Open Journal of Obstetrics and Gynecology, 2011, 1, 17-20
doi:10.4236/ojog.2011.12004 Published Online June 2011 ( OJOG
Published Online June 2011 in SciRes.
Medication induced fetal bladder rupture: a case report
Eldon Palmer1,2, Milette Oliveros1, Jason Fong3, George Graham3*
1Department of Neonatology, John A. Burns School of Medicine, University of Hawai’i, Honolulu, USA;
2Department of Pediatrics, Tripler Army Medical Center, Honolulu, USA;
3Department of Obstetrics, Gynecology and Women’s Health, John A. Burns School of Medicine, University of Hawai’i, Honolulu,
Email: *
Received 29 March 2011; revised 19 April 2011; accepted 27 April 2011.
BACKGROUND: Intrauterine bladder rupture is a
rare complication usually caused by structural blad-
der outlet obstruction. Some medications are known
to cause urinary retention or diuresis in fetuses and
preterm infants. CASE: A 31-year-old gravida 6, pa-
ra 3023 at 29 weeks and 2 days’ gestation required
intubation, mechanical ventilation, and medical ma-
nagement for severe chest pain and respiratory fail-
ure, eventually diagnosed as asthma and pneumonia.
An obstetrical ultrasound on hospital day three re-
vealed a markedly dilated fetal bladder. Repeat ul-
trasound the following day showed a decompressed
fetal bladder and significant ascites. A cesarean de-
livery was performed for a nonreassuring fetal heart
rate. Postnatal evaluation by voiding cystourethro-
gram and cystoscopy revealed bladder rupture with-
out evidence of outlet obstruction. Given the absence
of other plausible causes, the rupture was likely due
to exposure to maternal medications. CONCLUSION:
Transplacental exposure to maternal medications
may cause fetal urinary retention and intrauterine
bladder rupture. Fetal ultrasound surveillance dur-
ing treatment with medications known to cause uri-
nary retention may allow for early diagnosis and in-
Keywords: Bladder Rupture; Maternal Medication; Phar-
macology; Fetal Urinary Retention; Fetal Ultrasound
Megacystis and intrauterine bladder rupture are rare
complications usually resulting from structural bladder
outlet obstruction. Transplacental exposure to medica-
tions during pregnancy has been associated with fetal
urinary retention. Th is is the first case in the literature of
fetal urinary retention secondary to maternal medication
exposure resulting in intrauterine bladder rupture.
A 31-year-old gravida 6, para 302 3 with normal pr enatal
labs and a normal 22 week ultrasound presented to a
local emergency room at 29 2/7 weeks’ gestation with
symptoms of shortness of breath and severe chest pain.
Due to respiratory failure, she was intubated and placed
on mechanical ventilation. She was diagnosed with
asthma and bacterial pneumonia and transferred to the
medical intensive care unit (ICU) of a referral center.
The patient remained on a ventilator and was contin-
ued on sedation, pain control, asthma management, and
antibiotics. She was given a course of steroids for fetal
benefits. An obstetrical ultrasound performed o n hospital
day three was notable for an enlarged, thin-walled blad-
der with a mean diameter of 4.8 cm (Figure 1). There
was a trace amount of ascites seen. The amniotic fluid
volume appeared normal, with an amniotic fluid index of
20 cm. The renal pelvises measured five mm bilaterally
without evidence of dilated ureters. The gender was fe-
male. A biophysical profile was reassuring and the re-
mainder of the anat omical survey appeared normal.
Figure 1. Prenatal ultrasound showing an enlarged fetal bladder.
E. Palmer et al. / Open Journal of Obstetrics and Gynecology 1 (2011) 17-20
On hospital day four, fetal monitoring showed an ab-
sence of variability and recurrent late decelerations in
the fetal heart rate. A bedside ultrasound revealed a de-
compressed bladder and significant ascites (images not
A cesarean delivery was performed under general an-
esthesia for nonreassuring fetal status. A female infant
weighing 1531 g with Apgars of 3, 7, and 9 was deliv-
ered. On exam the neonate was noted to have a markedly
distended abdomen. Respiratory distress persisted be-
yond the initial resuscitation period and the baby was
transferred to a referral neonatal ICU for further evalua-
tion and management. An abdominal ultrasound per-
formed on the first day of life (DOL) showed ascites
with mild to moderate left hydronephrosis, left hy-
droureter, and a decompressed bladder (Figure 2).
Anuria was noted during the first DOL. A peritoneal
drain was placed on the second DOL yielding 140 mL of
fluid with an electrolyte profile consistent with urinary
ascites. Voiding cystourethrogram (VCUG) showed a
small bladder with leakage of con trast into the peritoneal
cavity (Figure 3). Cystoscopy revealed a defect in the
posterior bladder wall (Figure 4). Importantly, no anat-
omic bladder outlet obstruction was seen. Foley output
improved and peritoneal output eventually stopped on
DOL eight. A repeat VCUG on DOL 19 showed no evi-
dence of the previously seen defect. The baby was dis-
charged on DOL 21 wi th n or mal bladder functi on .
The mother did well postoperatively. She was extu-
bated on postoperative day one and discharged on hos-
pital day nine.
This is the first case in the literature of fetal urinary re-
tention and subsequent bladder rupture secondary to
maternal medication exposure. Previously described
causes of fetal bladder outlet obstruction include urethral
atresia, urethral valves, prolapsed ureterocele, megacys-
tis megaureter and megacystis microcolon. Although it is
Figure 2. Neonatal ultrasound showing a decompressed blad-
der and ascites.
