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766
GASTROINTESTINAL IMAGING

US of Right Upper Quadrant Pain

in the Emergency Department:
Diagnosing beyond Gallbladder
and Biliary Disease1
Gayatri Joshi, MD
Kevin A. Crawford, MD
Tarek N. Hanna, MD
Keith D. Herr, MD
Nirvikar Dahiya, MD
Christine O. Menias, MD
Abbreviations: ACR = American College of
Radiology, BCS = Budd-Chiari syndrome, ED =
emergency department, IVC = inferior vena
cava, MRCP = MR cholangiopancreatography,
RLL = right lower lobe, RUQ = right upper
quadrant, SLE = systemic lupus erythema-
tosus, UC = ulcerative colitis, UTI = urinary
tract infection, XGP = xanthogranulomatous
pyelonephritis
RadioGraphics 2018; 38:766–793
https://doi.org/10.1148/rg.2018170149
Content Codes:
1
From the Department of Radiology and Im-
aging Sciences (G.J., K.A.C., T.N.H., K.D.H.)
and Department of Emergency Medicine (G.J.,
T.N.H., K.D.H.), Emory University School
of Medicine, 550 Peachtree St, Atlanta, GA
30308; and Department of Radiology, Mayo
Clinic, Scottsdale, Ariz (N.D., C.O.M.). Recipi-
ent of a Certificate of Merit award for an educa-
tion exhibit at the 2016 RSNA Annual Meeting.
Received May 29, 2017; revision requested Au-
gust 8 and received January 29, 2018; accepted
February 2. For this journal-based SA-CME
activity, the author T.N.H. has provided disclo-
sures (see end of article); all other authors, the
editor, and the reviewers have disclosed no rel-
evant relationships. Address correspondence
to G.J. (e-mail: gayatri.joshi.md@gmail.com).
©
RSNA, 2018
SA-CME LEARNING OBJECTIVES
Acute cholecystitis is the most common diagnosable cause for right
upper quadrant abdominal (RUQ) pain in patients who present
to the emergency department (ED). However, over one-third of
patients initially thought to have acute cholecystitis actually have
RUQ pain attributable to other causes. Ultrasonography (US) is the
primary imaging modality of choice for initial imaging assessment
and serves as a fast, cost-effective, and dynamic modality to provide
a definitive diagnosis or a considerably narrowed list of differen-
tial possibilities. Multiple organ systems are included at standard
RUQ US, and a variety of ultrasonographically diagnosable disease
processes can be identified, including conditions of hepatic, pancre-
atic, adrenal, renal, gastrointestinal, vascular, and thoracic origin,
all of which may result in RUQ pain. In certain cases, subsequent
computed tomography, magnetic resonance (MR) imaging, MR
cholangiopancreatography, or cholescintigraphy may be considered,
depending on the clinical situation and US findings. Familiarity
with the spectrum of disease processes outside of the gallbladder
and biliary tree that may manifest with RUQ pain and recognition
at US of these alternative conditions is pivotal for early diagnosis
and appropriate management. Diagnosis at the time of initial US
can reduce unnecessary imaging and its consequences, including ex-
cess cost, radiation exposure, nephrotoxic contrast medium use, and
time to diagnosis, thereby translating into improved patient care and
outcome. This article (a) reviews the causes of RUQ pain identifiable
at US using an organ-system approach, (b) illustrates the US appear-
ance of select conditions from each organ system with multimodality
imaging correlates, and (c) discusses the relevant pathophysiol-
ogy and treatment of these entities to aid in efficient direction of
management.
Online supplemental material is available for this article.
©
RSNA, 2018 • radiographics.rsna.org

After completing this journal-based SA-CME

activity, participants will be able to:
■■List the causes of RUQ pain that are
identifiable at RUQ US using an organ- Introduction
system approach. Ultrasonography (US) is the primary imaging modality of choice for
■■Recognize the differentiating clinical initial assessment of acute right upper quadrant abdominal (RUQ)
and imaging features of each condition,
including complicating features.
pain, particularly in the emergency department (ED) setting (1,2).
The American College of Radiology (ACR) Appropriateness Criteria
■■Discuss the relevant pathophysiology
and next appropriate steps in manage- for US have a rating of 9 (out of 9) in patients with appropriate clini-
ment for patients with an identifiable cal indications (1,2). There are a variety of differential considerations
cause of RUQ pain at US who present for RUQ pain, and US is a fast cost-effective real-time dynamic mo-
to the ED.
dality, which does not use ionizing radiation or nephrotoxic intrave-
See www.rsna.org/education/search/RG. nous contrast medium and provides a definitive diagnosis or at least
a considerably narrowed list of differential possibilities.
An earlier incorrect version of this
article appeared online. This article
was corrected on Sept 12, 2018.
RG  •  Volume 38  Number 3 Joshi et al  767
TEACHING POINTS
■■ Overwhelmingly, gallbladder or biliary conditions, particularly
cholecystitis and choledocholithiasis, are the clinically suspect-
ed culprits for RUQ pain. However, although acute cholecys-
titis is the most common diagnosable cause for RUQ pain in
patients presenting to the ED, over one-third of patients have
RUQ pain attributable to other causes.
■■ In many cases, RUQ pain attributable to the liver is related to
liver capsular distention, which can be caused by inflamma-
tion, edema, and/or mass effect from a variety of underlying
causes.
■■ A pyogenic liver abscess can be caused by hematogenous
inoculation through the portal vein from a gastrointestinal
process, such as diverticulitis or appendicitis, or through the
hepatic artery in the setting of systemic infection, such as
sepsis or endocarditis. Direct extension of infection can occur
from infection of adjacent structures, such as RLL pneumonia.
Other routes of infection include ascending cholangitis and
direct inoculation, such as from penetrating trauma or an in-
vasive procedure.
■■ Pyelonephritis most commonly results from ascending UTI in
which the causative organism spreads from the urinary blad-
der into the upper urinary tract. This can occur in the absence
of reflux and is thought to be due to relative functional ob-
struction caused by bacterial endotoxins that inhibit ureteral
peristalsis.
■■ RLL parenchymal and pleural conditions, including pneu-
monia, infarction related to pulmonary embolism, pleural
effusion, and neoplasm involving the pleura and chest wall,
can result in pleuritis and RUQ pain. An intercostal imaging
approach is often required to visualize regions of the thorax
and thoracoabdominal junction, which may otherwise be
obscured owing to rib shadowing artifact. This is particularly
the case in patients who cannot tolerate large inspiration and
breath holding and consequently may have a greater portion
of the lung base and upper abdominal structures surrounded
by the ribcage.
Overwhelmingly, gallbladder or biliary condi-
tions, particularly cholecystitis and choledocho-
lithiasis, are the clinically suspected culprits for
RUQ pain. However, although acute cholecys-
titis is the most common diagnosable cause for
RUQ pain in patients presenting to the ED, over
one-third of patients have RUQ pain attribut-
able to other causes (3). Multiple organ systems
are included at standard RUQ US, and a variety
of disease processes that are diagnosable at US
can be identified, including hepatic, pancreatic,
adrenal, renal, gastrointestinal, vascular, and tho-
racic conditions, all of which may manifest with
RUQ pain (Table 1). Therefore, familiarity with
the spectrum of disease processes outside of the
gallbladder and biliary tree that may manifest with
RUQ pain and US recognition of these alternative
causes is pivotal for early accurate diagnosis and
efficient appropriate management.
Early accurate diagnosis is particularly critical
for those conditions that require timely interven-
tion such as pyonephrosis and appendicitis, among
others. In some cases, subsequent computed
tomography (CT), magnetic resonance (MR)
imaging including MR cholangiopancreatography
(MRCP), or cholescintigraphy may be considered
as the next appropriate management, depending
on the clinical situation and US findings (Fig 1).
US Evaluation of RUQ Pain
The standard RUQ US examination includes
dedicated evaluation of the liver, gallbladder,
intra- and extrahepatic biliary ducts, pancreas,
right kidney, and vasculature, with standard im-
ages that should be obtained from each of these
organs as part of every RUQ US examination
(Table 2). Obtaining additional images beyond
the standard protocol may be required for full as-
sessment of RUQ pain, tailored to the individual
patient and based on the patient’s clinical pre-
sentation, the clinical findings, and findings on
standard RUQ US images.
Several additional structures are within the
field of view of the standard RUQ US protocol
that may be the source of RUQ pain. For ex-
ample, real-time assessment can be performed of
the right lung base and right pleural space (when
evaluating the hepatic dome); the right adrenal
gland (when assessing the hepatorenal interface);
the hepatic flexure, right colon, and appendix
(when assessing the inferior margin of the liver
and right kidney); the stomach and duodenum
(when assessing the hepatic hilum and pancreas);
and the branches of the aorta (when assessing the
upper abdominal aorta). Additional images can
be obtained as appropriate if abnormalities are
identified within the field of view when perform-
ing the standard protocol for RUQ US (Fig 2).
During US assessment of the liver (Fig 2a),
if the patient can tolerate deep inspiration and
breath-hold instructions, a subcostal approach
may allow for near-full visualization of the liver. If
an intercostal approach is required to assess por-
tions of the liver above the costal margin, the US
probe should be placed in the intercostal space
and aligned parallel to the course of the ribs in an
oblique fashion. At each intercostal space, the US
probe should be angled upward and downward to
visualize the liver parenchyma above and below
each rib until the full liver is visualized.
Assessment for abnormal liver parenchymal
echogenicity and echotexture, liver surface
nodularity, mass lesions, abnormalities of the in-
tra- and extrahepatic ducts, and abnormalities of
the intrahepatic vessels are among the items to
include during an assessment of this region (4).
Attention to the right lung base and the right
pleural space can identify intrathoracic causes
of RUQ pain (Table 1, Fig 2a). US assessment
of the gallbladder (Fig 2a) includes evaluation
of gallbladder shape, size, wall, and intraluminal
768  May-June 2018 radiographics.rsna.org

