202 Letters to the Editor–Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 180 (2014)
d Reproductive Biology 180 (2014) 198–208
[(Fig._1)TD$IG]
Fig. 1. Detail scan at 21st week: elongated cervix with 82 mm of length (arrow) displaced upward and anteriorly, lying behind the pubic symphysis. No anatomical
malformations identified.
References
[1] Smalbraak I, Bleker OP, Schutte MF, Treffers PE. Incarceration of the retroverted
gravid uterus: a report of four cases. Eur J Obstet Gynecol Reprod Biol 39
1991;151–5.
[2] Newell SD, Crofts JF, Grant SR. The incarcerated gravid uterus: complications
and lessons learned. Obstet Gynecol 2014;123:423–7.
[3] Gardner CS, Jaffe TA, Hertzberg BS, Javan R, Ho LM. The incarcerated uterus: a
review of MRI and ultrasound imaging appearances. Am J Roentgenol
2013;201:223–9.
[4] Grossenburg NJ, Delaney AA, Berg TG. Treatment of a late second-trimester
incarcerated uterus using ultrasound-guided manual reduction. Obstet Gynecol
2011;118:436–9.
[5] Dierickx I, Van Holsbeke C, Mesens T, et al. Colonoscopy-assisted reposition of
the incarcerated uterus in mid-pregnancy: a report of four cases and a literature
review. Eur J Obstet Gynecol Reprod Biol 2011;158:153–8.
[6] Van Winter JT, Ogburn Jr PL, Ney JA, Hetzel DJ. Uterine incarceration during the
third trimester: a rare complication of pregnancy. Mayo Clin Proc 1991;66:
608–13.
Catarina Policianoa,* , Cláudia Araújoa
Susana Santoa,b
Mónica Centenoa,b
Luísa Pintoa,b
a
Department of Obstetrics and Gynecology, CHLN – Hospital
Universitário de Santa Maria, Lisbon, Portugal, bFaculdade de
Medicina da Universidade de Lisboa, CAM – Centro Académico de
Medicina de Lisboa, Av. Prof. Egas Moniz, 1649-035 Lisboa, Portugal
* Corresponding author at: Hospital Universitário de Santa Maria,
Department of Obstetrics and Gynecology CHLN, Av. Prof. Egas
Moniz, 1649-035 Lisboa, Portugal.
Tel.: +351 217805578; fax: +351 217805621.
E-mail address: catarinapoliciano@gmail.com (C. Policiano).
Received 24 March 2014
Received in revised form 18 May 2014
Accepted 20 May 2014
http://dx.doi.org/10.1016/j.ejogrb.2014.05.019
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A vaginal Gartner duct cyst presenting as a
cystocele during pregnancy
Dear Editor,
We observed a 33-year-old primigravida who presented at 29
weeks of pregnancy, after having discovered tumefaction of the
vagina. She reported pollakiuria, nycturia and a bladder filling
sensation. A pelvic examination revealed swelling of the anterior
wall of the vagina measuring 7 cm (Fig. 1(1), images have been
reproduced with permission of the patient), which increased in
volume during the following weeks, reaching a diameter of 8 cm
at 37 weeks of pregnancy. Different possible diagnoses were
made, including cystic vaginal lesion, real pelvic organ prolapse,
urethral diverticulum, and a vaginal Gartner’s or Sken’s duct cyst
[1]. The swelling exposed the patient to the risk of dystocia, and
rupture during labor or the expulsive stage. A diagnostic
procedure was carried out by means of MRI imaging, with a
non-enhanced fast protocol involving sagittal, axial and coronal
T2-weighted images, using turbo spin-echo sequences. The
appearance of the MRI was consistent with a wolffian duct
remnant in the vagina (Gartner’s duct cyst), as shown in Fig. 1(2)
(A, fetal head; C, vaginal cyst). Uroflowmetry did not reveal any
abnormality.
The cyst was punctured at the start of labor and an aseptic,
viscous, translucent liquid was evacuated. Delivery was performed
vaginally, without instrumentation, at 40 weeks. Surgical excision
of the cyst was performed 6 months later, as a result of recurrence
and vaginal symptoms (dyspareunia). The cystic mass extended to
the right lateral side of the bladder, but did not penetrate into the
urethra or the bladder (Fig. 1(3)). Pathology revealed a vestigial
paravaginalis cyst (mesonephrotic). Immunohistochemistry find-
ings revealed a high expression of CK7 and CK5/6, but no
expression of estrogen or progesterone receptors. No
 Letters to the Editor–Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 180 (2014) 198–208 203
[(Fig._1)TD$IG]

