400 Lettres à la rédaction / Gynécologie Obstétrique & Fertilité 43 (2015) 397–403
Déclaration d’intérêts
Les auteurs déclarent ne pas avoir de conflits d’intérêts en
relation avec cet article.
Références
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[5] Brunskill PJ. The effects of fetal exposure to danazol. Br J Obstet Gynaecol
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[6] Quagliarello J, Greco MA. Danazol and urogenital sinus formation in pregnan-
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dysplasia. J Pediatr 1979;95(3):399–402.
[9] Chen CP, Liu FF, Jan SW, Chang PY, Lin YN, Lan CC. Ultrasound-guided fluid
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hydrocolpos. Ultrasound Obstet Gynecol 2007;30(1):105–9.
[11] Salle JLP, Lorenzo AJ, Jesus LE, Leslie B, AlSaid A, Macedo FN, et al. Surgical
treatment of high urogenital sinuses using the anterior sagittal transrectal
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[12] Garel C, Dreux S, Philippe-Chomette P, Vuillard E, Oury JF, Muller F. Contribu-
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[13] Burc L, Volumenie JL, de Lagausie P, Guibourdenche J, Oury JF, Vuillard E, et al.
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with gastroschisis undergoing amnioexchange. BJOG 2004;111(4):292–714.
[14] Lecarpentier E, Dreux S, Blanc T, Schaub B, Ville Y, Mandelbrot L, et al.
Biochemical analysis of cystic fluid in the diagnosis of fetal intra-abdominal
masses. Prenat Diagn 2012;32(7):627–31.
D. Desseauvea,*,b, J.-L. Voluméniec, M. Gueneretc, J.-F. Colombanid,
B. Schaubc, F. Mullere
a
Université de Poitiers, CHU de Poitiers, 86021 Poitiers cedex, France
b
Service de gynécologie-obstétrique et médecine de la reproduction,
CHU de Poitiers, 86021 Poitiers cedex, France
c
Service de gynécologie-obstétrique, maison de la femme,
de la mère et de l’enfant, CHU de Fort-de-France,
97261 Fort-de-France cedex, Martinique
d
Service de chirurgie pédiatrique, maison de la femme,
de la mère et de l’enfant, CHU de Fort-de-France,
97261 Fort-de-France cedex, Martinique
e
Biochimie hormonologie, hôpital Robert-Debré, AP–HP,
75019 Paris, France
*Auteur correspondant
Adresse e-mail : david.desseauve@univ-poitiers.fr (D. Desseauve)
Reçu le 17 octobre 2014
Disponible sur Internet le 15 avril 2015
http://dx.doi.org/10.1016/j.gyobfe.2015.03.007
Toxic Shock Syndrome detected at 21 weeks’
gestation complicating acute chorioamnionitis
with intact sac
Toxic Shock Syndrome à 21 semaines d’aménorrhée compliquant une
chorioamniotite aiguë à membranes non rompues
We would like to report the case of a patient who presented a
group A beta-hemolytic Toxic Shock Syndrome (TSS) at
21 weeks’ gestation. Rare cases have been reported during
pregnancy, mostly during the third trimester, with a higher
maternal and/or fetal mortality than that observed in the
postpartum period or outside of pregnancy [1,2]. Indeed, during
pregnancy, the clinical picture is always complicated by early
major multi-organ failure.
1. Observation
The patient, aged 34, gravida 2, para 2, at 21 weeks’ gestation,
consulted a hospital center close to her home at 3 p.m. with a
clinical picture of febrile gastroenteritis worsening since that
morning. Her medical history included a cesarean section and type
2 diabetes. On examination, a persistent hypotension of 95/
63 mmHg was observed in spite of fluid replacement. Obstetric
examination was unrevealing. There had been no uterine
contractions and the cervix was closed. The uterus was tender
on palpation. Laboratory tests showed an impairment of renal
function (clearance less than 60 mL/min/m2, proteinuria on urine
sample of 4 g/L) associated with a hypokaliemia at 3.0 mmol/L,
signs of hemolysis (haptoglobin 0.20 g/L, LDH 1311 IU/L), a
beginning disseminated intravascular coagulation (DIC) (APTT
ratio 5, fibrinogen 0.60 g/L, PT < 10%, platelets 140,000/mm3, D-
dimers 4 mg/L) and an inflammatory syndrome (CRP 48 mg/L, PCT
13.71 ng/mL, leukocytes 12,000/mm3). Intravenous antibiotic
treatment started with Ceftriaxon 2 g and Ofloxacin 200 mg. The
patient was transferred to the medical intensive care unit at the
Strasbourg University Hospital. On admission, her temperature
was 38.8˚ C, heart rate 111 bpm, blood pressure 121/58 mmHg,
oxygen saturation 98% and respiratory rate 21/min. The patient did
not show any signs of cardiorespiratory or neurological distress
(Glasgow Coma Scale 15), but had significant suprapubic pain as
well as endobuccal hemorrhagic lesions. The onset of moderately
abundant metrorrhagia associated with cervical changes was
noted. Chest X-ray revealed a predominantly peripheral bilateral
interstitial syndrome. ECG showed sinus tachycardia at 110 bpm.