and extraluminal abnormalities. Assessment

Table 1: Sonographically Identifiable Differ-
should be performed in at least two different pa- ential Diagnosis Considerations for RUQ Pain
tient positions (supine, left lateral decubitus, up-
right, or prone). The presence of maximal inten- Adrenal
sity pain on graded pressure with the transducer Adrenal hemorrhage
(sonographic Murphy sign) must be evaluated Adrenal mass (benign, malignant)
(4). US evaluation of the pancreas (Fig 2a) in- Gallbladder/biliary
cludes assessment of pancreatic shape, size, and Acute cholecystitis
Chronic cholecystitis
echogenicity. Observation for pancreatic ductal
Cholelithiasis
dilatation, parenchymal abnormalities (includ-
Acalculous cholecystitis
ing mass lesions), and peripancreatic collections Gallbladder torsion
or masses should be performed. Assessment of Gallbladder carcinoma/metastasis
the patency of the portosplenic confluence and Postcholecystectomy complications
abnormalities of the stomach and duodenum Choledocholithiasis
can be performed when assessing the pancreas Mirizzi syndrome
(Fig 2a) (4). During assessment of the aorta, the Cholangitis
celiac artery and superior mesenteric artery can Biliary necrosis
be observed. Cholangiocarcinoma
Gastrointestinal
Hepatic Causes of RUQ Pain Subhepatic appendicitis
Abnormalities intrinsic to the liver, including acute Hepatic flexure colitis
hepatitis, hepatic steatosis with hepatomegaly and Bowel obstruction
Perforated viscus
capsular distention, hepatic abscess, and hepatic
Gastrointestinal neoplasm
neoplasm, without or with intratumoral hemor-
Bowel ischemia
rhage, can all result in RUQ pain and can mimic Gastritis
gallbladder or biliary causes of pain clinically. In Peptic ulcer disease
many cases, RUQ pain attributable to the liver is Hepatic
related to liver capsular distention, which can be Hepatic steatosis
caused by inflammation, edema, and/or mass effect Acute hepatitis
from a variety of underlying causes. Benign and ma- Liver abscess
lignant neoplasms without associated hemorrhage Liver neoplasm without or with tumoral hemor-
can cause capsular distention if large or subcapsular rhage (hepatocellular adenoma, hepatocellular
in location. A complication of tumoral hemor- carcinoma, metastases)
rhage can cause acute RUQ pain from hematoma- Pancreatic
related liver capsule (Glisson capsule) distention or Pancreatic neoplasm
rupture. Pancreatitis
Thoracic
Acute Hepatitis Right lower lobe (RLL) pneumonia
Acute inflammation of the liver parenchyma can Right lung base pulmonary infarct
result from a variety of underlying causes, includ- Chest wall mass
ing viral, parasitic, or bacterial infections, drug Pleural effusion
reaction, ischemia, and autoimmune dysfunction. Urologic
Acute hepatitis is ultimately a clinical diagnosis, Obstructive urolithiasis
and normal appearance of the liver at imaging Acute bacterial pyelonephritis
Pyonephrosis
does not exclude acute hepatitis (5).
Emphysematous pyelonephritis
With acute liver inflammation, the liver en- Renal abscess
larges, causing distention of the liver capsule, Subcasular hematoma secondary to hemor-
which may manifest as acute RUQ pain. Hepato- rhagic neoplasm (angiomyolipoma, renal cell
megaly may be the most sensitive finding at US carcinoma)
and can be identified with hepatic length exceed- Ruptured renal cyst
ing 15.5 cm in the midclavicular line or extension Vascular
of the right hepatic lobe inferior to the lower renal Portal vein thrombosis (bland and malignant)
pole in the setting of a normal-sized left lobe (6,7). Budd-Chiari syndrome (BCS)
Decreased hepatic echogenicity, thickening of the Hepatic artery compromise
walls of the portal veins (Fig 3a), and secondary
gallbladder wall thickening (Fig 3b) may also be
seen with hepatic inflammation (8). The “starry
sky” appearance of conspicuous portal triads on
RG  •  Volume 38  Number 3 Joshi et al  769

Figure 1.  Algorithm for the im-

aging workup of patients who
present to the ED with RUQ pain
(1). AC = acute cholecystitis.

Table 2. Imaging Protocol for Standard RUQ US*

Liver
Gray-scale transverse and longitudinal US images through the right hepatic lobe, left hepatic
lobe, and caudate lobe
Gray-scale US images through the hepatic dome to include the right diaphragm and pleural
space
Gallbladder
Gray-scale transverse and longitudinal US images through the gallbladder, evaluated in at
least two different patient positions
Gray-scale transverse US image of the gallbladder, with measurement of gallbladder wall
thickness
Assessment for a sonographic Murphy sign
Biliary tract
Gray-scale and color Doppler† longitudinal US images of the common bile duct, without
and with measurement of diameter in the proximal, mid-, and distal aspects
Color Doppler US† images of the right and left hepatic lobes to assess for intrahepatic bili-
ary ductal dilatation
Pancreas
Gray-scale transverse and longitudinal US images through the pancreatic head, uncinate pro-
cess, body, and tail, as visible
Right kidney
Gray-scale longitudinal US image without and with measurement of renal length
Gray-scale transverse US images through the upper, mid-, and lower poles
Color Doppler US image at the renal hilum‡
Vasculature
Gray-scale transverse and longitudinal US images of the aorta and inferior vena cava (IVC)
Gray-scale transverse and longitudinal images of the hepatic veins and main portal vein
Color Doppler US image to assess the patency of the portosplenic confluence
*Required images at a standard RUQ US examination. Additional images should be obtained if
abnormalities are found during acquisition of these standard protocol images.
†Color Doppler US may be used to differentiate hepatic arteries and portal veins from bile ducts.
‡Color Doppler US is used to differentiate between prominent hilar vessels and the collect-
ing system.

a background of hypoechoic edematous liver pa- US, CT, and MR imaging findings may
renchyma is often attributed to acute hepatitis, but include hepatomegaly, periportal edema, and
this sign has been shown to be neither sensitive periportal lymphadenopathy (9). Laboratory
nor specific (7). findings that support the clinical and imaging
770  May-June 2018 radiographics.rsna.org

Figure 2.  (a) Photograph shows the topographic regions for US assessment of the liver (gray oval 1), gallbladder (gray
oval 2), and pancreas and epigastric region (gray oval 3). Assessment of the intrahepatic biliary tree and intrahepatic
hepatic vasculature is also performed in the topographic region of the liver (gray oval 1). Assessment of the portal struc-
tures is performed at the confluence of these three regions. (b–d) Photographs show the topographic regions for US
assessment of the right kidney (gray oval 4) and the right pleural space and right lung base (gray oval 5). Assessment
for abnormalities of the right adrenal gland can be performed in real time while observing the hepatorenal interface (the
superior margin of gray oval 4) and by progressively moving the US probe medially in the longitudinal plane, obtaining
images as clinically warranted. (e) Photograph shows the topographic regions for US assessment of the IVC (gray oval
5a) and the aorta (gray oval 5b). Assessment for abnormalities of the celiac artery and superior mesenteric artery and
their respective branches can also be performed when viewing the aorta while obtaining additional nonstandard images,
if clinically appropriate. (f) Photograph shows the topographic region for US assessment of the hepatic flexure (gray oval
6) and right colon (gray oval 7). The appendix, if abnormal, can also be located in these regions. While dedicated assess-
ment of these structures is not part of the standard RUQ US, these regions can be observed in real time while assessing
the inferior margin of the liver, the right kidney, and the hepatorenal interface. If clinically warranted, image acquisition
of the bowel in these regions can be performed. Likewise, an assessment of the urinary bladder (gray oval 8) is not part
of the standard RUQ US protocol; however, focused assessment can be performed if an upstream urologic condition is
identified, including assessment for distal ureteral and bladder calculi, presence of right ureteral jet, signs of urinary tract
infection (UTI), and bladder wall abnormalities.

diagnosis of acute hepatitis include elevated
aspartate aminotransferase, alanine aminotrans-
ferase, and g-glutamyl transferase levels and
hypoalbuminemia (10).
Liver Abscess
Liver abscess, the most common type of visceral
abscess (11), can be categorized as pyogenic or
parasitic and cause RUQ pain with positive US
findings. Pyogenic abscesses can be caused by
bacterial or fungal organisms, and knowledge of
the patient’s medical history, risk factors, and
presentation are helpful in making the correct
diagnosis. Early diagnosis followed by timely in-
tervention has been reported to decrease mortal-
ity from 65% to 2%–12% (11).
Pyogenic Abscess.—A pyogenic liver abscess can be
caused by hematogenous inoculation through the
portal vein from a gastrointestinal process, such as
diverticulitis or appendicitis, or through the hepatic
artery in the setting of systemic infection, such as
sepsis or endocarditis. Direct extension of infection
can occur from infection of adjacent structures,
such as right lower lobe (RLL) pneumonia. Other
routes of infection include ascending cholangitis
and direct inoculation, such as from penetrating
trauma or an invasive procedure (11).
Most pyogenic abscesses in North America are
polymicrobial, with Escherichia coli and Klebsiella
pneumoniae being the most common offending
agents in all patients (11). Pure fungal or mixed
fungal and bacterial abscesses occur with greater
RG  •  Volume 38  Number 3 Joshi et al  771

Figure 3.  Acute hepatitis and liver failure secondary to cocaine-related vascular compromise in a
34-year-old woman with a history of polysubstance use who presented to the ED with worsening RUQ
pain for 2 days. Laboratory studies show markedly elevated liver enzyme and bilirubin levels and evidence
of cocaine use. (a) Transverse gray-scale US image through the porta hepatis shows thickening of the
walls (arrows) of the right, left, and main portal veins, with increased prominence of the portal triads
within the edematous hypoechoic liver. (b) Transverse gray-scale US image through the gallbladder
shows marked gallbladder wall thickening (arrow) due to hepatic dysfunction, notably without distention
or the presence of gallstones to suggest acute intrinsic gallbladder inflammation.

