Radiology Cases in Pediatric Emergency Medicine
Volume 7, Case 5
Daniel C.H. Kidani, Medical Student
Loren G. Yamamoto, MD, MPH
Kapiolani Medical Center For Women And Children
University of Hawaii John A. Burns School of Medicine
Three cases will be presented:

Case A
     This is a 16 year old female who presents to the 
emergency department with a one day history of severe 
right flank pain with associated vomiting.  She denies 
any fever, urgency, or dysuria.  Her past medical 
history is unremarkable.  
     Exam:  VS T 36.8 degrees C, P53, RR 24, BP 
120/80.  She is alert, cooperative, in moderately severe 
discomfort.  HEENT unremarkable.  Heart regular.  
Lungs clear.  Abdomen Diffuse tenderness on the right.  
Guarding and rebound are present on the right.  She 
has severe right CVA tenderness.
     UA:  >100 RBCs, 20-50 WBCs, positive nitrite.  
UCG negative.  WBC 10.1, Hgb 13.  BUN 11, Creat 
0.8.  An abdominal flat plate is ordered.

View her abdominal radiograph.

     This abdominal flat plate demonstrates a possible 
renal stone on the patient's right at the level of L3 and 

View the arrow to see where the stone is.  It is not 
easy to see.

     An IVP is ordered.

View her IVP at 5 and 20 minutes.
IVP at 5 minutes (below)

IVP at 20 minutes (below)

     The first IVP image is taken at 5 minutes following 
IV contrast.  This shows prompt excretion of contrast 
from the left kidney.  Contrast is seen excreted from the 
right kidney, but the ureter is not well visualized 
suggesting an obstruction in ureter.  The calyces are 
blunted indicating hydronephrosis.  The second IVP 
image is taken at 20 minutes following IV contrast.  This 
shows delayed retention of contrast on the right.  The 
calyceal blunting of the right kidney indicating 
hydronephrosis is more evident.  There is a narrowing 
of the ureter on the right in the area of the suspected 

View a close-up of this.

     This view shows a close-up of the same 20 minute 
IVP on the right in the area of the suspected stone.  
The black arrow points at this area. 

Case B
     This is a 15 year old male who presents to the 
emergency department with abdominal pain, vomiting 
and spots on his legs.  He vomited 15 times.  He also 
noted a red spot on his eye.  His pain is intermittent 
     Exam:  VS T 37.5 degrees C, P70, R20, BP 125/80.  
He is alert and comfortable.  He has a subconjunctival 
hemorrhage.  HEENT otherwise unremarkable.  Heart 
regular without murmurs.  Lungs clear.  Abdomen soft, 
non-tender with normal bowel sounds.  No CVA 
tenderness.  He has a moderate degree of purpuric 
lesions mostly on his lower extremities. 
     His CBC and coagulation studies are normal.  His 
UA shows 5-10 RBCs.  An abdominal series is ordered.

View his abdominal series.

Supine view (below)

Upright view (below)

View a close-up of the supine view.

     His abdominal radiographs demonstrate an 
incidental finding of a two calcifications superimposed 
on the right kidney, which are suggestive of kidney 
stones.  These are best seen on the supine (flat) view.  
The calcifications are present on the upright view, but 
they are superimposed over his 12th rib, making it more 
difficult to see.
     A CT scan is done.

View his CT scan.

     His CT scan is unremarkable except for the 
incidental finding of stones in his right kidney.  The 
arrow points to a stone in his right kidney.
     He is discharged with a diagnosis of probable 
anaphylactoid purpura, subconjunctival hemorrhage 
and nephrolithiasis.  Lithotripsy is considered.

