium (39). broids usuglly have a homogeneous or a concentrically
The most common benign uterine tumors, ttt" i$ti#}Es lamellated echo pattern with distinct demarcation and a
,(myom .lr, arise from the smooth musculature and are usu- smooth surface, but can contain calcifications with corre-
ally located in the corpus of the uterus. For planning the sur- sponding acoustic shadowing or a central necrosis.The size of
gical enucleation of fibroids, it is relevant to distinguish intra- fibroids should always be measured and controlled by serial
/transmural (Fig.60.1) and submucosal (Fig. 60.2) fibroids examinations to discover the rare sarcomatous transforma-
from subserosal fibroids on the surface of the uterus tion by revealing any rapid growth. Only in early pregnancy
(Fig.60.3) (54). The submucosal location close to the uterine can a sudden increase in size be attributed to a benisn lesion.
Fig.60.6a
rhe .b$-ii*f (91) are visualized on craniolaterally oriented 5.5 and 10.0 cm3for each ovary, with a mean value of just less
'
sagittal sections and are frequently in the immediate vicinity than 8 cm3.The ovarian volume does not change during prer-
of the iliac vessels(23) as seen in Figure 6L.1.To measure the nancy, but decreasessteadily by about 3.5 to 2.5 cm-' post-
volume of the ovaries, a transverse section has to be added. menopausally, relating to the length of time after the
The three diameters multiplied by 0.5 approximate the ovar- menoDause.
ian volume: in the adult female these volumes are between
Normally, several lfr1l{dib$ (93) are detectable in the 1st maturation, and that the time of the ovulation might be ob-
days of the menstrual cycle, seen as 4-6-mm small cycstsin served by endovaginal sonography.Signs considered to indi-
the ovary. After the 10th day of the cycle, one follicle be- cate imminent ovulation include a follicular size exceeding
comes dominant, the so-calledgraafian follicle, with a diame- 2 cm, Ihe visualization of the small, peripheral, ring-shaped
ter of about 10 mm (Fig. 61,.2).Thereafter, this follicle shows cumulus oophorus, and intrafollicular echos projecting from
linear growth, increasing in size by about 2 mm per day until the wall. Following ovulation, the leading graafian follicle
it reaches a size of 18-25 mm just before ovulation. In the "disappears" or at least diminishes markedly in size: at the
meantime the other follicles regress. same time a small amount of free fluid can be detected in the
iX,l-VF, cul-de-sac.Through invasion ofcapillary sprouts,the ruptured
It is relevantror deftI{$iyai$erti., that serialsono-
follicle becomes the progesterone-producing corpus luteum.
graphic examinations allow close monitoring of follicular
An ov.-ar,i#ir[*-'lt with a diameter exceeding 5 cm is suspi- unilateral ovarian tumors and can be classified as a primary
cious of tumorous growth and, especially if septations, wall benign tumor that rarely undergoes malignant transforma-
thickening, or solid internal echos (^.) are present (64) tion. A dermoid has to be distinguished from hemorrhagic or
(Fig.62.1), malignancy must be ruled out. A cyst containing endometrial cysts,which are filled with blood products and
sebum, hair, or other tissue components (:,) constitutes a der- can exhibit fluid-fluid interfaces (') (Fig. 62.3) or a homo-
moid (Fig. 62.2),which comprises about 15% of the usually geneous echo pattern (50) (Fig.62.a).
In a cycle stimulated as part of infertility therapy, merely About 5'/o of women truu" ipd$
measuring the serum hormone levels can neither rule out hy- *i{ffie$ caused by inhibited follicular maturation. Its most
perstimulated ovaries (Fig. 62.5) nor reliably estimate the common causeis adrenal androgen excess.It is characteristic
number of preovulatory follicles (93). It is for this reason that of PCOS for the ovary (91) to contain several small cysts
the number of i.ffi be monitored (64), predominantly around the periphery where they form a
sonographically so that therapy can be terminated and con- "pearls on a string" appearance within tissue of increased
traceptive measures advised when more than two preovula- echogenicity (Fig. 62.6).
tory follicles develop.
An elevated #$ffiHffi in the maternal serum or urine is an in- the last menstrual period or 14 days after conception. The ini-
dication of pregnancy, and sonography can confirm the preg- tially small cavity grows at a rale of about 1.1 mm per dav to
nancy. Furthermore, sonography can identify multiple preg- become the amniotic cavity (101), in which the embryo tsit is
nancy (refer to Figs. 66.3, 66.4), which is not always hor- later detectable (Fig. 63.2).
monally recognized, and it can exclude ectopic pregnancy
(EP). A gestational sac (chorionic 101) ourside rhe
uterus(39) constitutesan (Fig.63.3).