frequency in immunocompromised patients, such A search for an underlying biliary cause is

as those with malignancy or human immunode-
ficiency virus (HIV) infection (12). No source
is detected in approximately 50% of cases, and
blood cultures are positive in only 50% of cases
(11). A solitary abscess is often cryptogenic. Mul-
tiple abscesses suggest hematogenous dissemina-
tion through the portal vein or hepatic artery or
ascending cholangitis (5).
Clinical presentations of hepatic abscesses
vary. Fever (70%–90% of patients) and RUQ
pain (50%–75%) can mimic acute gallblad-
der disease (11). Alternatively, vague, indolent,
and constitutional symptoms or even a relative
absence of symptoms may be seen (5). Biochemi-
cal aberrations of the liver are nonspecific in the
setting of hepatic abscesses; however, elevations
of aspartate aminotransferase, alanine amino-
transferase, and total bilirubin levels and hypoal-
buminemia commonly manifest (5).
US and CT are 85% and 97% sensitive, respec-
tively, for detecting pyogenic liver abscesses (11).
The size, number, and location of pyogenic hepatic
abscesses can affect US sensitivity, with a smaller
solitary abscess in hepatic segment VIII having the
lowest overall sensitivity for diagnosis (13). Micro-
abscesses typically appear as hypoechoic nodules at
US, which may be distinct, ill defined, or conflu-
ent. Larger abscesses can have either increased
or decreased echogenicity and may have internal
debris and foci of gas (5). Abscesses may be single
nonloculated collections, single multiloculated col-
lections with echogenic internal septa and debris
(Fig 4a), solid or partially solid in appearance, or
may have multifocal involvement in the liver (5,11).
crucial, as obstructing biliary stones or a tumor
can result in cholangitis and peribiliary abscesses.
Some abscesses can be difficult to differentiate
from a solid necrotic neoplasm (11). However,
the presence of increased through transmission
suggests a cystic lesion with internal debris rather
than a necrotic albeit otherwise cystic-appearing
mass. Peripheral and septal blood flow may be
visualized at color Doppler US. However, the
debris-filled cavity itself remains avascular. Con-
trast material–enhanced CT may show a multiloc-
ulated cystic mass with surrounding parenchymal
edema. Aggregation of low-attenuating locules into
a single larger abscess cavity produces the “cluster
sign” (Fig 4b). MR imaging usually demonstrates
central T1 hypointensity and T2 hyperintensity,
although the internal T1 and T2 signal intensities
can vary with protein content (11).
Parasitic Abscess.—An amebic abscess, caused
by the parasite Entamoeba histolytica, is an ex-
traintestinal complication of amebiasis. Infection
is endemic in Central and South America, Africa,
and portions of Asia (11). E histolytica spreads
hematogenously through the portal vein from the
colon (5). Patients with an amebic abscess are
usually adult men who present with fever, RUQ
pain, and cough (11). Imaging findings may be
similar to those of pyogenic abscesses. However, a
history of recent travel to endemic areas accom-
panied by supporting laboratory values, including
mild elevation of total bilirubin and aminotrans-
ferase levels and hypoalbuminemia, can help to
establish the diagnosis (5).
772  May-June 2018 radiographics.rsna.org

Figure 4.  Pyogenic liver abscess in a 62-year-old man who presented to the ED with RUQ pain, fever,
and leukocytosis. (a) Longitudinal color Doppler US image through the liver shows a heterogeneous mul-
tiloculated intraparenchymal lesion (*), with echogenic internal septa and debris and prominent through-
transmission (arrows). Peripheral and septal blood flow is seen, but there is no internal blood flow in the
loculations. (b) Corresponding sagittal contrast-enhanced CT image shows a multiloculated abscess (*),
producing the cluster sign. Histologic analysis confirmed the presence of polymicrobial agents, including
E coli, the most common offending agent.

Typical US features of amebic abscess include
a homogeneously hypoechoic lesion with internal
echoes and an imperceptible wall and increased
through transmission. At contrast-enhanced
CT, an amebic abscess will appear as a round
fluid-attenuating lesion with rim enhancement
and surrounding edema (5,11). Internal septa
and a fluid-debris level are frequently associated
features (5). Extrahepatic extension is relatively
common (11). MR imaging demonstrates a le-
sion with low T1 and high T2 signal intensities;
perilesional edema may also be identified.
The tapeworm Echinococcus granulosus is the
most commonly implicated organism in echino-
coccal, or hydatid, disease (11,14). Patients are
infected by ingesting tapeworm eggs, and the
liver is the most common organ involved (11).
The clinical manifestation of hepatic echinococ-
cal disease varies widely, ranging from the absence
of symptoms to the presence of jaundice, severe
RUQ pain, a palpable RUQ mass, and anaphylaxis
(11). The US appearance depends on the stage of
disease and can range from an anechoic unilocular
cyst with a nearly imperceptible wall to a multi-
septated cyst with a hyperechoic wall containing
daughter cysts (11). At later stages, a partially or
completely calcified wall may be formed.
Nontraumatic Hemorrhagic
Hepatic Lesions
The most common hepatic tumors that manifest
with spontaneous nontraumatic hemorrhage are
hepatocellular adenomas and hepatocellular car-
cinomas. Rarely, hemorrhage can occur in focal
nodular hyperplasia, giant hemangiomas, peliosis,
and metastatic lesions. Other systemic causes of
hepatic hemorrhage in the absence of trauma or
anticoagulation include hemolysis, elevated liver
enzymes, and low platelet count (HELLP) syn-
drome or amyloidosis (15).
Hemorrhagic Hepatocellular Adenoma.—He-
patocellular adenomas (also known as hepatic
adenomas) are most commonly diagnosed in
women of childbearing age, often in the setting
of oral contraceptive use (3,16). Other high-risk
groups include patients with a history of andro-
gen-containing steroid use, iron overload second-
ary to b-thalassemia, and type 1 glycogen storage
disease, irrespective of sex (3,15). Adenomas may
be solitary (80%) or multiple (20%) and may be
clinically silent (15), particularly if they are small
or deep relative to the liver capsule, with inter-
vening liver parenchyma between the lesion and
liver surface. However, spontaneous hemorrhage
can occur, particularly in the setting of multiple
or large adenomas (3). A subcapsular location
results in RUQ pain due to capsular distention
and also increases the risk of massive hemoperi-
toneum due to large-volume hemorrhage into the
peritoneal cavity on capsular rupture (3).
Nonhemorrhagic adenomas may appear
hyperechoic at US owing to their relatively high
internal lipid content. Hemorrhagic adenoma, in
contradistinction, may appear heterogeneously
hypoechoic, with internal hyperechoic areas, or
RG  •  Volume 38  Number 3 Joshi et al  773

Figure 5.  Hemorrhagic hepatocellular adenoma with hemoperitoneum in a 34-year-old woman who presented to the ED with acute
RUQ pain. (a) Transverse gray-scale US image of the RUQ shows a relatively well-circumscribed heterogeneous liver mass (dotted circle),
with areas of hyper- and hypoechogenicity, signifying internal hemorrhage within an intrinsically hyperechoic hepatocellular adenoma.
(b) Transverse color Doppler US image shows prominent vessels at the periphery of the hepatocellular adenoma. (c) Longitudinal trans-
vaginal US image obtained at the same time shows complex free fluid with diffuse uniform echoes (*) adjacent to the uterus, signifying
hemoperitoneum extending into the pelvis. (d) Subsequent axial late-arterial contrast-enhanced CT image obtained during the same ED
visit shows a corresponding arterially enhancing heterogeneous intraparenchymal lesion (arrow) within the right hepatic lobe. Washout
was seen at a more delayed phase (not shown).

as a hyperechoic mass associated with fluid and
internal echoes, signifying intratumoral hemor-
rhage at gray-scale US (Fig 5a). Subcapsular he-
matoma and intraperitoneal hemorrhage can be
seen, particularly with hemorrhagic juxtacapsular
lesions, most commonly appearing as free fluid
with diffuse internal echoes (Fig 5c).
Color Doppler US may reveal prominent ves-
sels at the periphery of the mass (Fig 5b) (15).
Multiphase CT is often subsequently performed,
especially if there is concern for hepatocellular
adenoma rupture. At contrast-enhanced CT and
MR imaging, adenomas are usually well circum-
scribed with arterial enhancement (Fig 5d) and
washout in subsequent phases (15,16). At nonen-
hanced CT, hemorrhagic adenoma is suggested
by intratumoral hyperattenuation with adjacent
subcapsular hematoma or high-attenuation free
intraperitoneal fluid, particularly in high-risk
individuals such as a pregnant patient or a patient
taking oral contraceptives (15).
Hemorrhagic Hepatocellular Carcinoma.— Hem-
orrhagic hepatocellular carcinoma (HCC) is a
primary epithelial liver malignancy, with increasing
prevalence worldwide and in the United States
(15,17). Eighty percent of HCCs develop in
patients with cirrhosis. In individuals with cirrhosis,
annual HCC incidence ranges from 2% to 8% (17).
A ruptured HCC is a surgical emergency with
a high mortality rate. In endemic areas of Asia and
Africa, rupture occurs in approximately 7%–14%
of cases and is the most common cause of spon-
taneous nontraumatic acute hemoperitoneum in
male patients (15). By comparison, the prevalence
of ruptured HCC in western countries has been
reported to be less than 3%. This difference has
been attributed to a lower prevalence of hepatitis
B and C as compared to the Asian and African
populations, although differences in reporting may
also account for this apparent disparity (18).
When intratumoral hemorrhage occurs, bleeding
initially may be relatively minor, but it can progress
774  May-June 2018 radiographics.rsna.org

Figure 6.  Gallstone pancreatitis in a 25-year-old woman who

presented to the ED with RUQ pain. (a) Transverse gray-scale
US image shows a mildly edematous pancreas with an irregu-
lar indistinct ventral margin and hypoechoic peripancreatic
fluid (*). (b) Transverse gray-scale US image of the gallbladder
shows layering echogenic gallstones (arrow). (c) Axial contrast-
enhanced CT image shows fluid along the anterior margin of
the pancreas (arrow), with inflammatory stranding extending
into the perirenal fat (arrowheads).