Figure 3. Voiding cystourethrogram showing a contracted
bladder with contrast in the peritoneum.
Figure 4. Cystoscopy showing a perforation in the posterior
bladder wall.
not possible to prove that fetal urinary retention was due
to maternal medication exposure, the postnatal evalua-
tion excluding structural causes of bladder outlet ob-
struction makes transplacental medication exposure the
most likely etiology. This functional obstruction, com-
bined with medication induced diuresis, likely contrib-
uted to intrauterine bladder rupture.
opyright © 2011 SciRes. OJOG
E. Palmer et al. / Open Journal of Obstetrics and Gynecology 1 (2011) 17-20 19
Our diagnosis of acute fetal urinary retention is based
on a normal appearing bladder at 22 weeks’ gestation,
and the subsequent appearance of a thin-walled dis-
tended bladder with a normal amniotic fluid volume and
normal appearing fetal kidneys. The smooth appearance
of the abdomen after drainage of the ascites is also sig-
nificant, as chronic abdominal distension would likely
lead to a prune belly app earance of the abdominal wall.
Transplacental exposure to maternal antipsychotic
medications has been proposed as a cause of fetal uri-
nary retention, with subsequent resolution after discon-
tinuation of the medications [1]. We reviewed the ma-
ternal medications used in this case for their potential to
cause urinary retention and to cross the placenta. Of the
medications used, fentanyl, morphine, ipratropium, dil-
tiazem, and aminophylline have been reported to cause
urinary retention.
Opioids, specifically morphine and fentanyl, rapidly
cross the human placenta with equilibration between the
mother and fetus [2]. Opioids decrease the sensation of
bladder fullness by blocking parasympathetic nerves and
increase the tone of the bladder neck by stimulating
sympathetic nerves, both of which can result in urinary
retention. Urinary retention requiring bladder drainage
has been reported in premature infants within 24 hours
of exposure to morphine [3]. Ipratropium bromide is an
inhaled anticho linergic medication us ed for th e treatment
of asthma and has been associated with urinary retention
[4]. Systemic absorption of inhaled ipratropium is mini-
mal and it is not known whether ipratropium crosses the
placenta. Calcium channel antagonists, such as diltiazem,
reduce contractility o f the bladder and can cause urin ary
retention in adults. Diltiazem crosses the placenta with a
similar concentration in the mother and fetus [5].
Aminophylline is a compound of the bronchodilator
theophylline and ethylenediamine, and is used for the
treatment of asthma. Theophylline has been associated
with urinary retention and diuresis. It is thought that
theophylline inhibits contractility of the detrusor muscle
by increasing cyclic adenine monphos phate [6]. Theo-
phylline crosses the placenta rapidly, with a similar con-
centration in the mother and fetus [7]. Maternal fu-
rosemide has been used to distend the fetal bladder for
evaluation of urinary tract anomalies [8].
Maternal rocuronium and propofol were specifically
investigated for urinary effects given their infrequent use
in pregnancy. Rocuronium is a nondepolarizing, neuro-
muscular blocking agent that paralyzes skeletal muscle,
but not smooth muscle. Paralysis of skeletal muscle re-
sults in relaxation of the external urethral sphincter and
therefore would not be expected to cause urinary reten-
tion. Propofol is a short acting h ypnotic ag ent, which has
not been associated with urinary retention.
Due to the nature of the mother’s presentation to the
outlying hospital, a large number of medications were
administered in the work-up and treatment of her under-
lying medical conditio n (Table 1). Since the medications
used in this case have not previously been associated
with fetal bladder rupture, it is likely the dose and com-
bination of medications that contributed to the outcome
in this case (Table 2).
Ta b le 1 . Maternal medications given prior to first evidence of
bladder distension.
Medication Known urinary effect s
Acetaminophen None
Aminophylline Aminophylline- dif ficulty voiding, diuresis
Azithromycin rare nephritis, acute renal failure
Betamethasone Early neonatal diuresis
Ceftriaxone rare renal insufficiency
Cisatracurium None
Diltiazem Urinary retention
Enoxaparin None
Fentanyl urinary tract spasm, urinary retention, oli guria
Insulin None
Furosemide Induces diuresis
Ipratropium dysuria, urinary retention
Levalbuterol hematuria
Morphine urinary tract spasm, urinary retention, oliguria
Oseltamivir None
Propofol Green urine
Rocuronium None
Table 2. Most likely contributors to fetal bladder rupture.
Medication Urinary Effect
Fentanyl Increase bladder neck tone
Decreases intensity of afferent
distension signal 1750 mcg
Furosemide Induces diuresis 80 mg
Diltiazem Decreases bladder contractility 50 mg
Aminophylline Decrease detrusor contractility
Induces diuresis. 250 mg
Morphine sulfateIncrease bladder neck tone
Decreases intensity of afferent
distension signal 335 mg
opyright © 2011 SciRes. OJOG
E. Palmer et al. / Open Journal of Obstetrics and Gynecology 1 (2011) 17-20
Copyright © 2011 SciRes.
Periodic ultrasound examinations to evaluate for me-
gacystis could be considered when medications associ-
ated with urinary retention are used during pregnancy;
especially when multiple med ications and h igh doses are
used. If significant bladder distention develops, a change
in medication or a vesicocentesis could be considered to
decrease the risk of intrauterine bladder rupture.
Norman Sato, MD; Ronald Sutherland, MD; Devin Puapong, MD;
Janet Burlingame, MD.
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