Case C	
     This is a 19 year old female who presents to the 
emergency department with a chief complaint of 
abdominal pain.  She has a two-day history of 
abdominal pain progressing to right CVA tenderness 
with radiation to the groin region.  She also has fever, 
vomiting, nausea, chills, dysuria, urinary frequency, 
diarrhea, and general malaise.
     Exam:  VS:  T 37 degrees C, P 67, RR 20, BP 
105/68.  She is alert, oriented, not toxic and in no 
apparent distress.  Her oral mucous membranes are 
pink and moist.  Heart regular without murmurs or extra 
heart sounds.  Lungs clear to auscultation and 
percussion bilaterally.  She has mild CVA tenderness 
on the right side.  Abdomen is soft and nondistended 
with normal bowel sounds.  She has some RUQ 
tenderness.  No rebound tenderness or peritoneal 
signs.  No masses were palpated.  Her pelvic exam is 
significant for mild right adnexal tenderness.  There is 
no cervical motion tenderness.  Extremities 
     Her lab studies show:  WBC 17.0, Hgb 13, platelet 
count 295,000.  UA 1+ protein, 4+ blood, positive 
leukocyte esterase, many bacteria, 20-50 WBCs and 
5-10 RBCs per high power field.  UCG negative.  An 
abdominal series is ordered.

View her abdominal series.
Supine view (below)

Upright view (below)

     There is nothing obvious on the supine (flat) view.  
The upright view is significant for a calcification 
overlying the right kidney.   Another abdominal flat 
plate is ordered to see if the calcification has moved.

View later abdominal radiograph.

     This follow-up radiograph shows persistence of the 
calcification over the right kidney.  A CT scan is 

View the patient's CT scan.    

     The first CT image shows a contrast enhanced left 
kidney with prompt excretion of contrast.  The right 
kidney is excessively contrast enhanced with no 
excretion of contrast.  The black arrow points at two 
stones in the renal collecting system.
     The second CT image shows a dilated ureter on the 
right kidney (black arrow).  The third CT image shows a 
dilated ureter on the right without contrast flow 
compared to the normal sized contrast filled ureter on 
the left.  The fourth CT image shows another stone in 
the right ureter just as it enters the bladder.
     The patient is diagnosed with pyelonephritis, 
hydronephrosis and urolithiasis.  She is hospitalized 
and treated with IV antibiotics, fluids and ketorolac.
     Her urine culture later grows proteus species which 
is a urea splitting organism suggesting that these are 
struvite stones.  