to subcapsular hemorrhage and finally rupture
through the liver capsule and into the peritoneal
cavity. The acute distention of the liver capsule ac-
counts for associated epigastric or RUQ pain (15).
On US images, intratumoral bleeding may
appear as a complex mass, with cystic and solid
elements and variable echogenicity, depending on
the age of intratumoral blood products. Capsular
rupture results in free intraperitoneal fluid, most
commonly complex free fluid in the acute set-
ting, although notably, anechoic fluid can reflect
hyperacute blood from active hemorrhage.
Pancreatic Causes of RUQ Pain
Patients with pancreatic conditions classically
present with epigastric pain radiating to the back,
but they can present with RUQ pain as well (19).
CT, MR imaging, and endoscopic US are the tradi-
tional modalities of choice for dedicated pancreatic
imaging, but patients with nonspecific RUQ pain
are often initially imaged with RUQ US, which also
may reveal a range of pancreatic conditions (20).
Acute Pancreatitis
Acute inflammation of the pancreas is usually at-
tributable to obstructing gallstones, alcohol use, and
the use of certain drugs such as steroids and sulfa-
containing medications. Still, many cases are idio-
pathic. The reported prevalence of US abnormali-
ties in acute pancreatitis ranges from 33% to 90%
(21) and includes peripancreatic inflammation,
heterogeneous pancreatic parenchyma, decreased
gland echogenicity, indistinct ventral pancreatic
margin, and gland enlargement (Fig 6a) (21,22).
The diagnosis of acute pancreatitis at US is
complicated both by findings that change over the
course of the disease and the relatively subjective
nature of certain findings, in particular the fea-
tures of parenchymal heterogeneity and indistinct-
ness of the ventral margin (21–23). The pancreas
should be the most echogenic solid intra-abdom-
inal organ, and pancreatic hypoechogenicity can
be a useful indicator of pancreatitis. However, this
parameter should be used with caution, as the
same population of patients with pancreatitis tend
to have echogenic liver parenchyma due to hepatic
steatosis, confounding the relative assessment of
pancreatic echogenicity (21).
When pancreatitis is identified, careful US
evaluation for gallstones and choledocholithiasis
should be performed (Fig 6b), since over 25% of
gallstones are occult at CT in comparison with
those seen at US (21,24). Subsequent CT is not
required for diagnosis, but it can be performed in
RG  •  Volume 38  Number 3 Joshi et al  775

Figure 7.  Pancreatic adenocarcinoma in a 48-year-old man

who presented with epigastric and RUQ pain. (a) Transverse
color Doppler US image shows a hypoechoic lesion (*) in the
pancreatic body, without appreciable internal blood flow. The
lesion exerts mass effect on the portosplenic confluence (ar-
row). (b) Axial contrast-enhanced fat-saturated T1-weighted
MR image shows a low-signal-intensity mass (*) in the pan-
creatic body, with upstream dilatation of the main pancreatic
duct (arrow) and pancreatic parenchymal atrophy within the
upstream pancreatic tail. (c) Coronal maximum intensity pro-
jection MRCP image shows the dilated main pancreatic duct
in the pancreatic tail (arrow), with abrupt cutoff in the pan-
creatic body at the site of the obstructing pancreatic mass
(arrowhead).

situations of diagnostic uncertainty (eg, to exclude
alternative diagnoses), in patients who develop or-
gan failure or other clinical or laboratory features
of severe pancreatitis, and to evaluate for compli-
cations (eg, necrosis, peripancreatic collections
[Fig 6c], and mesenteric vein thrombosis) (25).
Pancreatic Cysts and Neoplasms
Pancreatic cysts may be benign or malignant,
increase in frequency with age, and are often
incidental (26). These are asymptomatic in 70%
of patients, but they may manifest with abdomi-
nal or back pain (26). Cysts associated with pain
have a greater likelihood of malignant or prema-
lignant conditions (26,27). Acute presentations
may arise with internal spontaneous hemorrhage,
superimposed infection, obstructive pancreatitis,
or biliary colic related to pancreatic head lesions
with mass effect on the distal common bile duct.
Pancreatic neoplasms may be solid or cystic.
Solid lesions include pancreatic adenocarcinoma,
pancreatic neuroendocrine tumors, solid pseu-
dopapillary tumor, pancreatic lymphoma, and
metastases (28). Cystic neoplasms include serous
cystadenoma, mucinous cystic neoplasm, and
intraductal papillary mucinous neoplasm (29).
Pancreatic adenocarcinomas are the fourth leading
cause of death from malignancy in adults, with the
majority of symptomatic tumors occurring in the
pancreatic head (20). The typical manifestation is
pain and jaundice owing to simultaneous pancre-
atic and common bile ductal obstruction (20).
US findings vary based on the type and loca-
tion of the lesion. Pancreatic adenocarcinomas
are usually depicted as a hypoechoic hypovas-
cular mass with mass effect on the surrounding
structures, including the portosplenic venous
confluence, common bile duct, and main pancre-
atic duct (Fig 7). If a previously unknown solid
or cystic pancreatic neoplasm is identified at ab-
dominal US, MR imaging with MRCP sequences
should be performed for a more comprehensive
imaging evaluation.
Gastrointestinal Causes
of RUQ Pain
US is often underused in the diagnosis of gastro-
intestinal conditions; its potential for detecting
disease of the stomach and bowel is often un-
derestimated owing to diminished confidence in
inexperienced investigators, commonly owing to
concern for nonvisualization due to bowel gas or
nonspecific nature of bowel wall thickening when
visualized. However, when used as a directed
imaging tool, US can have excellent diagnostic
results. A variety of conditions that cause RUQ
776  May-June 2018 radiographics.rsna.org

Figure 8.  Subhepatic acute appendicitis in an 8-year-old boy with RUQ pain, nausea, fever, and leukocytosis. (a) Longitudinal
gray-scale US image shows a blind-ending fluid-filled tubular structure with bowel architecture (dotted oval), located adjacent to
the inferior tip of hepatic segment VI (*), consistent with an inflamed subhepatic appendix. (b, c) Transverse gray-scale images
without (b) and with (c) transducer pressure show noncompressibility and a targetoid appearance of the appendix.

pain can be identified at US, including gastro-
intestinal neoplasm, bowel obstruction, bowel
perforation, subhepatic appendicitis, and hepatic
flexure colitis of varying causes.
Subhepatic Appendicitis
Appendicitis has a prevalence of approximately
14% in patients presenting to the ED with abdom-
inal pain (30). Although the typical presentation
involves visceral periumbilical pain followed by
migration to the right lower quadrant, appendicitis
can localize to the RUQ in cases with subhepatic
location of the inflamed appendix, which can oc-
cur as normal anatomy (such as with high-riding
cecum or retrocecal appendix), in patients with
altered anatomy (eg, in the setting of prior abdom-
inal surgery), and in pregnant patients (owing to
displacement from the gravid uterus) (30).
Acute appendicitis is the most common surgi-
cal emergency during pregnancy. Imaging may be
especially important in the workup of abdominal
pain in a pregnant patient, as clinical evaluation
poses a unique challenge due to difficult physical
examination, altered anatomy, physiologic leu-
kocytosis, and atypical presentation. Progressive
cephalad migration of the cecum and appendix
occurs during pregnancy owing to displacement
by the enlarging gravid uterus. As a result, pa-
tients presenting with appendicitis in the late sec-
ond or third trimester will often have RUQ pain
due to the subhepatic location of the appendix.
Prompt accurate diagnosis of appendicitis in
the pregnant patient is especially critical, as delay
in diagnosis leads to a 10%–15% perforation rate,
which is associated with a fetal mortality rate of
35%–55%, as compared to 1.5% in uncompli-
cated appendicitis. There is also an increased risk
of premature delivery and maternal complica-
tions (31). US is the first-line imaging modality
for the evaluation of suspected appendicitis in
pregnant women (ACR Appropriateness Criteria
rating of 8). MR imaging may be useful if US
findings are equivocal (rating of 7) (1,2).
Reported sensitivity and specificity rates for US
detection of appendicitis range from 80% to 93%
and 94% to 100%, respectively (32). Typical US
findings of acute appendicitis include dilatation
greater than 7 mm in diameter (with measurements
made from outer wall to outer wall), targetoid ap-
pearance at transverse US, absence of peristalsis,
and noncompressibility, particularly in conjunc-
tion with focal pain at the site of the appendix with
transducer pressure (Fig 8) (33). Echogenic appen-
dicoliths with posterior shadowing are commonly
present but are not required for diagnosis.
The surrounding mesenteric fat usually dem-
onstrates increased echogenicity secondary to
periappendiceal inflammation. Reactive inflam-
mation of the cecum or terminal ileum may also
manifest. Free fluid is not required for diagnosis
but can sometimes be seen at imaging. The pres-
ence of substantial extraluminal fluid or appendi-
ceal wall discontinuity should raise the suspicion
for perforation. Color Doppler US may dem-
onstrate hyperemia of the hypoechoic muscular
layer; note that isolated hyperemia of the mucosal
layer has been associated with enteritis and is not
a specific finding for appendicitis (32,34).
Hepatic Flexure Colitis
Hepatic flexure colitis can occur in isolation or as
a part of diffuse colitis and results in RUQ pain.
Underlying causes include infectious, inflam-
matory, ischemic, or diverticular disease. The
normal appearance of the bowel wall includes five
concentric layers of differing echogenicities. The
three innermost layers are relatively echogenic
and consist of the mucosal interface, the deep
RG  •  Volume 38  Number 3 Joshi et al  777

Figure 9.  Acute infectious hepatic flexure colitis in a

36-year-old man who presented to the ED with RUQ
pain and bloody diarrhea. (a) Initial longitudinal gray-
scale US image of the RUQ obtained with a curved
transducer shows a segment of dilated fluid-filled
bowel with wall thickening (arrow), located along the
inferior margin of the right hepatic lobe. (b) Longitu-
dinal gray-scale US image obtained with a linear trans-
ducer for improved near-field visualization shows dif-
fuse colonic wall and haustral thickening (arrow), with
trace pericolonic free fluid (arrowhead). (c) Subsequent
axial contrast-enhanced CT image shows hepatic flex-
ure wall thickening, with pericolonic fat stranding and
trace fluid.

mucosa (including the muscularis mucosa), and
the submucosa and muscularis propria interface.
This is followed by the hypoechoic muscularis
propria and finally the hyperechoic serosa (32).
In the setting of bowel inflammation, however,
bowel wall thickening creates concentric promi-
nence of these bowel wall layers, resulting in a
targetoid appearance, which is nonspecific and
can manifest in a variety of bowel conditions.
Transmural inflammation or fibrosis can lead
to complete loss of typical gut layers, resulting
in a thick hypoechoic rim at transverse assess-
ment (32). Reactive pericolonic free fluid may
manifest. A careful evaluation for organized fluid
collection or abscess should be performed.
Infectious Colitis.—As with most causes of he-
patic flexure inflammation, bowel wall thickening
with a prominent hypoechoic muscularis propria
layer can be visualized. Haustral thickening and
small-volume pericolonic fluid may be seen (Fig
9). While infectious causes often manifest as pan-
colitis, some cases are left or right predominant,
depending on the causative agent. Right-sided
colitis is characteristically caused by Salmonella,
Yersinia, tuberculosis, and amebiasis (35).
Inflammatory Bowel Disease–related Colitis.—
Reported sensitivity and specificity for US detec-
tion of inflammatory bowel disease range from
67% to 96% and 79% to 97%, respectively (32).
Crohn disease (CD) often extensively involves
the right colon and terminal ileum, which mani-
fests as right-sided abdominal pain. Ulcerative
colitis (UC) is less likely to manifest as isolated
RUQ pain, since the expected pattern of involve-
ment of UC is continuous distal-to-proximal
inflammation of the colon.
Distinguishing between CD and UC is possible
on the basis of the location of the disease and the
presence of skip lesions, pericolic abscesses, and
fistulas resulting from transmural inflammation,
any of which, when manifested, favor a diagnosis
of CD over UC. The degree of bowel wall thicken-
ing is less pronounced with UC as compared with
that of CD, with relatively preserved anatomic
bowel wall layers in UC relative to those of CD
(32). However, definitive diagnosis with US is
challenging, and confirmation with CT or MR
imaging and colonoscopy is often warranted.
The classic targetoid appearance of the bowel
related to inflammatory bowel wall thickening is
a common finding in areas of acute inflammation
778  May-June 2018 radiographics.rsna.org