Vaginalsonographycan detect #1$.ffi-iffi#
"urly
na*ct' (Fig. 63.1)when the gestational sac(chorioniccavity) ffi# can be detectedfrom the 6th ses-
measures2 to 3 mm in diameter.This sizeis generallyfound tational week. At this time, the normal rate is about 80 to 90
at the beginningof the 4th gestationalweek plus 3 daysafter beats per minute.
Biophysical limits: According to the guidelines of the mended tissue exposure limits. Though no adverse biologic
-\merican Institute of Ultrasound in Medicine (AIUM), effects have been reported so far with these higher sono-
acoustic energies below 100 mW/cmz or less than 50 J/cm graphic tissue exposures,'it is prudent to refrain from non_
have no confirmed biologic effect and can be considered safe essential (color-) Doppler sonography during the sensitir.e
[1]. Since the sonographic exposure delivered with conven- phase of organogenesis(1st trimester)
[2, 3].
tional real time sonography is far below those values,neither
1 AIUM Bioeffects Committee: Bioeffects considerations for safet\ in ulrrasour;
thermal nor cavitation effects are to be expected. Ultrasound Med., Suppt. T (1988): 1 38
-i
In the sonographic evaluation of pregnancy, :F.i,ffi is prl- sac is fetal in origin. Figure 64.2 shows a yolk sac (102) adja-
marily used to assesintrauterine growth retardation but also cent to the spine (35) in a fetus of a gestational age of 7 weeks
assistsin diagnosing anomalies.The normal biometric values and 6 days.
for the gestational age and their percentiles are also found as
i:€gffi A normal ferus is de-
tables at the end of the book
tectable at a gestational age of 6 weeks and 3 days, and has a
e..e€*Al rhe CRL of approximately 5 mm. At this time, the amniotic cav-
initially anechoic chorionic cavity (101) becomes surrounded ity measures 15-18 mm. As soon as the fetus (95) is visible,
by an echogenic rim of reactic endometrium (78) (Fig. 6a.1) the CRL replaces the GSD since it more accurately deter-
and is detectable after the 14th day of conception. It should mines the gestational age (within the range of a few days) up
be detectable if the serum HCG exceeds about 750-1000 to the 12th gestational week (Fig.6a3). Thereafter, mea-
U/l-otherwise an ectopic pregnancy must be excluded suring the biparietal diameter of the head (BPD) becomes
(compare p.63) more accurate (compare p. 65).
fh" iiffi is seen as echoic ring-like structure at about If a fetus is not detectable in the chorionic cavity as ex-
the 5th gestational week and increasesto 5 mm in size by the pected for gestational age, the calculation of gestational age
10th gestational week. A diameter of the yolk sac of less than should be checked first. If follow-up examination fails to
3 mm or more than 7 mm is associatedwith a higher risk of show appropriate development of the still empty chorionic
developmental anomalies.A yolk sac clearly seen within the cavity, the finding may indicate a blighted ovum without a
uterine cavity excludes an ectopic pregnancy since the yolk developing fetus, which occurs with an incidence of about 5%
of all gestations.
8 9 101112
7 +1 S D
o
o
5 E
4 ll
3
-o
(I
1
Iweeksp.c.]
0
2 3 4 5 6 7 8 I 101112
-2 SD
Y
p
(E
I
c)
E
week l
B Beginning wirh the 12th ges- lel to the midline echo of the falx (106), which is interrupted
tational week, measuring the BPD becomes feasible and in the anterior third by the cavum septi pellucidi. Cerebellum
more accurate than measuring the CRL. At this time, the or orbits should not be in the imaging plane because the
choroid plexus (104) appears bilaterally and is seen as an diameter would be measured too far inferiorly. In the same
echogenicstructure. To make the measurement reproducible imaging plane, the occipitofrontal diameter (OFD) and the
and accurate,the same reference plane (Fig. 65.1) should be head circumference (HC) can be measured as well. The re-
selected,with visualization of the entire circumference of the spective normal values can be found at the end of the book.
oval skull (105). It is important to select an orientation paral-
12 15 20 24 28 30 36 40 44
.ffi The ossified femoral diaphysis the length of the remaining tubular bones to exclude growth
(107) is easilymeasured:The upper leg (108) should be as retardation or malformation is only necessaryif the FL falls
closeas possibleto the probe and orientedlengthwise,thus outside the reference range or if the percentile changes on
perpendicularto the axisof the probe (Fig. 65.2).Measuring sequential examinations.
+2 SD
-2 S D
50
40
30
20
10
12 15 20 24 28 30 36 40 44
The reference plane The bilateral ribs should be displayed symmetrically to as-
"
(Fig. 65.3) is the level of the liver (9), possibly with visualiza- sure that the section was not obtained in an oblique plane.
tion of the dorsal third of the umbilical and portal veins (11).