Repeat laboratory tests showed a deteriorating renal function (GFR
34 mL/min/m2, creatinine 160 mmol/L), inflammatory syndrome
(CRP 122 mg/L), DIC (PT < 10%, APTT 106.3 s, factor V 8%, factor II
48%, factor VII 63%, factor X 56%, platelets 114,000/mm3) and
hemolysis (LDH 657 IU/L, haptoglobin 0.11 g/L). Blood gas results
were as follows: pH 7.43, PaCO2 38 mmHg, PaO2 76 mmHg,
HCO3–15 mmol/L, BE 8.8 mmol/L, lactates 6.7 mmol/L.
Management of the shock syndrome consisted of vascular
filling with isotonic saline solution, administration of noradrena-
lin, oxygen therapy via a facial mask, broad-spectrum antibiotic
therapy with Piperacillin-Tazobactam-Amikacin and blood pres-
sure monitoring. CT scan of the abdomen and pelvis revealed no
specific abnormality. Vaginal swab and blood cultures taken the
previous evening proved to be positive for group A beta-hemolytic
Streptococcus pyogenes, and the antibiotic treatment was accord-
ingly modified with the addition of Clindamycin and Metronidazol.
The patient was also transfused with several packs of red cells and
fresh frozen plasma. The diagnosis of group A beta-hemolytic
streptococcal TSS complicating probable chorioamnionitis was
made in the light of this clinical picture of septic shock with multi-
organ failure. After multidisciplinary discussion and with the
 Lettres à la rédaction / Gynécologie Obstétrique & Fertilité 43 (2015) 397–403
Fig. 1. Acute placentitis: infiltration of villosities by polynuclear leukocytes with
necrosis of the trophoblast (" hematoxylin and eosin stain, magnification  200).
consent of the couple it was decided to proceed with medical
termination of the pregnancy in order to ensure maternal rescue. In
view of the rapid and sudden worsening of the patient’s ventilatory
parameters, we performed a cesarean section under general
anesthesia at 2 p.m. It took place without major complication via a
subumbilical midline incision and median corporeal hysterotomy
with extraction of a lifeless female fetus weighing 360 grams. The
exploration of the abdominopelvic cavity was normal. Histological
examination confirmed the presumtive diagnosis of acute chor-
ioamnionitis (Fig. 1). The day following the operation, the
appearance of lesional edema was observed on the chest X-ray
which, together with a persisting multi-organ failure, required us to
begin intermittent conventional dialysis (creatinine 850 mmol/L).
Placental and vaginal swabs were positive for group A Streptococcus
pyogenes, as was mass spectrometry analysis of specimens which
had been sent to the French National Reference Center for
Streptococci at the Cochin-Broca-Hôtel Dieu hospital group
(department of Prof. Poyart, 27, rue du Faubourg Saint-Jacques,
Paris): emm3 (M protein gene) sequences were identified and the
specimens were positive for streptococcal A and B superantigens.
Throat swabs were negative for group A S. pyogenes. The patient was
extubated 5 days after the cesarean. There were no abnormal
features on the gynecological follow-up examination two weeks
after the operation. The patient was transferred to the nephrology
unit for ongoing daily dialysis because of acute tubular necrosis. This
was discontinued 15 days after the cesarean following resumption of
renal function (446 mmol/L). The patient was reviewed two months
after the event without major sequelae.