Figure 10.  UC in a 32-year-old man who presented with right-

sided abdominal pain. (a, b) Longitudinal (a) and transverse (b)
gray-scale US images in the right midabdomen show the fluid-
filled right colon with abnormal irregular wall thickening. Dashed
curved lines in b = demarcating wall. (c) Color Doppler US cine
clip shows targetoid appearance of the right colonic wall, with
haustral thickening and wall hyperemia. (Also see Movie 1.)

(Fig 10, Movie 1). Strictures may appear as a seg-
ment of wall thickening with a fixed hyperechoic
narrowed lumen in conjunction with fluid-filled di-
lated upstream bowel (32). The “creeping fat” sign
can manifest as mass-like echogenic fat adjacent
to the cecum and terminal ileum (32). Prominent
right lower quadrant lymph nodes may be visual-
ized. Complications such as abscesses and fistulas
can also be detected at US. Abscesses are usually
poorly defined hypoechoic areas, which may con-
tain echogenic gas and debris. Fistulas, a hallmark
of CD rather than UC, may appear as hypoechoic
tracks containing gas extending between segments
of bowel or adjacent structures (32).
Colonic Diverticular Disease.—Although the ma-
jority of acute colonic diverticulitis cases will result
in localized pain in the left abdomen, one-third of
cases are missed clinically, as this entity may mani-
fest in a similar manner as acute appendicitis (30).
In a recent meta-analysis, the diagnostic accuracies
of US and CT for acute diverticulitis were 92%
and 94%, respectively, and the overall specificities
were 90% and 99%, respectively (30,36). While
CT remains the superior imaging modality in the
diagnosis of acute diverticulitis, the diagnosis can
occasionally be made at US when an inflamed fo-
cal outpouching along the course of a hypoechoic
inflamed segment of colon is identified, often with
adjacent reactive echogenic fat. Evaluation for ex-
traluminal abscess formation should be performed,
including careful assessment for intraparenchymal
hepatic abscess from the direct spread of infection.
Gastritis and Peptic Ulcer Disease
Individuals with gastric or duodenal inflamma-
tion may present with diffuse abdominal pain or
isolated RUQ pain. Other complaints may in-
clude a sensation of abdominal fullness, bloating,
nausea, early satiety, and heartburn (37). Duo-
denal ulcer disease is characterized by exacerba-
tion of pain in the fasting state and relief after
eating (37). Infection with Helicobacter pylori is
implicated in the majority of cases of gastritis and
peptic ulcer disease (38). Certain medications, in
particular nonsteroidal anti-inflammatory drugs
RG  •  Volume 38  Number 3 Joshi et al  779
and aspirin, are other leading causes (37). Peptic
ulcer disease affects the duodenal bulb most
frequently (35%–65% of cases), followed by the
pylorus and distal gastric antrum (30%–45%)
and gastric body (5%–15%) (39). When infec-
tious gastritis or peptic ulcer disease is suspected
clinically, patients first undergo noninvasive test-
ing for H pylori and, if positive for infection, treat-
ment with antibiotics is initiated.
US is not indicated for the imaging workup of
gastric or duodenal disease, but portions of the
stomach and duodenum are included within the
field of view at abdominal US when any num-
ber of entities are being considered for RUQ
pain, and, under certain conditions, gastritis and
peptic ulcer disease can be identified. The most
reliable indicator of gastric or duodenal inflam-
mation is focal wall thickening and obliteration
of the multilaminar bowel architecture. Thicken-
ing of the gastric antrum beyond 4 mm suggests
gastritis (38). When the stomach or duodenum
is sufficiently distended with fluid, a peptic ulcer
may be identified as a focal or linear echogenic
region, with varying degrees of extension into the
bowel wall (39,40). The presence of inflammatory
changes, free fluid, or gas around the stomach or
duodenum raises the possibility of perforation and
can be confirmed at CT (38–40).
Perforated Viscus
Underlying causes for bowel perforation include
peptic ulcer disease, bowel obstruction, diverticu-
litis, and, less commonly, neoplastic perforation or
bowel ischemia (30). Bowel wall thickening with
fluid-filled distention should raise suspicion for a
bowel condition as the cause of abdominal pain.
In this setting, perforation should be suspected
if echogenic reflectors with reverberation artifact
(signifying gas) are found that cannot be localized
to the intraluminal space and instead significantly
change in location by altering patient position.
Among experienced sonographers, US has an
accuracy of 89%, a sensitivity of 96%, and a speci-
ficity of 82% for pneumoperitoneum; however,
the accuracy among less experienced clinicians
has been reported to be much lower, at 68% (41).
Variability in bowel position as well as obscuration
of structures deep relative to gas by its charac-
teristic dirty shadowing can cause uncertainty in
the localization of gas within the abdomen at US,
particularly when differentiating between small-
volume free gas, pneumatosis intestinalis, and
intraluminal gas (Figs 11–13, Movie 2). In such
settings, CT is indicated.
If pneumatosis related to bowel ischemia is
suspected at the time of US, assessment for portal
venous gas should be performed, appearing as
echogenic mobile reflectors within the main portal
vein and its major branches at gray-scale US, with
accumulation within the smaller peripheral intra-
parenchymal portal veins in a branch-like pattern,
if enough portal venous gas is present. At spectral
Doppler US, the passage of gas locules corre-
sponds with audible crackles and visible patho-
pneumonic sharp spikes superimposed on a portal
venous waveform (Fig 14, Movie 3) (42, 43).
Renal Causes of RUQ Pain
Renal causes for RUQ pain include obstructive,
infectious, neoplastic, traumatic, and hemorrhagic
conditions, and often these factors may coexist.
Obstructive Urolithiasis
Obstructive right nephroureterolithiasis, or stones,
typically manifest as right abdominal or right
flank pain in the acute setting, with hematuria at
urinalysis and hydronephrosis at US (Fig 15a).
However, the absence of hydronephrosis at US
does not preclude ureterolithiasis as a clinical diag-
nosis, but it may prompt further workup with CT
or MR imaging. Ureteral stones are not commonly
visualized at US, but when visualized, color Dop-
pler US may reveal twinkle artifact and upstream
hydroureteronephrosis. With the right US set-
tings, twinkle artifact can facilitate identification
of stones that may otherwise be poorly visualized
or missed (Fig 15c). Assessment for ipsilateral
ureteral jet can confirm at least partial passage of
urine despite a suspected ureteral stone (Fig 15c),
although absence of ureteral jet is not diagnostic of
obstruction. The presence of obstructive urolithia-
sis should always prompt clinical assessment for
superimposed urinary tract infection (UTI), as
urine stasis is a known risk factor.
Renal Infections
Interstitial nephritis refers to inflammation of the
renal interstitium and is most commonly caused
by infection, although other less common causes
include drug reaction, granulomatous disease,
and metabolic disorders (44). Renal infection
presenting in the ED can be acute, chronic,
complicated, or uncomplicated. Acute bacterial
pyelonephritis is commonly seen in the ED and
often occurs in women aged 15–40 years (45).
Acute Bacterial Pyelonephritis.—Acute bacterial
pyelonephritis is commonly seen in the ED and
often occurs in women aged 15–40 years (45).
Pyelonephritis most commonly results from an
ascending UTI, in which the causative organism
spreads from the urinary bladder into the upper
urinary tract. This can occur in the absence of re-
flux and is thought to be due to relative functional
obstruction caused by bacterial endotoxins that
inhibit ureteral peristalsis (44). Pyelonephritis can
780  May-June 2018 radiographics.rsna.org

Figure 11.  Free intraperitoneal gas anterior to the liver. (a) Trans-
verse gray-scale US image obtained using a phased-array trans-
ducer shows a poorly marginated anterior liver surface owing to
echogenic reflectors with posterior dirty shadowing, signifying
gas (arrows). (b) Gray-scale US cine clip obtained using a linear trans-
ducer for improved near-field resolution and localization of gas shows
gas interposed between the anterior margin of the left hepatic lobe
and the peritoneal reflection, signifying free intraperitoneal gas (ar-
row). (Also see Movie 2.) (c) Axial contrast-enhanced CT image (lung
window) shows free gas anterior to the liver (arrow).

Figure 12.  Pneumatosis intestinalis. (a) Longitudinal gray-scale US image shows echogenic
reflectors (arrowheads), diffusely associated with a segment of bowel located along the interior margin
of the liver but not clearly localized within the bowel lumen. On changes in patient position, these
reflectors remained relatively unchanged in location (not shown). (b) Sagittal contrast-enhanced CT
image (lung window) shows gas within the hepatic flexure wall.
RG  •  Volume 38  Number 3 Joshi et al  781

Figure 13.  Diagnostic challenge in localization of gas associated with a loop of bowel abutting the peritoneal reflec-
tion. (a) Transverse gray-scale US image at the midline, near the level of the umbilicus, shows echogenic reflectors
in a lobulated configuration, similar to that of the outline of the bowel (arrows), along the peritoneal reflection with
posterior dirty shadowing, which completely obscures the structures deep relative to this gas. (b) Corresponding axial
contrast-enhanced CT image (lung window) shows extensive pneumatosis, including a loop of bowel with the same
lobulated contour seen at US, abutting the peritoneal reflection near the umbilicus (arrows). The pneumatosis, in con-
junction with intraluminal gas, accounts for substantial obscuration at US, resulting in difficult localization.