     Urolithiasis affects 2-10% of industrialized 
populations, with a lower incidence in 
non-industrialized countries.  Most, 80%-85%, of 
stones pass spontaneously; however, 20% of patients 
require hospitalization.  Recurrence rates are 14%, 
35%, and 52% at 1, 5, and 10 years respectively, after 
the first stone is passed.  The peak onset of 
symptomatic kidney stones is in the 3rd and 4th 
decades of life, with a male to female ratio of 3:1(1).  
High humidity and elevated temperatures seem to be 
contributing factors to the development of renal calculi.  
Symptomatic stones also have their highest incidence 
in the higher temperatures of the summer months (4).
Nephrolithiasis is rare in children; however, the 
incidence of urinary calculi in the United States is 
increasing.  Approximately 5-10 cases of urolithiasis 
between 10 months and 16 years of age are seen at a 
typical US pediatric center annually (1).  Although 
urolithiasis is uncommon in children younger than 2 
years of age, the incidence does not seem to favor any 
age group or gender (2).  Approximately 66% of urinary 
calculi in North American children are found in the 
kidneys at the time of diagnosis, the remaining 1/3 are 
located in the ureters (2).
     The etiology of kidney stones is derived from an 
imbalance of a delicate equilibrium within the kidneys.  
The kidneys must both conserve water and excrete 
substances with a low solubility, two opposing factors.  
This balance must be maintained with the adaptation to 
diet, climate, and activity.  When this balance is 
disrupted, the urine may become supersaturated with 
insoluble materials which may aggregate into a 
calculus (3). 
     There are four basic types of renal calculi: calcium, 
struvite, uric acid, and cystine stones.  Calcium stones, 
which account for 75%-85% of all renal calculi, consist 
of calcium oxalate, calcium phosphate, or calcium 
urate.  Since most renal calculi are composed of 
calcium, most urinary stones are radioopaque (4).  
They are more common in males, often arise in the 3rd 
decade of life, have a recurrence rate between 2 and 3 
years, and is frequently familial (3).  They are 
associated with idiopathic hypercalciuria, 
hyperuricosuria and primary hyperparathyroidism which 
accounts for 50%, 20% and, 5% of calcium stones, 
respectively.  Another 20% are idiopathic (3).
     Struvite (magnesium ammonium phosphate) stones 
are relatively common, making up 10%-15% of all renal 
calculi (3).  These stones are due to chronic urinary 
tract infections with gram-negative urease-producing 
bacteria and therefore are commonly found in women 
and in those patients requiring chronic bladder 
catherization (3).  Common organisms are Proteus, 
Pseudomonas, and Klebsiella species.  Struvite is 
visualized on radiograph when it complexes with 
calcium carbonate or calcium phosphate.  These 
stones are capable of obtaining large sizes, large 
enough to fill the renal pelvis and calyces to produce 
staghorn calculi (3).  
     Uric acid stones make up 5%-8% of renal calculi (3).  
They are radiolucent, are more common in males, and 
are commonly familial.  Since pure uric acid stones are 
radiolucent, CT, ultrasound, or intravenous 
ultrasonography may be implemented for detection; 
however, uric acid frequently complexes with calcium 
oxalate making these stones radioopaque via 
radiograph (4).  About 25% of patients with uric acid 
stones have gout.
     Cystine stones are rare and account for 
approximately 1% of all renal calculi (3).  Because of 
their sulfur content, cystine stones are only slightly 
radioopaque, so are poorly visualized on x-ray.  They 
are due to a hereditary metabolic defect resulting in 
proximal tubular and jejunal transport of the dibasic 
amino acids: cystine, lysine, arginine, and ornithine.  
Thus, a large amount of these amino acids are lost in 
the urine; however, because of its relative insolubility, 
cystine is the only one of these amino acids to form 
stones (1). 
     Stones initially form on the renal papillae or within 
the collecting system.  Stones need not be 
symptomatic; however, pain and obstruction arise when 
stones break loose and enter the ureter or 
ureteropelvic junction (3).  It is not uncommon for 
struvite, cystine, or uric acid stones to grow too large to 
enter the ureter; these stones gradually fill the renal 
papillae and even the renal calyces, forming staghorn 
calculi (3). 
     As the stone traverses the ureter it commonly 
produces severe colicky pain and bleeding, termed 
renal colic (5).  The pain develops gradually, 
manifesting initially in the flank progressing downward 
and anteriorly toward the lower back and genitalia.  
Stones obstructing the ureteropelvic junction may 
present with mild to severe flank pain without radiation 