2. Discussion
Over the past twenty-five years, there has been a rise in invasive
group A streptococcal infections [1,7,8] during pregnancy, with an
incidence 20 times higher in pregnant women compared to non-
pregnant women [1,9]. The greater susceptibility of parturient
women to contract such an infection has been demonstrated [8] and
is due to skin and mucosal lesions on delivery, vaginal pH variation
after the rupture of the amniotic sac, which promotes microorgan-
ism growth, and temporary immunosuppression linked to preg-
nancy [1,3]. The low incidence of these infections and considerable
variability in the severity of the clinical pictures suggest that an
innate or acquired immunity against group A streptococci exists
among pregnant or postpartum women [1,4].
Group A streptococcal toxicity is linked to its virulence factors
[9]: the antiphagocytic surface protein M, and pyrogenic exotoxin
(Spe-A) essentially produced by the M1 and M3 serotypes
401
[2]. Although there are almost 150 different M serotypes, only
some are responsible for invasive infections. Byrne [4] showed that
the morbidity of parturients with puerperal endometritis was
significantly associated with the M1 and M28 serotypes; an
association between the morbidity of non-puerperal group A
streptococcal invasive infections and M1 and M3 serotypes had
already been found [4], with the latter being associated with TSS in
38% to 40% of cases versus 10% to 15% for the other strains. The rise in
invasive forms appears to be linked to an increase in the virulent M1
and M3 strains [5,10,11]. Spe-A is responsible for severe invasive
infections due to significant lymphocyte stimulation, bypassing the
conventional pathway, and gives rise to a massive production of
cytokines and massive inflammatory response. In the study by Byrne
[4], most of the strains expressing Spe-A were implicated in severe
clinical pictures, notably TSS, with high morbidity. The type B
pyrogenic exotoxin (Spe-B) does not appear to be linked to
morbidity [4]. In our case report, a type M3 group A streptococcus
expressing type A and B pyrogenic exotoxins was identified. These
strains are relatively uncommon in France and account for only 3% to
4% of the strains responsible for invasive group A streptococcal
infections. Although identification of the strain is not of immediate
clinical benefit, it can be used retrospectively to show a relationship
with and understand the severity of a particular clinical picture.
As in all cases of TSS, our patient presented a relatively non-
specific initial clinical picture with adverse progression in less than
24 hours. The early diagnosis of these invasive forms is difficult to
make on account of the paucity of initial symptoms, thus leading to
delayed recognition [6]. Streptococcal A infections complicated by
TSS are rare (6%) [3], and occur in most cases (85%) within the first
2 to 3 postpartum days, preponderantly after normal vaginal
delivery [3,5,6,10,12].
During pregnancy, the clinical picture is always complicated by
early major multi-organ failure [2–6], suggesting an immunity
different from that observed in the postpartum [2,11,12] and only
medical interruption of pregnancy and comprehensive intensive
care can ensure a favorable outcome. A shorter delay between the
onset of infection and surgical treatment is correlated to a lesser
degree of morbidity and mortality [3,4,11]. Because of the term and
the non-viability of the fetus, a cesarean with a transvaginal
approach could have been done to reduce maternal morbidity.
Considering the germ and to reduce the risk of hematoma associated
with DIC, we preferred to realize a subumbilical midline laparatomy,
instead of a transverse laparotomy, looking for other infectious
localizations. In spite of optimal medical and surgical management,
the mortality of group A streptococcal infections complicated by TSS
is 30%, and the condition remains associated with a severe and
extensive morbidity [11]. In our case study, the entire dilemma was
bound up with the fact that in view of the rapidly deteriorating
clinical picture a therapeutic decision with very serious conse-
quences had to be taken before there was any diagnostic certainty
about the primary focus of infection. The decision to proceed with
medical termination of pregnancy in order to ensure maternal
rescue was taken less than 24 hours after the onset of signs and
indisputably contributed to the favorable outcome.
Disclosure of interest
The authors declare that they have no conflicts of interest
concerning this article.
References
[1] Hamilton SM, Stevens DL, Bryant AE. Pregnancy-related group A streptococcal
infections: temporal relationships between bacterial acquisition, infection
onset, clinical findings, and outcome. Clin Infect Dis 2013;57:870–6.
[2] Sugiyama T, Kobayashi T, Nagao K, Hatada T, Wada H, Sagawa N. Group A
streptococcal toxic shock syndrome with extremely aggressive course in the
third trimester. J Obstet Gynaecol Res 2010;36:852–5.