Figure 14.  Portal venous gas in a patient with bowel ischemia. Longitudinal gray-scale US cine clip (a) and spectral analysis image (b)
show hepatopetal flow in the main portal vein, with mobile echoes moving in the direction of blood flow in the main portal vein. The
portal venous waveform shows spectral spikes (arrows in b), diagnostic of portal venous gas. (Also see Movie 3.)

also develop from hematogenous spread or direct
inoculation under relevant clinical circumstances.
The patient’s clinical presentation varies but can
include fever, chills, dysuria, and RUQ or right
flank pain. Nonspecific nausea and vomiting may
manifest as well (44).
The imaging appearance can be occult at US.
When findings are apparent, they include hydrone-
phrosis, renal enlargement, and effacement of renal
sinus fat due to edema and segmental, geographic,
or diffuse loss of corticomedullary differentiation,
with areas that may be increased or decreased in
echogenicity (Fig 16). Involved areas can exhibit
hypoperfusion, best identified with careful power
Doppler US evaluation of the renal parenchyma.
Complicating features include abscess formation or
the presence of gas within the parenchyma (44,46).
Emphysematous Pyelonephritis.—Emphysematous
pyelonephritis is a life-threatening necrotizing infec-
tion that is commonly seen in the setting of poorly
controlled diabetes. Other risk factors include
immunocompromised status or underlying urinary
tract obstruction from calculi or a neoplasm (44).
Patients with RUQ or flank pain from right-sided
emphysematous pyelonephritis are usually criti-
cally ill and may additionally pre­sent with fever,
hyperglycemia, metabolic acidosis, dehydration,
782  May-June 2018 radiographics.rsna.org

Figure 15.  Obstructing right ureterovesical junction

(UVJ) calculus in a 34-year-old patient presenting with RUQ
pain. (a) Longitudinal gray-scale US image of the right kid-
ney shows anechoic dilatation of the renal collecting sys-
tem (*), confirmed by absence of internal blood flow at
color Doppler US (not shown). (b) Transverse gray-scale
US image through the urinary bladder shows an echogenic
stone (arrow) at the right UVJ, with upstream right hydro-
ureter (arrowhead). (c) Transverse color Doppler US image
through the urinary bladder shows twinkle artifact (arrows)
deep relative to the right UVJ stone and absence of a right
ureteral jet. Contralateral left ureteral jet is also seen.

Figure 16.  Acute bacterial pyelonephritis in a febrile 25-year-old woman who presented to the ED with RUQ and right
flank pain. Urinalysis showed findings of a UTI. (a) Longitudinal gray-scale US image of the right kidney shows a rela-
tively well-demarcated segmental area of increased echogenicity in the upper-to-interpolar region, with associated loss
of corticomedullary differentiation. (b) Axial contrast-enhanced CT image shows striated nephrogram in the interpolar
region of the right kidney (dashed circle).

and electrolyte imbalance. The culprit organism is
most commonly E coli.
On gray-scale US images, parenchymal em-
physema appears as echogenic reflectors with
posterior dirty shadowing and, when extensive,
can entirely obscure visualization of the kidney
(44) (Fig 17a). If emphysematous pyelonephri-
tis is suspected at initial RUQ US, CT is often
performed to assess the extent of involvement, in
order to guide management. In the more severe
form, gas may replace the renal parenchyma and
can extend into the ureter and ureteral wall and
even the contralateral kidney (Fig 17b–17d).
Pyonephrosis.—Pyonephrosis is a medical emer-
gency with a high mortality rate and is fittingly
RG  •  Volume 38  Number 3 Joshi et al  783

Figure 17.  Emphysematous pyelonephritis in a febrile middle-aged patient who presented to the ED
with RUQ and right flank pain. (a) Transverse gray-scale US image at the level of the hepatorenal interface
shows echogenic reflectors (arrow) along the inferior margin of the liver, with associated posterior dirty
shadowing (*) that obscures the right kidney entirely. (b) Corresponding abdominal radiograph shows
gas in the RUQ (arrow), conforming to the expected shape and location of the right kidney and right
renal collecting system. (c, d) Subsequent axial (c) and coronal (d) nonenhanced CT images show gas
nearly replacing the right renal parenchyma (arrow), with gas (arrowhead in d) transecting into the wall
of the right ureter throughout its course.

referred to as “pus under pressure,” indicating
infection of an obstructed kidney in which the re-
nal collecting system becomes distended with pu-
rulent exudate containing infectious organisms,
inflammatory cells, and debris (47). Obstructing
masses, strictures, calculi, and complications of
pyelonephritis such as sloughed papilla may serve
as underlying contributing factors (44).
US is 90% sensitive and 98% specific for
pyonephrosis, but consideration of this diagnosis
and knowledge of the patient’s clinical presenta-
tion are integral to rendering the diagnosis (47).
US findings include diffuse urothelial thicken-
ing (including along the nondependent aspects
of the distended collecting system and ureter);
layering echogenic debris along the dependent
collecting system, ureter, and urinary blad-
der; and mobile or shifting echoes related to
debris, stones, and even gas (Fig 18) (44–48).
However, these mobile echoes are not required
for diagnosis, and pyonephrosis can be indistin-
guishable from noninfected hydronephrosis at
US in approximately 10% of cases, making the
correlation with the patient’s clinical status of
the utmost importance, as a diagnosis of pyone-
phrosis would substantially change management
and prognosis (48).
Pyonephrosis must be treated promptly by
decompressing the collecting system, usually with
a nephrostomy tube or ureteral stent placement,
and administration of antibiotics, as this entity
can lead to rapid renal parenchymal destruction,
sepsis, and even death (46–48).
Xanthogranulomatous Pyelonephritis—Xantho-
granulomatous pyelonephritis (XGP) is a chronic
granulomatous process in which the renal paren-
chyma is replaced by lipid-laden macrophages
and occurs as a result of an immune response to
a recurrent bacterial UTI (45,49). Involvement
is most commonly unilateral but can be bilateral,
and it is usually diffuse but can be segmental
(particularly in the setting of duplicated collect-
ing system) (44). Staghorn calculi manifest in the
784  May-June 2018 radiographics.rsna.org

Figure 18.  Pyonephrosis in a 24-year-old pregnant woman with a history of sickle cell disease who presented to the ED with RUQ
pain and fever. Urinalysis showed findings of UTI. (a) Longitudinal gray-scale US image though the right kidney shows renal calyceal
dilatation with urothelial thickening and dependent echogenic debris (arrows). (b) Longitudinal color Doppler US image through the
midabdomen shows right hydroureter with urothelial thickening, as well as layering debris (arrow). (c) Longitudinal gray-scale US
image through the urinary bladder shows diffuse mobile intraluminal echoes, consistent with mobile debris.

Figure 19.  XGP in a 20-year-old patient

who presented to the ED with right thora-
coabdominal pain. (a) Longitudinal gray-
scale US image of the right kidney shows
blown-out dilated calyces (*) with marked
renal cortical thinning, loss of the normal
renal architecture, and a large amorphous
calculus with posterior shadowing centered
within the renal pelvis and extending into the
calyces (arrow). (b) Abdominal radiograph
shows a large calculus with staghorn configu-
ration (arrow) in the expected location of the
right kidney. (c) Coronal nonenhanced CT
image shows a staghorn calculus (arrow) with
diffuse marked dilatation of the right renal
calyces (*), with overlying cortical thinning
(“bear paw” sign).

majority of cases. Clinical symptoms include ab-

dominal and flank pain, low-grade fever, malaise,
pyuria, and hematuria.
At US for the evaluation of RUQ pain, findings
of right-sided XGP include renal enlargement, tion of normal renal architecture, and the presence
hydronephrosis with marked dilatation of the renal of large amorphous calculi with posterior acous-
calyces and loss of overlying renal cortex, distor- tic shadowing (Fig 19a) (44,49). The remaining
RG  •  Volume 38  Number 3 Joshi et al  785

Figure 20.  Renal abscess in a patient presenting with RUQ and flank pain with fever. (a) Transverse gray-scale US image shows
fluid-filled structures with internal debris within the right kidney parenchyma (arrows), including within the cortex, which did not
correspond with the expected configuration of a collecting system. (b) Corresponding coronal contrast-enhanced CT image shows
a complex fluid-filled structure with internal septa (*) and peripheral enhancement, with hypoenhancement of the surrounding renal
parenchyma, in keeping with edema (arrow). (c) Single fluoroscopic image obtained from subsequent percutaneous abscess aspira-
tion and irrigation of two large fluid loculations in the upper pole of the right kidney. The irrigation solution contained contrast media,
thus opacifying these collections. Aspirated material revealed Staphylococcus aureus at histologic analysis.

renal parenchyma may appear hypoechoic owing
to edema and inflammation (48). Inflammatory
changes may extend to adjacent structures, includ-
ing the psoas muscle (46). Staghorn calculus is
often seen at radiography and CT (Fig 19b, 19c).
Renal Abscess.—Liquefactive parenchymal ne-
crosis and coalescence of microabscesses in the
setting of renal infection result in renal abscess
formation (46,47). Diabetes is a strong predis-
posing risk factor for the development of renal
abscess. Other risk factors include vesicoureteral
reflux, ascending infection, renal calculi, and
anatomic abnormalities. The US appearance is
variable, in part owing to the potential for rapid
change in the appearance over the course of days.
Renal abscess can appear as a hyperechoic or
hypoechoic focal intrarenal mass or a complex
cystic mass containing echogenic debris with ab-
sence of internal vascularity (Fig 20). Extension
into and beyond the perirenal space can occur
(46–48).
Renal Neoplasms
Spontaneous hemorrhage related to right-sided
renal neoplasm or cyst rupture can cause RUQ
and right flank pain. According to a 2002 meta-
analysis, the most common cause of spontaneous
unilateral renal hemorrhage is angiomyolipoma,
followed by renal cell carcinoma (50,51). Angio-
myolipomas larger than 4 cm have increased risk
of hemorrhage. As with hemorrhage anywhere,
the appearance at US is variable, depending
on the time course. Subcapsular hematoma or
hemoperitoneum may be observed. If the cause
of hemorrhage is not discovered at initial imag-
ing, follow-up imaging after hematoma resolution
should be performed (50–52).
Adrenal Causes of RUQ Pain
Adrenal Hemorrhage
An adrenal condition as the cause of acute RUQ
pain is relatively uncommon. When it occurs,
it is almost always attributed to intraglandular
hemorrhage. Although most cases of adrenal
hemorrhage are diagnosed incidentally at imaging
for an unrelated condition or at autopsy, when
acutely symptomatic, patients most often present
with upper abdominal or flank pain and low-
grade fever (53–57). When only the right gland is
affected, an adrenal hematoma can be a cause of
acute RUQ pain (55).
Adrenal insufficiency as a result of adrenal
hemorrhage is relatively uncommon, and it is
more likely to develop in bilateral involvement
and when more than 90% of each adrenal gland
is destroyed; however, most affected patients do
not present with clinical or laboratory findings
of adrenal dysfunction (53,55,56). Predispos-
ing factors for spontaneous adrenal hemorrhage
include stress (such as surgery, severe burns, or
sepsis), pregnancy, bleeding diathesis, and an-
ticoagulation therapy (53,55–58). Both benign
(80%) and malignant (20%) adrenal tumors
(53), such as pheochromocytoma, myelolipoma,
adrenocortical carcinoma, and metastases, can
be predisposed to bleeding, and adrenal hem-
orrhage may be the initial manifestation of the
underlying neoplasm (53,54,58).
Unless the adrenal hemorrhage results in a
large hematoma, it is likely to be undetectable at
786  May-June 2018 radiographics.rsna.org