Fig. 1. A vaginal Gartner duct cyst presenting as a cystocele. (1) Pelvic examination during pregnancy (a pelvic examination revealed swelling of the anterior wall of the vagina
measuring 7 cm, mimicking a cystocele (International Continence Society’s pelvic organ prolapse quantifiation system: stage 3 cystocele; Ba = +3; C = 3; D = 7; Bp = 3)). (2)
T2-weighted MRI parasagittal image that revealed a cystic lesion arising from right vaginal wall extended to vulva and measuring 70 mm  30 mm  20 mm (A = fetal head;
C = vaginal Gartner cyst enhanced with contrast). (3) Pelvic examination 6 months after delivery (C = left vaginal Gartner cyst).

complications were observed post-operatively, and at 3 months
follow-up the patient no longer suffered from dyspareunia.
Pelvic organ prolapse does not usually occur during pregnancy
[2]. The assessment of a vaginal lesion during pregnancy, by means
of a pelvic examination and imaging of the surrounding organs, is
needed in order to make a reliable diagnosis and avoid
inappropriate management. Conservative management may be
preferable [3].
Conflict of interest
None.
Source of financial support/funding
None.
References
[2] Cil AP, Basar MM, Kara SA, Atasoy P. Diagnosis and management of vaginal
mullerian cyst in a virgin patient. Int Urogynecol J Pelvic Floor Dysfunct 2008;19
(May (5)):735–7.
[3] Montella JM. Vaginal mullerian cyst presenting as a cystocele. Obstet Gynecol
2005;105(Pt 2):1182–4.
Jeremy Boujenaha,b , Guillaume Ssi-yan-kanc
Sophie Prevotd
Gihad E. Chalouhie
Xavier Deffieuxa,b,f,*
a
AP-HP, Hôpital Antoine Béclère, Service de Gynécologie-Obstétrique
et Médecine de la Reproduction, Clamart F-92141, France, bUniversité
Paris-Sud, Faculté de Médecine, Orsay F-91405, France, cAP-HP,
Hôpital Antoine Béclère, Service de Radiologie, Clamart F-92141,
France, dAP-HP, Hôpital Antoine Béclère, Service d'Anatomopatho-
logie, Clamart F-92141, France, eAP-HP, Hôpital Necker, Service de
Gynécologie-Obstétrique, Paris F-75007, France, fGREEN GRC 01
(UPMC), Groupe de RecherchE cliniquE en Neuro-Urologie, Site
Antoine Béclère, Clamart F-92141, France

[1] O’Boyle AL, Woodman PJ, O’Boyle JD, Davis GD, Swift SE. Pelvic organ support in * Corresponding author at: Service de Gynécologie Obstétrique et
nulliparous pregnant and nonpregnant women: a case control study. Am J Médecine de la Reproduction, Hôpital Antoine Béclère, 157 rue de
Obstet Gynecol 2002;187(July (1)):99–102.

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204 Letters to the Editor–Brief Communications / European Journal of Obstetrics & Gynecology and Reproductive Biology 180 (2014) 198–208
[(Fig._1)TD$IG]
la Porte de Trivaux, F-92140 Clamart, France. Tel.: +33 1 45 374
487; fax: +33 1 45 374 963.
E-mail address: xavier.deffieux@abc.aphp.fr (X. Deffieux).