due to distention of the renal capsule.  Pain which 
migrates downward suggests that the stone has passed 
to the lower third of the ureter.  In the absence of 
migrating pain, the position of the calculi cannot be 
predicted.  If the stone makes its way to the 
ureterovesical junction, symptoms consistent with 
urinary tract infection may manifest; frequency, 
urgency, dysuria (3).  When the stone passes into the 
bladder, the pain subsides; however, unique symptoms 
arise if the stone enters the urethra (5).  There is no 
correlation between stone size and severity of 
symptoms (4).  The symptoms surrounding urolithiasis 
in the pediatric patient varies with age.  The 
excruciating flank pain associated with stone passage 
in the adult patient is rarely seen in children; however, 
50% of children experience abdominal, flank, or pelvic 
pain.  The pain from renal calculi may mimic colic in 
infants.  Pre-school aged children commonly 
experience the symptoms of urinary tract infections 
while adolescents more commonly experience pain 
similar to adults (2).   
     The patient who presents with a renal stone may be 
mistaken for a patient with an aortic dissection, acute 
appendicitis, mechanical back pain, bowel obstruction, 
cholecystitis and biliary colic, constipation, epididymitis, 
gastritis or peptic ulcer disease, UTI and 
pyelonephritis, PID, pneumonia, testicular torsion, or 
urinary obstruction (1).  Thus, these differential 
diagnoses must be considered.
     Upon physical examination, the patient with renal 
colic is typically writhing in pain and is unable to keep 
still; in contrast to patients suffering from peritoneal 
irritation who remain motionless to minimize the pain 
(4).  Fever is absent in uncomplicated cases of 
urolithiasis.  Pyelonephritis, pyonephrosis, or 
perinephric abscess should be suspected if fever is 
present.  An abdominal examination is typically 
unremarkable; although hypoactive bowel sounds may 
indicate an ileus, which is common in patients suffering 
from severe, acute pain.  In male patients, pain may 
radiate to the testicles; however, the testicles should 
appear normal and be only mildly tender.  One should 
be wary of the older patient (>60 years old) with a 
suspected primary case of nephrolithiasis and should 
take care to rule out an aortic aneurysm (1).
     The evaluation of a patient with a suspected renal 
calculi should consist of a metabolic evaluation, urine 
and dipstick, as well as imaging.  Recovered stones 
should be examined for composition, as treatment 
differs according to stone type.  Controversy exists as 
to which patients require a thorough metabolic work-up; 
however, abnormalities of serum calcium, phosphate, 
electrolytes, and uric acid should be screened for in 
first time stone formers.  In recurrent stone formers or 
patients with a family history of stone disease, a more 
extensive evaluation is required.  An initial 24 hour 
urine collection on a random diet should be analyzed 
for volume, urinary pH, and calcium, uric acid, oxalate, 
phosphate, and citrate excretion.  If necessary, a 
second 24 hour urine collection can be made on a 
restricted calcium diet.  PTH and calcium load tests can 
be performed to further clarify metabolic abnormalities 
     Urinalysis may reveal microscopic or gross 
hematuria.  85% of patients with ureterolithiasis have 
hematuria on microscopic exam of the urine, while 95% 
have hematuria when both microscopy and urine 
dipstick are used (1).  Although hematuria is commonly 
associated with urinary calculi, the degree of hematuria 
is not predictive of stone size or passage.  
     Infection must be excluded in cases of renal calculi.  
If a urinary tract infection is present with 
hydronephrosis, hospital admission is mandatory 
unless follow-up is readily available within 24 hours (1).
     Non-contrast helical CT is currently the gold 
standard imaging study for the diagnosis of 
ureterolithiasis in the emergency department.  
Non-contrast helical CT has been shown to have a 
sensitivity of 95%-100% and a specificity greater than 
that of an intravenous pyelogram (IVP).  Advantages of 
non-contrast helical CT are that it can be done in less 
than 5 minutes and avoids the use of IV contrast.  
However, helical CT does not provide information on 
kidney function, the degree of obstruction, and does not 
visualize indinavir stones well (1).  
     Prior to helical CT, IVP was the gold standard 
imaging technique.  Since IVP is dependent on the flow 
of IV contrast from the kidney to the ureters, both 
kidney function and degree of obstruction can be 
assessed.  It is also the test of choice for diagnosing 
indinavir stones.  However, an IVP is not as rapid as a 
helical CT and exposes patients to both radiation and 
