Medication induced fetal bladder rupture: a case report

doi:10.4236/ojog.2011.12004

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Open Journal of Obstetrics and Gynecology, 2011, 1, 17-20

doi:10.4236/ojog.2011.12004 Published Online June 2011 (http://www.SciRP.org/journal/ojog/ OJOG

Published Online June 2011 in SciRes. http://www.scirp.org/journal/OJOG

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,

USA.

Email: *[email protected]

Received 29 March 2011; revised 19 April 2011; accepted 27 April 2011.

ABSTRACT

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-

tervention.

Keywords: Bladder Rupture; Maternal Medication; Phar-

macology; Fetal Urinary Retention; Fetal Ultrasound

1. INTRODUCTION

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.

2. CASE REPORT

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

available).

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.

3. DISCUSSION

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.

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

MethylprednisoloneNone

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

Cumulative

Dose

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

E. Palmer et al. / Open Journal of Obstetrics and Gynecology 1 (2011) 17-20

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.

OJOG

4. ACKNOWLEDGEMENTS

Norman Sato, MD; Ronald Sutherland, MD; Devin Puapong, MD;

Janet Burlingame, MD.

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