300 -2 SD
259
200 =(E
I
150
o
100 E
I week ]
50
Fig.66.1b Fig.66.2b
Fig.66.3
AVHR PVHR
IlT"-"
U ,bT
--:
O
l' \ E
0,4f = *i=
l -2sD
o,2l
ft-r- tc 16 17 18 19 20 21 22
Gestationalage I weeks ]
Spina bifida consists of incomplete closure of the spinal since this will best reveal any interruption of the chain of the
,-:r:l tosether u'ith a defect in the spinal arches of varying posterior elements, including the spinous process.The trans,
:.{ree. The spine (35) is visualizedin the sagittal (Fig. 68.1) verse section (Fig. 68.3) must delineate the three ossification
.nJ coronal (Fig.68.2) plane. Subsequentlyeach vertebra is centers (35) of each segment as a triangle of closely adjacent
:;r'ieued in the transverseplane in a craniocaudaldirection structures. The fetal aorta (15) is seen anteriorlv.
In spina bifida (Fig. 68.4), both posterior ossification spina bifida occulta. The indirect sonographic signs of spina
centers are splayed laterally and the spinal canal is dorsally bifida ("banana" and "lemon" signs) have already been il-
open ('.:). Measuring the maternal serum a-fetoprotein lustrated on page 67 (refer to Figs. 67.2,67.3).
identifies only spina bifida aperta, but not the covered form.
Fig.68.4a Fig.68.4b
69
:
:
e t lt$eG*il if;:.ffisl Transverse and coronal sections of the face are usually
evaluated for decreased (hypotelorism) or increased (hypertelorism) interorbital
distance,and the sagittal sectionsfor an atypical profile. A lip-palate cleft generally
is lateral and can best be appreciated as a gap in the echogenic upper lip on the
coronal section. The normal upper lip (' , r ) appears as continuous structure
(Fig.69.1).
(Ref':Pandvaet al)
1O0T[ % 1
20 22 24 26 28 30 32 34 36 38
ageI years]
Maternal
Fi g.69.4a Fig.69.4b
7D
A small ASD or VSD as well as cardiac anomalies with (TGA) might not be apparent on the four-chamber view and
right-toJeft shunts can be definitively excluded only by it is therefore necessaryto look for crossedoutflow tracts and
citor-endeti!,,,s'eh$*6tdi,*$iatj performed by an' ex- aortic and pulmonic valves on the short axis view.
perienced examiner. Tiansposition of the great arteries
,Malformations
71
+2 SD
c
E. m
o+u
b
E -2 SD
o
!J U
o)
c
!
Yzv
(E
.E
E 10
c
Gestationalage I weeks ]
'ffi
16 20 24 28 32 36 40
Fig.71.2a Flg.71.2b Fig.71.2c
+j$W!L{t:*!;ri9r*nirii"rtri+;iirrlilieMfitriAijitstjlHrqril$x-f.:!il*rlqEr+l!!a-tti$rntlh\iqitq
Skeletal$yqtem: In the secondand third trimester, Furthermore, supernumerous phalanges can be found, such
(Fie.72.ll and Fig.72.2) are checkedfor complete as hexadactyly as seen in Figure 72.3. A polydactyly can be
developmentof 'f,6q[
the phalangealossificationcenters(121)and associatedwith shortened ribs and concomitant pulmonary
the metatarsalbones(122).In this way,syndactylyaspart of hypoplasia. Not only are the shortened ribs apparent, but
other consenitalmalformationsyndromescan be excluded. also the bell-shaoed thorax.
The search for a l$iii.$,fg,g:tanomaly should not be ne- Impaired enchondralossificationas part of i#
glected (Fi9.72.$. The clubfoot does not only appear as a ifui*iffj is frequently recognizedonly in the 3rd trimester by
club-like deformity, but also as deviated shortened tubular shortenedtubular bones and a head of disproportionately
bones. large appearence.
Fig.72.4a Fig.72.4b
TTi1,,.Glnita|s andPrenatal
Diig:norii Self-Assessment
Questi0nSr:for ;3
To conclude this section, you can again test how much detail preceding pages,the answer to the quiz image of question I is
you remember and how much still has to be memorized. The given on page 77 at the end of the book.
answersto question 1 and questions 3 to 6 can be found in the
Fig.73.2 Fig.73.3
r| Lrl-lnq
The thyr-ei.d.gf$ndtis examined with a 7.S-MHz linear trans- (89) and the more lateral sternocleidomastoid muscle (85).