the risk of nephrotoxicity or anaphylactoid reactions 
due to contrast agents.  The cost of an IVP is 
comparable to a helical CT (1).
     Although less sensitive or accurate than either an 
IVP or helical CT in diagnosing ureteral calculi, 
ultrasound is useful in the pregnant or unstable patient.  
It is also a useful imaging modality in the course of 
ruling out an abdominal aortic aneurysm in patients 
older than 60 who present with a first or atypical 
nephrolithiasis.  Ultrasound may also be able to 
elucidate stones at the ureterovesical junction that may 
have been missed by helical CT or IVP (1).
     Treatment of nephrolithiasis is dependent on stone 
type.  However, IV access should be obtained to 
administer pain and antiemetic medications.  IV 
hydration is controversial as some believe fluid loading 
forces the stone through the urinary tract at a faster 
rate; however, some feel as if this may increases renal 
colic (1).  However, it is generally accepted that 
increased fluid intake is beneficial in diluting the urine 
and impeding stone formation.
     In some instances, purely medical treatment is not 
sufficient and surgical intervention is indicated.  
Ureterolithiasis coupled with a fever, suggesting a 
urinary tract infection represents a true medical 
emergency.  IV antibiotics and immediate drainage of 
the infected hydronephrosis are indicated, either 
through percutaneous nephrostomy or ureteral stent 
placement.  Antibiotics alone, in this situation, may be 
insufficient (1).  
     When stones fail to pass spontaneously and impede 
urine flow, surgical measures are often indicated.  
Typically, stones lodge at three main sites: the 
ureteropelvic junction, the point at which the ureter 
crosses the iliac vessels, and the ureterovesical 
junction.  Although stones less than 6mm in diameter 
commonly pass spontaneously, it is difficult to 
determine which stones will pass.  Conservative 
observation with the proper pain medications is 
appropriate for the first 6 weeks; if the stone has not 
passed by the 6th week, more aggressive intervention 
is required.  Indication for intervention before the 6th 
week includes severe pain that does respond to 
medication, fever, chronic nausea and vomiting that 
requires IV hydration, and social factors (e.g. need to 
return to work or travel) (4).  
     Distal ureteral stones are best extracted via 
ureteroscope or in situ extracorporeal shock wave 
lithotripsy (ESWL).  Ureteroscopic extraction involves 
passing an endoscope through the urethra into the 
ureter.  With the aid of direct visualization, the stone is 
removed via basket extraction.  In situ ESWL involves 
the use of external energy that is focused at the point of 
the stone, resulting in stone fragmentation and 
eventually stone passage.  This technique is not 
advised for women of childbearing age with stones in 
the lower ureter since the effects of such treatment on 
the ovaries is unknown (4).
     Proximal and midureteral stones (i.e. above the 
inferior margin of the sacroiliac joint) can also be 
treated with ureteroscopy or in situ ESWL.  With 
ESWL, the stone can be pushed back via a retrograde 
ureteral catheter into the renal pelvis so as to provide a 
larger area for stone fragmentation.  Stents may be 
placed in the ureter to facilitate passage and prevent 
obstruction (4).  
     Renal stones that are asymptomatic do not need to 
be treated.  However, they should be monitored via 
serial abdominal radiographs or renal ultrasound.  If the 
stone is growing and becomes symptomatic, the 
appropriate procedures should be undertaken.  Stones 
less than 3cm in diameter should be treated with 
ESWL; while larger stones, and stones that reside in 
the inferior calyx are best treated with percutaneous 
nephrolithotomy (4).
     1.  Craig S.  Renal Calculi.  Available online at 
June 28, 2000.
     2.  Kroovand LR.  Pediatric Urolithiasis.  Urologic 
Clinics of North America 1997;24(1):173-184.
     3.  Asplin JR, Coe FL, Favus MJ.  Nephrolithiasis.  
In:  Braunwald E, Fauci AS, Hauser SL, Isselbacher KJ, 
Kasper DL, Longo DL, Martin JB, Wilson JD (eds).  
Harrison's Principles of Internal Medicine, 14th Edition 
CD-ROM.  McGraw-Hill, New York, 1998, 
     4.  Presti JC, Stoller ML, Carroll PR.  Urology: 
Urinary Stone Disease.  In:  Tierney LM, McPhee SJ, 
Papadakis MA (eds).  Current Medical Diagnosis and 
Treatment, 39th edition.  Lange Medical Books, New 
York, 2000, pp929-933.
     5.  Hruska K.  Renal Calculi (Nephrolithiasis).  In:  
Goldman L, Bennett JC (eds).  Cecil Textbook of 
Medicine, 21st ed.  W.B. Saunders Company, 
Philadelphia, 2000, pp622-627.

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Web Page Author:
Loren Yamamoto, MD, MPH
Professor of Pediatrics
University of Hawaii John A. Burns School of Medicine