402 Lettres à la rédaction / Gynécologie Obstétrique & Fertilité 43 (2015) 397–403
[3] Aronoff DM, Mulla ZD. Postpartum invasive group A streptococcal disease in
the modern era. Infect Dis Obstet Gynecol 2008;796:892.
[4] Byrne JLB, Aagaard-Tillery KM, Johnson JL, Wright LJ, Silver RM. Group A
streptococcal puerperal sepsis: initial characterization of virulence factors
in association with clinical parameters. J Reprod Immunol 2009;82:74–83.
[5] Lurie S, Vaknine H, Izakson A, Levy T, Sadan O, Golan A. A Group A Streptococ-
cus causing a life-threatening postpartum necrotizing myometritis: a case
report. J Obstet Gynaecol Res 2008;34:645–8.
[6] Schummer W, Schummer C. Two cases of delayed diagnosis of postpartal
streptococcal toxic shock syndrome. Infect Dis Obstet Gynecol 2002;10:
217–22.
[7] Stevens DL. The flesh-eating bacterium: what’s next? J Infect Dis 1999;179
(Suppl. 2):S366–74.
[8] Mason KL, Aronoff DM. Postpartum group A Streptococcus sepsis and maternal
immunology. Am J Reprod Immunol 2012;67:91–100.
[9] Rimawi BH, Soper DE, Eschenbach DA. Group A streptococcal infections in
obstetrics and gynecology. Clin Obstet Gynecol 2012;55:864–74.
[10] Anteby EY, Yagel S, Hanoch J, Shapiro M, Moses AE. Puerperal and intrapartum
group A streptococcal infection. Infect Dis Obstet Gynecol 1999;7:276–82.
[11] Crum NF, Chun HM, Gaylord TG, Hale BR. Group A streptococcal toxic shock
syndrome developing in the third trimester of pregnancy. Infect Dis Obstet
Gynecol 2002;10:209–16.
[12] Busowski MT, Lee M, Busowski JD, Akhter K, Wallace MR. Puerperal group A
streptococcal infections: a case series and discussion. Case Reports Med
2013;2013:751329.
A.-S. Gassmanna, A. Kocha,*, E. Boudiera, G. Averousb,
N. Sananesa, I. Nisanda, F. Schneiderc, B. Langera
a
Département de gynécologie-obstétrique, hôpital de Hautepierre,
hôpitaux universitaires de Strasbourg, 67100 Strasbourg, France
b
Département d’anatomie et de cytologie pathologiques,
hôpitaux universitaires de Strasbourg, 67100 Strasbourg, France
c
Service d’anesthésie réanimation médicale, hôpital de Hautepierre,
hôpitaux universitaires de Strasbourg, 67100 Strasbourg, France
*Corresponding author.
E-mail addresses: anne-sophie.gassmann@chru-strasbourg.fr
(A.-S. Gassmann),
antoine.koch@chru-strasbourg.fr (A. Koch),
eric.boudier@chru-strasbourg.fr (E. Boudier),
gerlinde.averous@chru-strasbourg.fr (G. Averous),
nicolas.sananes@chru-strasbourg.fr (N. Sananes),
israel.nisand@chru-strasbourg.fr (I. Nisand),
francis.schneider@chru-strasbourg.fr (F. Schneider),
bruno.langer@chru-strasbourg.fr (B. Langer).
Received 9 September 2014
Available online 21 April 2015
http://dx.doi.org/10.1016/j.gyobfe.2015.03.025
La césarienne vaginale doit-elle toujours se
pratiquer ?
Shall vaginal caesarean section still be practiced?
La césarienne vaginale ou opération de Dührssen est une
technique obstétricale très peu utilisée. Bien que réputée simple à
réaliser, elle effraie de nombreux gynéco-obstétriciens. D’ailleurs,
la transmission de la connaissance aux plus jeunes n’est quasiment
plus assurée. On la retrouve pourtant citée, voir décrite, dans la
plupart des livres traitant de l’obstétrique et de ses techniques. Sa
paternité est attribuée à Dührssen en 1895 [1]. Nous essayerons à
travers un report de cas de montrer que la césarienne vaginale
garde une place intéressante dans certaines indications.