rlucer. With the head slightly extended, transversesectionsof On cross section (Fig.74.2), the carotid artery (82) is some-
the entire gland are obtained or, if the entire width of the what posteromedial in location and is visualized as a round
sland cannot be encompassed, of each lobe separately noncompressible structure. In contrast, the jugular vein (83)
(Fig.74.1a). Thereafter, sagittal sections are obtained runs more anterolaterally, exhibits a typical phasic pulse and
through eacn *hgiUiti toUe iFig. 74.lbl. The trachea (84) can be compressed by applying graded (!) pressure. To
nith its air shadows in the midline and the carotid arteries i*$3F*ilhd$i**$dhei+h.$,q$jg+" di, the maximumtransverse
(82) and jugular veins (83) with their echo-free lumina later- and sagittal (anteroposterior) diameters of each lobe are
allv serve as general orientation on the transverse sections. measured on transverse sections (Fig.7a.2b). Both values
The thyroid parenchyma (81) is situated between the trachea are multiplied by the maximum length as measured on the
and the vessels.Anterior to the trachea, a thin parenchymal sagittal sections (Fig.75.3b) and are divided by two. Within
t'and .{i*{X$iiffi connects both thyroid lobes (compare an error range of approximately I}Y", the result corresponds
Fig.75.r). to the volume (in ml) of each lobe. Excluding the isthmus,
\\'ith the patient performing a Valsalva maneuver (bearing which can be ignored becauseof its small size,the volume of
down with the vocal chords closed), the jugular veins distend the thyroid gland should not exceed 25 mlin men and 20 ml
due to blocked venous drainage (Fig.74.1c). This makes in women. Small thyroid cysts (64) might not causeany distal
orientation even easier. acoustic enhancement (Fig.74.3) and must be differentiated
from hypoechoic nodules (compare p.75). Intrathyroidal
The normal S.b-l$ffi[+$, {ij (81) is slightly more vesselsare rarelv delineated.
echogenic than the anteriorly located sternohyoid muscle
Fig.74.2b Fig.74.2c
Fig.74.2a
Fig.74.3b Fig.74.3c
Fig-74.3a
azlrhvroidGland Diffuseand FocalChanges ?q
Fig.75.2a Fig.75.3a
Fig.75.4a
"" 89/90
84
I
45
II
I l-L
Fig.75.2b Fig.75.3b Ir
Fig.75.4b
76
Solution to Fig. 16.2 (question 7): Solution to Fig.22.1 (question 4): Solution to Fig.33.1 (question 6):
//r
//-
Sonographic section: sagittal section of Sonographic section: sagittal section of Sonographic section: oblique subcostal
-
the upper abdomen, paramedian over the upper abdomen at the level of the section of the right upper quadrant of
the inferior vena cava (1,6). left renal vein crossing the aorta. the abdomen.
Organs: liver (9), heart, and pancreas Vessels and structures: refer to key on Diagnosis: Focal fatty infiltration (63)
(33). the unfolded back cover. of the liver (9) and multiple hepatic
Structures:diaphragm(13), hepatic Dilatation?: no, only dilated left renal metastases (56) with hypoechoicirim.
veins (10), portal branch (1L), connec- vein due to compression between aorta Note: two episodes of metaststic
tive tissue (5), caudate lobe between 5 (15) and SMA (17), still physiologic. spreading since new and older meta-
and 16. static foci are visible!
Abnormal finding: echo-free space be- Differential diagnosis: none, the find-
tween the myocardium and diaphragm. ing is pathognomonic.
Diagnosis:pericardial eflusion (79).
Differential diagnosis: epicardial fat.
/7
45
Sonographic section: intercostal plane Sonographic section: intercostal plane Sonographic section: high section of
of the right flank in left lateral decubi- of the right flank in left lateral decubi- the left flank in the right lateral decubi-
tus position. tus position. tus position.
Organs: liver (9), renal parenchyma Organs: liver (9), abdominal oblique Organs: spleen (37), lung (47). colon
(29) with renal pelvis (3L), lung (47), vasculature (4), interstinal loop (46) (43), diaphragm (13).
abdominal oblique musculature (4), with acousticshadowing (45), renal par- Parenchyma: not normally homo-
diaphragm (13), intestinal loop (46). enchyma (29),renal pelvis (31), upper geneous,but patchy with several inter-
Diagnosis: renal cyst (64) with distal renal pole (27), lower renal pole (28). spersedhyperechoicfoci.
acoustic enhancement (70). Diagnosis: renal cell carcinoma (54), Diagnosis: multiple splenic heman-
Differential diagnosis: adrenal tumor hypoechoic tumor with space-occupy- gromas.
wi th c y s t icc om pon e n t. ing effect. Differential diagnosis: hyperechoic
Differential diagnosis: renal lym- metastases, vasculitisdue to SLE. his-
phoma, metastasis,hyperplastic column tiocytosisX.
of Bertin, hemorrhagic renal cyst.
Imaging plane: endovaginal visualiza- Sonographic Section: suprapubic longi- Sonographic Section: oblique section
tion of the uterus. tudinal (sagittal) section of the lower of the left lower quadrant of the abdo-
Diagnosis: endometrial hyperplasia abdomen. men.