Figure 21.  Spontaneous adrenal hemorrhage in a 21-year-old

woman with uncomplicated pregnancy to date (27 weeks and 2
days), who presented with sudden-onset acute sharp epigastric
and RUQ pain. (a) Transverse color Doppler US image shows a
heterogeneously hyperechoic lesion (*) without internal vascular-
ity wedged within the hepatorenal space in the expected location
of the right adrenal gland. (b) Axial contrast-enhanced CT image
shows heterogeneous hyperattenuating material and fluid (*) in
the expected location of the adrenal gland. (c) Follow-up coro-
nal nonenhanced fat-saturated T1-weighted MR image obtained 5
days later shows a heterogeneous lesion with areas of intrinsic high
signal intensity (arrow) superior to the right kidney in the expected
location of the right adrenal gland, reflecting blood products.
There is preservation of a fat plane between the liver and kidney.

abdominal US, particularly in adults, and will be

identified more readily at CT (53,59). When an
adrenal hematoma is visible at US, its appearance
varies depending on the time course. In the acute
phase, when a patient is likely to present to the
ED, a solid avascular masslike appearance with
diffuse or heterogeneous echogenicity may be ob-
served (Fig 21a) (53,55,57,58). As the hematoma
evolves, a more heterogeneous pattern emerges,
with a central hypoechoic or cystlike area reflect-
ing clot lysis (58). Peripheral calcification can be
detected at US as early as 1 week (53).
As with that seen at US, the imaging ap-
pearance of adrenal hemorrhage at CT and
MR imaging varies with time and in most cases
will resolve completely, develop into a chronic
pseudocyst, or persist as dystrophic calcifica-
tions (53,57,58). In the acute setting, an adrenal
hematoma is depicted at nonenhanced CT as a
rounded or ovoid mass with the attenuation of
clotted blood (50–90 HU) replacing the normal
Y-shaped configuration of the adrenal gland (Fig
21b) (53,54,57,58). At contrast-enhanced CT,
the hematoma will usually appear less attenuat-
ing than normal enhancing adrenal tissue, if still
visible (57). Periadrenal fat stranding, reflect-
ing an uncontained hemorrhage, is a frequent
additional finding (53,56). In less severe cases
of hemorrhage, the normal adreniform shape is
maintained, and the hematoma is contained to
the central portion of the gland with preservation
of peripheral enhancement, giving rise to a “train
track” appearance (57).
The primary use of MR imaging in the
evaluation of adrenal hemorrhage is to evaluate
for an underlying mass once the hemorrhage
has been established and to estimate when the
hemorrhage occurred. Although distinguishing
an adrenal mass from a large hematoma is not
always possible at MR imaging, the presence
of enhancing components argues strongly for
a neoplasm (53,57,58). Comparison with any
prior imaging studies, when available, is also
valuable in determining whether a preexisting
mass is the likely cause (57). The MR imaging
characteristics of a bland adrenal hematoma
depend on the evolving magnetic properties of
blood over time. Depending on the temporal
relationship between hemorrhage onset and
RG  •  Volume 38  Number 3 Joshi et al  787

Figure 22.  RLL pneumonia with transdiaphragmatic extension,

resulting in hepatic and perihepatic abscess in a patient presenting
to the ED with RUQ pain and fever. (a, b) Longitudinal gray-scale
US images at the thoracoabdominal junction show an ill-defined
soft-tissue focus (arrow) above the level of the diaphragm in the
expected location of the right lung base, with abrupt loss of the
echogenic right hemidiaphragm interface (arrowhead). A cystic-
appearing lesion with scattered internal echoes (*), located inferior
to the disrupted right hemidiaphragm, involves the liver paren-
chyma and extends into the hepatorenal space. (c) Sagittal con-
trast-enhanced CT image shows a heterogeneously enhancing RLL
consolidation (arrow) consistent with RLL pneumonia that extends
through the right hemidiaphragm and is continuous with a track
into a rim-enhancing fluid collection (signifying intra-abdominal
abscess) (*) involving the posterior right hepatic lobe and hepa-
torenal space, with perirenal inflammation.

awareness and recognition to quickly and accu-

MR imaging, high T1 signal intensity or rapidly
evolving signal intensity may be observed within
bland hemorrhage (Fig 21c) (53,55,57,58).
Thoracic Causes of RUQ Pain
RLL parenchymal and pleural conditions, includ-
ing pneumonia, infarction related to pulmo-
nary embolism, pleural effusion, and neoplasm
involving the pleura and chest wall can result in
pleuritis and RUQ pain. An intercostal imaging
approach is often required to visualize regions
of the thorax and thoracoabdominal junction,
which may otherwise be obscured owing to rib
shadowing artifact. This is particularly the case
in patients who cannot tolerate large inspiration
and breath holding and consequently may have
a greater portion of the lung base and upper ab-
dominal structures surrounded by the ribcage.
RLL Pneumonia
RLL pneumonia or pleural effusion can result
in pleuritis that manifests as RUQ pain. Both
RLL consolidation and right pleural effusion are
often readily identifiable at RUQ US but require
rately make the diagnosis. A minority of patients
with RLL pneumonia will develop transdiaphrag-
matic spread of infection, which can result in
intra-abdominal abscess formation (Fig 22).
Pulmonary Embolism
Abdominal pain has been reported in 6.7% of
patients with pulmonary embolism (60,61).
Although the mechanism is not fully understood,
one hypothesized theory for this pain is distention
of the liver capsule owing to hepatic congestion
from right heart strain, which can occur regardless
of pulmonary embolism location. Other theories
include diaphragmatic pleurisy resulting from
pulmonary infarction with the right lung base
specifically (61). While some centers use bedside
transthoracic US to diagnose pulmonary embolism
(62), most pulmonary embolisms are not directly
identified at RUQ US. However, secondary signs
at RUQ US and clinical examination, such as RLL
consolidation with unexplained tachypnea and
tachycardia, should raise suspicion (63,64). Some
of these patients may present with low-grade fever
and abnormal liver function test results (64).
Chest Wall Mass
Chest wall tumors can be benign or malignant and
when malignant may be primary or metastatic. US
788  May-June 2018 radiographics.rsna.org

Figure 23.  B-cell lymphoma with involvement of the right chest wall and anterior liver capsule in a 57-year-old
woman with RUQ pain. (a) Transverse color Doppler US image shows a nearly anechoic mass (*) along the anterior
margin of the liver, which may be confused for a complex pleural or chest wall fluid collection. However, there is ab-
sence of posterior acoustic enhancement and presence of internal blood flow, both of which should raise suspicion for
a hypoechoic solid mass. (b) Corresponding axial contrast-enhanced CT image shows enhancing soft tissue (arrow)
anterior to the right hepatic lobe with loss of fat planes along the chest wall and liver margin, with resulting contour
deformity of the liver surface.

Figure 24.  Chronic small vessel occlusive vasculitis related to systemic lupus erythematosus (SLE) resulting in ischemic
infarct of the left hepatic lobe in a 14-year-old boy with a history of SLE who presented with RUQ and epigastric pain
and jaundice. (a) Transverse gray-scale US image shows heterogeneous abnormal echogenicity and echotexture within
the left hepatic lobe, with abrupt sharp demarcation between involved and uninvolved liver in the distribution of the
left hepatic artery branches. (b) Axial contrast-enhanced CT image shows corresponding heterogeneous enhancement
of the left hepatic lobe.

findings of chest wall masses are often nonspecific,
and CT or MR imaging are used as complemen-
tary studies to narrow the differential diagnosis
and provide additional information regarding the
extent of disease (65). However, superficial chest
wall masses can be identified at US, particularly
with RUQ US obtained in the ED for RUQ pain.
Identification of the chest wall mass is not only
important because it can provide a cause for the
patient’s pain, but it is also important for stimu-
lating workup for a lesion that may otherwise be
missed in its early stages. A superficial chest wall
mass is often amenable to US-guided biopsy (66).
A lymphomatous soft-tissue mass in the chest
wall can appear hypoechoic or nearly anechoic
at US and can be mistaken for a cystic lesion
when improper technique is employed. Posterior
acoustic enhancement or through transmission is
more characteristic of a cystic or fluid-filled lesion;
absence of through transmission suggests the pres-
ence of a solid mass (Fig 23). The use of appro-
priate gain settings can aid in detecting low-level
echoes, which otherwise may not be apparent. It is
also crucial to carefully evaluate for internal blood
flow. When blood flow is not appreciated at color
Doppler US, power Doppler US should be used
for greater sensitivity. Evaluation for lymphade-
nopathy or splenomegaly may be helpful.
Vascular Causes of RUQ Pain
Thrombosis of the hepatic vasculature, including
the portal venous, hepatic arterial (Fig 24), and
RG  •  Volume 38  Number 3 Joshi et al  789

Figure 25.  Bland portal vein thrombosis secondary to SLE-associated coagulopathy in a