1. Observation
Madame D., 31 ans, deuxième geste primipare, a consulté à
22+3 semaines d’aménorrhées (SA) aux urgences pour douleurs
abdominopelviennes et métrorragies. Elle n’avait aucun antécé-
dent médico-chirurgical. Elle a accouché par voie basse spontanée
à terme d’un garçon en bonne santé de 3310 grammes, quatre ans
auparavant. La grossesse ne posait aucun problème particulier. Elle
est de groupe sanguin O+. La patiente ne prenait aucun traitement
ni toxique. Les constantes cliniques étaient normales (TA = 120/70,
pouls = 80 battements par minute), la bandelette urinaire ne
révélait pas de protéinurie. La hauteur utérine était conforme, mais
l’utérus était « tendu », les métrorragies étaient en quantité
modérée, de sang rouge foncé. Le toucher vaginal objectivait un col
mi-long, en position intermédiaire, fermé. L’examen au spéculum
confirmait l’origine utérine des pertes sanguines. L’échographie
retrouvait un fœtus sans activité cardiaque, eutrophe (poids fœtal
estimé à 577 g) en présentation céphalique, une quantité de liquide
amniotique normale, le placenta était postérieur non bas inséré
avec une image hétérogène de 80 mm sur 75 mm fortement
évocatrice d’un hématome rétroplacentaire.
Le bilan biologique réalisé objectivait une anémie normocytaire
modérée (Hb = 9,8 g/dL), une hyperleucocytose, une thrombopénie
modérée (plaquettes = 90 G/L), un TCA allongé avec un ratio à 3,16,
une fibrinolyse majeure avec un fibrinogène indosable, un TP
inférieur à 10 %, un facteur V à 12 %. Devant le diagnostic de
coagulation intravasculaire disséminée (CIVD) sévère, les pre-
mières mesures de réanimation médicale ont été débutées
(transfusion de deux culots de plasma frais congelé (PFC), d’un
concentré plaquettaire et d’un flacon de fibrinogène humain). Face
à l’instabilité hémodynamique maternelle rapidement croissante
(TA = 80/50, pouls = 120 battements par minute), l’évacuation
chirurgicale de la grossesse a été décidée : une césarienne par voie
abdominale exposant à un risque hémorragique important du fait
de la sévérité de la CIVD, une césarienne vaginale pour sauvetage
maternel a été préférée.
La césarienne vaginale fut réalisée sous anesthésie générale,
selon la technique de Dührssen modifiée par Schauta (technique
résumée dans le Tableau 1). La délivrance artificielle a retrouvé un
volumineux hématome confirmant le diagnostic d’hématome
rétroplacentaire. Une révision utérine a été réalisée. Le temps de
réfection n’a posé aucun problème. En fin d’intervention, le globe
utérin était tonique et l’hémostase satisfaisante. La patiente a
ensuite été mutée dans le service de réanimation. Au total, la
patiente a reçu 5 PFC, 6 concentrés globulaires, 2 flacons de
fibrinogène humain et 1 concentré plaquettaire.
Les suites post-opératoires ont été simples au niveau clinique et
biologique. La patiente est sortie à j4 avec un traitement préventif
par héparine de bas poids moléculaire (HBPM) et la poursuite d’une
antibioprophylaxie pendant 7 jours.
Le compte-rendu anatomo-pathologique du placenta confir-
mait l’existence d’un hématome rétroplacentaire.
Tableau 1
Principaux temps opératoires de la césarienne vaginale selon la technique de
Dührssen modifiée par Schauta.
Principaux temps opératoires
Incision sagittale médiane du col et du vagin
Décollement vésico-utérin
Exposition du segment inférieur
Hystérotomie/incision du segment inférieur* (doit être strictement
verticale pour être peu hémorragique et remonter jusqu’au cul-de-sac
péritonéal, sans l’inciser)
Extraction fœtale, délivrance et révision utérine
Suture du segment inférieur
Suture du vagin antérieur
Nous décrivons ici la technique classique au 3e trimestre de la grossesse lorsque
le segment inférieur est formé. *La technique reste réalisable à des termes plus
précoces comme dans notre cas, l’incision est alors isthmo-corporéale.
L’hystérotomie dépend du terme auquel on opère : courte au 2e trimestre
(4–5 cm), elle est beaucoup plus étendue au 3e trimestre (9–10 cm) (segment
inférieur formé).