(78) )8mm in a postmenopausal Organs: urinary bladder (38), uterus Organs: abdomial oblique muscles (.1).
woman without estrogen replacement (39, intestinal loop (43). colon (43).
therapy (refer to question). Diagnosis: blood clot (52) layered along Diagnosis: multilayered wall-thicken-
Recommendation: fractionated dilata- the posterior wall of the urinary blad- ing caused by colitis.
tion and curettage to exclude an endo- der. Differential Diagnosis: ischemia of the
metrial carcinoma. Differential Diagnosis: Arch artifacts intestinal wall causedby thrombosis of
(51) and reverberation echoes (51) in the mesenteric vein or occlusion of the
the anterior aspect of the urinary blad- mesenteric artery.
der; layered concrements,thickness ar-
tifacts -----+ shaking!
In preparation for the practical sections,the student should become familiar with planes propagate from the transducer
the spatial oiieafafi,on it a},br,q'e,r,.dimensig '$.p,acg,As an introduction, only two through the body.
planes that are perpendicular to each other should be considered: the vertical All sagi!,-ta!,seationsare convention-
(sagittal) plane and the horizontal (transverse) plane. As suggestedon page 4, a
ally viewed as seen from the patient's
cone coffee filter should be used to envisase how the sound waves in these two right side (Fig. 78.1b). Consequently,
the crani al aspectoI the patient is dis-
Sagittalviews:
pl ayed on the l eft and the caudal
aspect on the ir.ighf (Fig. 7S.1d).
After turning the transducer 90o
(Fig. 7$.1d), the sonographic erosp-
lsectigits, like axial CT sections, are
viewed from the patient's feet, result-
::::::r:,1i::
i ng i n an i nverted di spl a y of t he
vi sual i zed structures (Fig. 78. lc) .
W hat both secti onshave i n com m on is
that the image displays the anterior
abdominal wall, including transducer,
on the top and the posterior structures
Fig.78.1a Fig.78.1b on the bottom. This orientation con-
forms to the customary display of con-
ventional radiographs, CT, and MRI.
Standing in front of the patient, the
views:
Transversal liver, for instance, is seen on the left
though in actual fact it is on the
patient's right side.
// \..-..
)'-''-\ / \
t\
rioht / \ tett
<-*
Fig.78.1c Fig.78.1d
The next difficulty consistsof visualizingstructuresamidstacousticshadowscast If, despite every maneuver, the porta
bv intestinalair. The solutionis not the additionof more couplinggel, asthe nov- hepatis could not be visualized because
ice often believes,but a gradedincreasei" t$e$.f-b*Sqle3$,p{.[.i$$ , of meteorism or a postprandial state,
togetherwith:pfU$H.t$ieatninginstructions for the patient, explainedfurther and an attempt should be made to visualize
illustratedon the next page. tne.p-Ah_Xi:beFAtier
thortiseir (Fig.7s.2). Should this also
fail. the patient is asked to turn onto
the l ett si de and to cont inue t ur n-
ing beyond the lateral decubitus
fobition (Fig.7S.3). The liver is
pushed by its own weight against the
anterior abdominal wall and displaces
the air-containing intestinal loops
laterally. This frequently opens up the
view for the portal vein and lesser
omentum.
Fig.78.2 Fig.78.3
79
Optimal adaption of the pressure on the transducer The solution lie s in liqilt$:$slngtthe pressure. appli,ei$'tro:;*i[e]
To aroid any patient discomfort, the beginner is often reluc- transdueer (lO l), but the increase should be gradual
tant to press the transducer firmly on to the abdomen. If this rather than sudden to avoid any defense reflex or antagonis-
is the case ( J J J ), physiologic air remains in the intestinal tic reaction by the patient. By carefully displacing the intesti-
lumen (46), causing acoustic shadowing (45) that can, for in- nal air, this maneuver displaces the interfering air shadows
,stance.interfere with visualizing the posteriorly located pan- (45), and the pancreas (33) and common bile duct (66) come
,,/ creas {33) (Fig.79.la). Even the bile duct (66) or the portal into view (Fig.79.1b). The same principle can be applied to
vein (11) is frequently obscured by duodenal air or an air-dis- the mid and lower abdomen, for instance, for improving the
tended stomach. visualization of retroperitoneal lymph nodes.