Received 1 February 2014

Received in revised form 26 March 2014
Accepted 20 May 2014

http://dx.doi.org/10.1016/j.ejogrb.2014.05.015

Wernicke’s encephalopathy complicating

gestational hyperemesis

Dear Editor,

Wernicke’s encephalopathy (WE) is an acute, severe neuropsy-

chiatric syndrome arising from thiamine (vitamin B1) deficiency.
Although it is often thought confined to alcohol abuse, WE may
occur in any nutritionally deficient state including pregnancy-
related conditions such as hyperemesis and thyrotoxicosis [1,2].
During pregnancy, a delayed diagnosis of WE results in serious
complications in both mother and baby [1,2].
A previously healthy 24-year-old pregnant woman, G1P0, was
admitted to hospital at 18 weeks of gestation and following 5
weeks of vomiting and weight loss totaling 8.6 kg. Abdominal
ultrasounds were normal. Her nausea improved with intravenous
metoclopramide and mildly elevated liver enzymes normalized
with hydration. Three days later she was discharged home only to
be readmitted 2 weeks later with intractable vomiting, and with
additional neurological symptoms of headache, double vision,
weakness and dizziness. Physical examination showed normal
consciousness, reduced deep tendon reflexes, multidirectional
nystagmus, paralysis of the left VI cranial nerve, and finger-noise
ataxia. The following day the patient became stuporous with a
Glasgow Coma Scale score of 10 and was transferred to the
intensive care unit. Laboratory evaluation revealed elevated 2–3
fold elevated hepatic enzymes. Her cerebrospinal fluid (including
PCR for neurotropic viruses) was normal. Magnetic resonance
imaging (MRI) of the brain showed normal vessels and bilateral,
abnormal T2 hyperintensities in the superior colliculi, periaque-
ductal gray, fornix, mammillary bodies, and in anterior and
posterior thalamus (Fig. 1). Based on clinical and radiological
findings, WE was diagnosed and therapy with intravenous
thiamine 300 mg/day was begun. During the next five days the
patient gradually improved her consciousness and became able to
walk on a wide base and tolerate solid food. Fetal ultrasounds
were normal on admission but nine days later they were
consistent with death in utero. Fetal delivery was medically
induced.
WE is a potentially fatal, but reversible, medical emergency if
recognized and treated promptly [1,2]. WE is featured by the classic
triad of ataxia, ophthalmoplegia and altered mental status.
However, in approximately 70% of non alcoholic patients, WE
presents with non specific symptoms (i.e., dizziness, headache,
fatigue, depressive or visual problems) rather than with the
classical triad which is often absent or a late finding [1,2]. As a
consequence, WE is often underdetected or misdiagnosed for other
disorders and is found approximately 10–20 fold more frequently
in autopsy than in clinical studies [1–3]. Because of delayed
treatment, WE in pregnancy leads to high rates of permanent
cognitive impairment (60–80%), the Korsakoff’ syndrome, or death
of the mother (10–20%) [2].
Fig. 1. T2-weighted axial MRI images of the brain taken at the level of
mesencephalon (above) and thalamus (below). Open arrows indicate areas of
abnormal hyperintensity. Abbreviations: AT: anterior thalamus; F: fornix; PAC:
periaqueductal gray; PT: posterior thalamus; SC: superior colliculi.
Besides causing WE in the mother, thiamine deficiency has
adverse effects also on fetal outcome, likely because thiamine
deficiency impairs oxidative energy metabolism and central
nervous system development [1,3]. Based on literature, the risk
of spontaneous abortion and of fetal intrauterine death in WE is,
respectively, 25% and 1%. Further, in asymptomatic pregnant
women, low thiamine levels have been associated to intrauterine
growth retardation of the fetus and low weight at birth [1]. Our
case of intrauterine death during mother’s recovery from WE adds
evidence that thiamine deficiency may damage the fetus despite
the reversal or even in absence of neurological symptoms in the
mother.
The diagnosis of WE remains primarily clinical [4]. Brain MRI,
however, plays an important role in supporting the diagnosis of WE
(level B evidence) [4] because classical clinical signs are often
lacking and thiamine determination may not be readily available.
Also, brain MRI allows differential diagnosis of WE (sensitivity
90%) from other neurological emergencies in pregnancy (i.e., deep
cerebral vein thrombosis, thalamic stroke, encephalitis, central
pontine myelinolysis) [4,5]. The typical MRI findings in WE, seen
also in our patient, include T2-weighted hyperintense areas in the
periaqueductal and periventricular gray matter and are potentially
reversible [4,5]. When they involve cerebellar and cerebral
cortices, hyperintense abnormalities on MRI predict a poor
outcome.

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