19-year-old man with a history of SLE. (a) Transverse color Doppler US image shows near oc-
clusion of the main portal vein by an echogenic filling defect, with a small focus of remaining
visible hepatopetal blood flow. (b) Color Doppler US spectral analysis image in this region of
blood flow within the main portal vein shows a monophasic hepatopetal waveform.

hepatic venous vasculature, can cause RUQ pain.
Each thrombosis pattern is associated with reli-
able findings at RUQ US.
Portal Vein Thrombosis
Main portal vein thrombosis can be asymptom-
atic but can also cause RUQ pain, particularly
when there is associated mesenteric venous
thrombosis (67). A portal vein thrombus can be
bland or malignant, and accurate distinction is
critical because the underlying cause, treatment,
and prognosis change substantially when throm-
bosis is determined to be malignant.
Bland Portal Vein Thrombosis.—Thrombosis
of the portal vein is commonly associated with
hepatic cirrhosis due to relative stasis of blood
flow in the portal vein. In the noncirrhotic patient,
bland portal vein thrombosis may be related to hy-
percoagulable states, for which there are numerous
underlying causes, including intrinsic or genetic
coagulation factor aberrations, autoimmune
disorders (such as SLE), inflammatory conditions
(such as pancreatitis, inflammatory bowel disease,
diverticulitis, cholangitis, and peritonitis), known
malignancy, oral contraceptive use, and pregnancy
(67,68). Superior mesenteric vein and portal vein
thrombosis can lead to RUQ pain, but it can also
cause diffuse abdominal pain if complications of
venous bowel infarction develop.
In the setting of occlusive bland portal vein
thrombus, US will show a filling defect within
the portal vein without internal vascularity, and
spectral analysis will show absence of blood flow
within the thrombus (aphasic waveform) (68).
Areas of blood flow with hepatopetal monopha-
sic waveform can be seen in nonocclusive bland
portal vein thrombus (Fig 25).
Malignant Portal Vein Thrombosis.—Patients
with hepatic cirrhosis are at increased risk for
hepatocellular carcinoma, which is the most com-
mon cause of malignant portal vein thrombosis.
Other differential diagnosis considerations in-
clude pancreatic carcinoma, cholangiocarcinoma,
and metastatic disease (68).
At gray-scale US, an echogenic filling defect
within the portal vein is typically seen, some-
times with portal vein distention. However,
neither the echogenicity of the thrombus nor the
presence of portal vein distention can reliably
discriminate bland from malignant portal vein
thrombosis. The most reliable gray-scale US
findings of malignant thrombus are the com-
bination of an echogenic filling defect with an
adjacent liver mass (68), but even these features
are not diagnostic.
The use of color or power Doppler US with
spectral analysis is crucial in the diagnosis of
malignant thrombus. Internal blood flow within
the thrombus at color or power Doppler US
(termed the thread and streak sign) with pulsatile
arterialized hepatofugal flow at spectral analy-
sis are specific and definitive findings (Fig 26a)
790  May-June 2018 radiographics.rsna.org

Figure 26.  Malignant portal vein thrombosis in a 72-year-old man with RUQ pain. (a) Transverse color Doppler US image
with spectral tracing through the main portal vein shows an echogenic filling defect with internal blood flow in the main
portal vein (thread and streak sign) and a pulsatile arterial hepatofugal waveform at spectral analysis. The adjacent liver
shows a nodular contour with coarsened parenchymal echotexture, compatible with hepatic cirrhosis. (b) Axial contrast-
enhanced arterial phase CT image shows the thread and streak sign (arrows), with prominent neovascularity in and around
the portal venous tumor thrombus. (c) Axial contrast-enhanced portal venous phase CT image shows cirrhotic liver mor-
phology, with a partially shown multifocal hepatocellular carcinoma (arrows). Enhancing soft tissue is seen in the expanded
main portal vein (*).

(68–70). This sign can also be observed at arte-
rial phase contrast-enhanced CT (Fig 26b) (70).
Careful assessment for a primary lesion should
be performed (Fig 26c).
Hepatic Vein Thrombosis and BCS
BCS is a relatively uncommon condition of
hepatic venous outflow obstruction of any cause,
from the level of the hepatic veins to the inferior
cavoatrial junction, with a reported prevalence
of one in 100 000 worldwide (71,72). BCS is
considered primary when the obstruction is
related to a primary venous condition, such as
thrombosis, stenosis, or web formation. BCS
is categorized as secondary when related to ex-
trinsic compression, as seen with a mass lesion
(71). An underlying hypercoagulable state can
be identified in about 75% of BCS cases (73).
BCS can be classified as fulminant, acute, sub-
acute, or chronic, depending on the time course
and its associated clinical presentation, which
ranges from absence of symptoms to fulminant
liver failure. Abdominal pain, hepatomegaly, and
ascites manifest in almost all cases (71).
US is the imaging modality of choice, with
sensitivity and specificity of 85% or higher (73).
Hepatomegaly, particularly with caudate lobe
enlargement, with a coarsened echotexture, non-
visualization of the hepatic veins, a compressed
IVC, enlarged intrahepatic collateral hepatic
veins, splenomegaly, and ascites are often seen
(Fig 27a, 27b) (72). Secondary gallbladder wall
thickening should not be mistaken for acute
cholecystitis (Fig 27a) (73). Color Doppler US
RG  •  Volume 38  Number 3 Joshi et al  791

Figure 27.  BCS in a 32-year-old woman with RUQ pain and distention who reported current oral
contraceptive use. (a) Transverse gray-scale US image through the liver shows coarsened hepatic pa-
renchyma and a right pleural effusion (*). Partially visualized secondary gallbladder wall thickening (ar-
row) should not be mistaken for acute cholecystitis. Ascites and splenomegaly (not shown) also reflect
postsinusoidal portal venous congestion owing to hepatic venous obstruction. (b) Transverse color
Doppler US image shows numerous collateral vessels within the caudate lobe but no morphologic right
or middle hepatic vein extending into the IVC. (c) Color Doppler US image with spectral analysis shows
a dilated caudate lobe vein (arrow) extending into the IVC, with a venous waveform. (d) Fluoroscopic
image from transjugular hepatic venography shows near-complete thrombosis of the right hepatic vein
and moderate thrombosis within the middle hepatic vein with the presence of collateral vessels and the
spiderweb appearance (arrow). Arrowhead = catheter.

may reveal absent or reversed flow in the hepatic
veins, IVC, or both, with intrahepatic collateral
veins (Fig 27b) (72). An engorged caudate lobe
vein (>3 mm in diameter) draining directly into
the IVC may be seen (Fig 27c) (71,72). The
presence of collateral vessels with drainage into
the subcapsular or intercostal veins is highly
sensitive and specific for BCS (72).
The diagnosis of BCS is confirmed by a spi-
derweb pattern or frank occlusion at venography
(Fig 27d), and confirmation is necessary even
with negative US results when clinical suspicion
remains high (73). Type I BCS is limited to the
IVC, type II BCS involves only the hepatic veins,
and type III is a mixed type with hepatic vein and
IVC involvement (71). Treatment varies with the
severity of disease and includes anticoagulation
therapy, surgical shunt creation, endovascular
stent placement, and liver transplantation (72).
Conclusion
Several disease entities involving a variety of
organ systems can manifest as RUQ pain, which
can be reliably identified at initial RUQ US,
even when performed solely for the purpose of
evaluating for gallbladder or biliary conditions.
It is important for the radiologist to be familiar
with this spectrum of diseases, including their
792  May-June 2018 radiographics.rsna.org
respective clinical manifestations and appear-
ances at US, as US can often provide an ac-
curate diagnosis if recognized by the radiologist
or sonologist. Diagnosis at the time of initial
US can reduce unnecessary imaging and its
consequences, including excess cost, radiation
exposure, nephrotoxic contrast medium use,
and time to appropriate management, enabling
improved patient care and patient outcomes.
Disclosures of Conflicts of Interest.—T.N.H. Activities related to
the present article: disclosed no relevant relationships. Activities
not related to the present article: education grant from the Ameri-
can Society of Emergency Radiology. Other activities: disclosed
no relevant relationships.
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TM
ERRATA This copy is for personal use only. To order printed copies, contact reprints@rsna.org

1590

Errata
September-October 2018 • Volume 38 • Number 5

Originally published in:

Table 1: Sonographically Identifiable Differ- RadioGraphics 2018; 38(3):766–793 • https://doi
ential Diagnosis Considerations for RUQ Pain .org/10.1148/rg.2018170149
Adrenal US of Right Upper Quadrant Pain in the Emer-
Adrenal hemorrhage gency Department: Diagnosing beyond Gallblad-
Adrenal mass (benign, malignant)
der and Biliary Disease
Gallbladder/biliary
Gayatri Joshi, Kevin A. Crawford, Tarek N.
Acute cholecystitis
Chronic cholecystitis Hanna, Keith D. Herr, Nirvikar Dahiya, Christine
Cholelithiasis O. Menias
Acalculous cholecystitis
Gallbladder torsion
Erratum in:
Gallbladder carcinoma/metastasis RadioGraphics 2018; 38(5):1590 • https://doi.org/
Postcholecystectomy complications 10.1148/rg.2018184007
Choledocholithiasis Table 1: The text under the subheadings “Pancreatic”
Mirizzi syndrome
and “Vascular” was inadvertently switched. Table 1 is
Cholangitis
Biliary necrosis reprinted here with the correct text under these sub-
Cholangiocarcinoma headings. The online version has been corrected.
Gastrointestinal
Subhepatic appendicitis
Hepatic flexure colitis
Bowel obstruction
Perforated viscus
Gastrointestinal neoplasm
Bowel ischemia
Gastritis
Peptic ulcer disease
Hepatic
Hepatic steatosis
Acute hepatitis
Liver abscess
Liver neoplasm without or with tumoral hemorrhage
(hepatocellular adenoma, hepatocellular carcinoma,
metastases)
Pancreatic
Pancreatic neoplasm
Pancreatitis
Thoracic
Right lower lobe (RLL) pneumonia
Right lung base pulmonary infarct
Chest wall mass
Pleural effusion
Urologic
Obstructive urolithiasis
Acute bacterial pyelonephritis
Pyonephrosis
Emphysematous pyelonephritis
Renal abscess
Subcasular hematoma secondary to hemorrhagic neo-
plasm (angiomyolipoma, renal cell carcinoma)
Ruptured renal cyst
Vascular
Portal vein thrombosis (bland and malignant)
Budd-Chiari syndrome (BCS)
Hepatic artery compromise