Competent breathing instructions Should this approach fail, the stomach can be filled with de-
Initially, there is some reluctance to tell the patient how to gassedwater (tea), following administration of Buscopan (to
breathe during the examination, though the quality of the eliminate any peristaltic activity). This results in good sound
sonographic examination of the abdomen strongly depends transmissionthrough the stomach.The water should be taken
on the depth of the inspiratory effort necessary,for example, through a straw to avoid inadvertent swallowing of air.
to displace the liver caudally adequate for its visualization. In
Finally, the examiner can sustain the patient's cooperation
:*,e,iirxslii_l-$ffir,e.t$*l (Fig.79.3a),
not onlyarerhe
"liver and spleen obscured by the overlying lung bases,but
betterby nor ontvgivtngifi$tfw&riiit*gifui1e', suchas"take
a deep breath through your mouth and hold your breath,"
also the pancreas by an air-containing stomach (26). The low
but also by telling the patienr to exhale befoterri:,,8rd,6fig'.€
position of the liver (q) iiii:$flHtlr (Fig. 79.3b)
displacesair-containing intestinal loops and stomach (26) in- thp.ldiryot,hils,*f.fid+i;Ul-.eath (or after the desired imige has
been captured by freezing the display). This advice is not as
feriorly and opens the pancreatic region (33) for sonographic
trivial as it seemsbecausethe inexperienced examiner often
viewing. The same principle can be applied to facilitate the
fails to achieve good respiratory cooperation, thereby dis-
evaluation of the kidneys. Respiratory maneuvers rarely play
couraging the patient and further straining the patient's res-
a role in the lower abdomen.
piratory condition.
Fig.79.3a Fig.79.3b
80
This workbook is intended for physicians, technicians, and cept of teaching sonography combined with practical exer_
medical students who are new to sonography and wish to fa_ cises in small groups could not have been achieved without
miliarize themselves with the technique of ,sonographic the feedback and constructive criticism of the students and
image formation and the interpretatiorrof sonographiCim_ pyhsicians in our program and without the continuous
ages.It also takes into consideration the fact thaiminv nov_ cooperation of numerous instructors taken from the ranks of
ices generally have a limited budget for purchasing texttooks our students.I wish to thank Jorg Kambergs, Andreas Saleh"
on their chosen field. Ghazaleh Tabatabai, and Jochen Tiirk, who supported my
I therefore thank everybody who contributed to the work_ work for many years and offered valuable iuggestions
book and strived for a low production cost. The members of Furthermore, I wish to mention the willing support of the
Georg Thieme Verlag accommodated all our special requests models Simone Katzwinkel, Wolfgang Bongeri, Joana and
and.wishesconcerning the layout of the material, and accom_ Wi.irmchen Hofer for the photographs illustiating the posi_
panied and supported the progress of the workbook tioning of the probe.
at all
times. Owing to the exceptional engagement and support I am obliged to prof. U. Modder, prof. H._G. Hartwip. and
of
Dr. Liithje, Dr. Bergman, and Mr. Lehnert, the third G^"r-u., Dr. Tanja Reihs for their counsel and for providing sJveral
edition and the English translation, with Dr. Winter as trans_ cases.A special note of gratitude goes to my wife Stefanie,
lator, could be completed in a very short period of time. who advised me during the planning stage, helped train our
The
Department of Science and Research of irlorth Rhine_West_ assistants,and reviewed the manuscript.
phalia and Toshiba contributed to the printing costs,
making
the affordable price a reality. I thank the graphic artists Mrs. Susanne Kniest, and Nfrs.
,
Sabine zarges for their valuabre help in drawing an sketches
This interactive workbook is based on the experience I and diagrams, and Mr. Markus pietrek for the professional
have gathered since 1992 in Diisseldorf as head o1 the pilot photographic displays that demonstrate the handlins of rhe
project on medical didactics ,Anatomy of Imaging Modali_ Iransducer.
The pilot project is gratefully supported bylhJprogram
]igs."
*Quality
in Teaching,' conducted Uy ttre Dlpartmerit of
Science and Research of North Rhine-Westphaiia. The
con_ Diisseldorf, fall 1998 Matthias Hofer
The normal valueslisted here are subjectto individual varia- the statedstandardsections.For vessels,the inner diameter
tions and should be consideredonly as guidelines.Different of the vascularlumen is siven.without considerationof the
tables apply for children. These representativevalues were vascularwall.
takenfrom the literatureand apply only to measurements in
-dbdominal aorta luminal diameter: Ovaries volume:
5.5-10.0cm3 (each ovary.pre-
menopausal)
2.5-3.0cm = ectasia 2.5-3.5 cm3(each ovary post-
menopausal)
.{&enal glands maximal size: Pancreas size of the head:
Superiormesenteric luminaldiameter:
(with collapse during forced expiration!)
arterv
suspicious of right cardiac insufficiency
Thyroid gland
Jffi -*?*ilfilfrfr?,TTtrffi;a,ffi
nD-iffi;itrffi ffifr
HU 4.0-7.0 cm (craniocaudal)
1.0-3.0cm (transverse)
rLD ffiffi***:*3'.0"ffi1;f"' t" pr g 1.0-2.0 cm (sagiual)
distance
volume (both lobes combined):
Kklneys maximal size: < 20 ml (women)
10.0-12.0cm (lengthwise) < 25 ml (men)
4.0-6.0cm (transverse)
respiratory mobility: Urinary bladder wall thickness:
3.0-7.0cm
parenchymal width:
1.3-2.5cm postvoid residual:
Parenchym a- p y elon in dex : < 100ml
(under30 years) volume: /
1.2:1-1.6:1(31-60years) < 550 ml (women)
(above 60 years) < 750 ml (men)
Liver size in right MCL:
< 13.0cm (craniocaudal) Uterus maximal size:
< 15.0cm (dependingon body habitus) 5.0-8.0 cm longitudinal (nullipara)
marginal angle: 1.5-3.0cm width
< 30" (left hepatic lobe, lateral)
< 45'(right hepatic lobe, caudal) Volume calculation 0.5 xAxB xC
!hin*[ GBF
Bdarurerriiirs*
l*'lfeuatss @ nrieme @ tticmo
SCW(sinucortical
width): < 3 mm
CCW(craniocerebral
width) < 4m m Excetpt frum: Ercerpt.hcm:
IHW(lnterhemispheric
width) < 6m m t ltra$suEdTdeching
mHrHal Ultrffi shdT$aeftirE
ilan-ual
Width
oflateral (frontal
ventricles horn):
< 13mm ls8!t3 131110414 r$0N3 +3111041 4
-
llwm*lr*let ufirfisnis rFrbn*lal
Ultrarsnofffi y ricolpeH: jou ?
o
Estimation
of FetalWeiqhl I
o = n n n cq e? q !q c! cq c! q n I \
-.E g= ::S P K X N R SSgSS
@
g
E€ O€ 6 ON o OO@r r So @
= F ot cj ni + N ot + <t €j d Gi d +
TN N-N N OOOm
'6
-E
G
.E = q9-qo?enr?(q\eqRqc !\
Ffr6OFOQNo-ooN@OO
o
E
=
+
s
EN
It
o Q tcotpeH : leu :
E rE 96;
logFW= 1.36+ 0.05AG+ 0.18FL- 0.0037
(AGx FL) It
6 ;
6 .- F _ooo@ N N o@ oN '_s N @
€o
Ref.:
Hadl0ck
FBetal:Sonographic of{etal
estimation weight. (1984)536
Radiology d e; ; nj d d + + rj rj <t cj N N N N
5 J
FW=Fetalweight F LL
AC= Abdominal
circumference d
c\t oq c? oq c? cq q q q c\ c?
9n
t! E 3.:..t \
FL = Femur
length s
e.
- h - N N m O$ s@O@@@N N
E
:>
F=
gE o eZ
E
Kidneys:
NolmalWeight ltg 6s nqnqnqnqc?\'-=I\c q
r@'--NNooss@@@@@@
+2 SD F
TO
E
E s
; E Q.9
tct
E z €d
'6c
!
'6
o
Ct ZE
o-E $ ON Sr @@r € O@N @O ^E
! O 93 d + + rj @ @ N cj { t ot.J =
= =
>s
6
b E @
E':
>t
ffiffi?ilanda'l :o
=
O
t@@oN$@@oNs@@o
TTr-NNNNNOOmOOO
:-
9u
e' p i:'iiir":lifi!,1"ti.:::i;*.$$
A gland maximum
(Pediatric canbefoundontheback)
measurements
gland)
. Dilation venacavato > 2.0cm(2.5cm intrained
oftheinferior athletes) Adrenal dimension cm(length
oi entire
cm(thickness
<l ofeach limb)
. Dilated
hepaticvein> 6 mminthehepatic periphery present
Biliary
ducts diameter0tcommon bileduct < 0.6 cm(gallbladder andnormal)
. Absentcavalcollaosewithforced inspiration < 0.9 cm(status postcholecystectomy)
. diameterofintrahepatic
ducts < 0.4 cm
pleural
Possible initially
effusion, almostalways ontheright
Gallbladder wallthickness < 0.4 cm(postprandialupto 0.7cm)
maximum dimensions (preprandial)
< I1.0 cmlongitudinal
< 4.0 cmtransverse (preprandial)
maximum dimensions 10-12 cmbipolar length
4-6 cmwidthathilum
rangeofrespiratory
movement 3-7 cm
parenchymalthickness '1.3-2.5cm
a
Normal lumen: suprarenal < 2.5cm cortical
index 30y ears )
> 1.6:1 (under
1.2-1.6:1(31-60y ears )
a
Ectasia: 2.5-3.0 cm '1. l :1 (above60 years)
a Aneurysm: >3cm Liver craniocaudal rightmedio-
span, 15.0c m
< 13.0cm upto max i mal
progressing line
clavicular (dependingon bodyhabitus)
a Riskof rupture
increased
by: dilation marginal
angulation < 30" (lefthepaticlobe,laterally)
diameter > 6 cm < 45' (righthepatic
l0be,caudally)
excentriclumen Lymphnodes maximum
dimension <'1 cm
sacculardilation(instead Ovary volume 5.5-10.0cms(prernenopausal)
2.5- 3.5 cm3(postmenopausal)
of fusiformdilation) Pancreas APdiameter ofthehead < 3.0 cm
APdiameter ofthebody < 2.5 cm
APdiameter ofthetail < 2.5 cm
APdiameter oftheduct < 0.2 cm
gland dimensions
Prostate < 5.0x 3.0x 3,0c m
v0tume <25 ml
Spleen maximum dimensions < 11 cm (intercostal
length)
("4711" rule) < 7 cm (depth)
Demonstrationof portocaval attheportahepatis
collaterals ("4711" isa wellknown German < 4 cm (widthat hilumto outersurface)
Diameteroftheportalveinattheportahepatis> 15mm brand ofcologne water)
Dilatation
of thesplenicvein> 1.2cm bladder wallthickness
Urinary < 0.4 cm (fullbladder)
< 0.8 cm (aftervoiding)
Splenomegaly postvoid
residual < 100 ml
Demonstrationof ascites normal
volume < 550 ml (females)
(AxBxCx0.5) < 750 ml (males)
Recanalized
umbilicalvein(Cruveilhier-Baumgaften
syndrome) maximumdimensions 5 -8 cm in length(nulliparous)
Esophageal (by
varices endoscopy) 1.5-3 cm in width(nulliparous)
width
endometrial < 1smm/<8 mm (pre-/postmen0pausal)
yolksac 3.0-7.0 mm
IUD-fundus
distance <20 mm
IUD-endometrium
distance <5 mm
-F
3= = :{ :{ :{ sD I
i , No@@o
o
P P I P P St St St 9n St Sn Sn
o@N o@ @oo o No
= S@@@@ONNNNNJJJ
€
O :l
:'
o o60sNo@o5NQ@o5 0 ,
- . l
E)
= N !'r !'., N !'.) !t^) lo
ooa@NJo@@!ooa@NJo
:' :' :' :' :' :' :t
6
F
- - -
o: - d'r
E =, , GONNNNNNNJJJJ A
so so so !o I I 90 90 90 90 9o 90 90 :J : :J }l € P I 90 :{ Sn } N 99" P 9D r @ @o
ed o_
--=
!oo@No@@oo@No@@oo o o6@!s@NssaJ!obo o'
o -
= e
9d
- r
55 5 5 @@OOO@@@@@NNN t
@.. i a E --
o JO@@!OO5 6 NJO@6!
Y-
@N
trt 3:
g
o=
= @ @ o @ @ N N N N N J TJ oi -' o ,-,
l$ Is :- r. r. :' :' :' P I P I P P I So o € 5 Sd !'.r rr I 90 I
o6@oJSOOSJ!r5!
+ !..' I :J Sr P So e=E=
o
NO@\OOONO@! O O O NO @ o
-
P Sr 9n 9n Sr Ir Sh Sr Sn 9n 9n 5 5 i I i i o o =
o@@!oqSaNJo@@!oo5 a
= *
@OOOOONNNNJ.fJJ @
#'
:PS'!N:'9Pf:'SoPS!9
!@@@@oo@@@@ooo
!=
s
:K': Eft
F
#
il.
tEt'
:l *\
E;
t
:t s \\\, t
s
o
o
F
F
rl}:'
B-
-l ,\
e \\\ l\ n
O! T> tsl
o
11;
o
=o
C
-
<<
TT
E
:li \\l=' =s
4
=3 PP
no'.nr"u"
] LI
"",.' :- - x :. oo
9!
3H g.
4
= r*-
Hp s 9 6'
q6
0 ct
H fl
!!!!!!! ooooooo o <*il
++++++
oo s@NJ
++++++
oo5@NJ Ed E o=
Nc gd x6 o .:i
3 = q;
-.E E6
qq = ::ii
aN 6'
JJJJJJ@ 6 !OO 5@@
9nlSDN-Ptn
oooqoo
tn i rb ,\\b o b =:,
er o
= _ i t'
@@ @@@ @@ @@@@@ @@ g€ c
++++++ ++++++ =o
=' OO A @N J oo 5@ N J
-
- ,i";
=
-6
+ d +. +:
= O@N N NN N NNNNJJJ
sDI.r:'99o:JP
JO
i$t
? .i. l
!.o9!opo:Jsni
- o!o@o@o ooro@@!
=
o rt'
f:'
i:
?€ r .l
++++++ ++++++
;.,
3 oo 5@NJ oos@NJ
't'-
q5 55 5S5 5@ @ @ O 66 NO
- ,r:
:r !o 90 P sn | !.o :- !o po:r sh + sD l!
N@@@5 00 @ @ oN@oo F
::'