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Severe midtrimester oligohydramnios: Treatment strategies

Article  in  Current opinion in obstetrics & gynecology · April 2014

DOI: 10.1097/GCO.0000000000000051 · Source: PubMed

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REVIEW

CURRENT
OPINION Severe midtrimester oligohydramnios: treatment
strategies
Zoltan Kozinszky a, János Sikovanyecz b, and Norbert Pásztor b

Purpose of review
Nearly 1% of pregnancies are affected by some type of midtrimester oligohydramnios. Evidence is
currently accumulating that suggests the better efficacy of the new therapeutic procedures relative to
conventional management. This review summarizes the available evidence.
Recent findings
The prolongation of the period between the diagnosis of oligohydramnios and delivery following
amnioinfusion and amniopatch techniques appears to be strongly associated with the gestational age
and whether the situation was based on rupture of the membranes or not. Case series reveal that
amnioinfusion significantly improves the perinatal outcome and prolongs the pregnancy in severe
second-trimester oligohydramnios in both idiopathic cases and those involving rupture of the amniotic
membranes [preterm prelabor rupture of the membranes (PPROM)]. There is clear evidence of a lower
frequency of perinatal complications and successfully prolonged gestation in iatrogenic PPROM after the
amniopatch technique relative to population controls.
Summary
Identification of potentially modifiable risk factors for the successful prolongation of pregnancy complicated
with midtrimester oligohydramnios, and previable PPROM is needed for the improvement of treatment
strategies and prognosis. Randomized trials are needed to determine whether amniotic fluid-replenishing
strategies can improve pregnancy outcomes.
Keywords
amnioinfusion, amniopatch, midtrimester oligohydramnios, rupture of the membranes

INTRODUCTION of amniotic fluid in the midtrimester increases

Oligohydramnios, a deficiency of amniotic fluid
volume (AFV) below the 10th percentile correspond-
ing to the gestational stage, is a complicating
feature in 0.8–5.5% of pregnancies [1,2]. There is
no consensus on the sonographic assessment of the
AFV, which can be based either on the measurement
of the deepest vertical pocket (<2 cm defining oligo-
hydramnios) [3] or on the depths of the amniotic
fluid in four quadrants [as the amniotic fluid index
(AFI)] [1]. It is noteworthy that the severe form is
not clearly defined, though a clinically relevant AFI
of less than 5 cm appears to be the best predictive
value for an abnormal fetal outcome which might
require therapy [1,2,4], as opposed to a border-
line reduced fluid with an AFI of 6–8 cm, in which
case treatment is not required and the perinatal
outcome is generally favorable [5].
There are two peaks in the incidence of oligo-
hydramnios, between 13 and 21 weeks, and
between 34 and 42 weeks [4]. Since the production
progressively [6], extreme and persistent oligo-
hydramnios prior to 22–24 weeks may impede
the fetal lung development, resulting in a level of
pulmonary hypoplasia that poses a risk of perinatal
mortality as high as 80% [7–9], or possibly in a
growth delay, compression-related skeletal de-
formities (muscle hypotrophy or joint constriction),
and pregnancy loss [9]. A poor perinatal outcome
with an overall survival rate of only 10.2–14.4%
may be observed in the second trimester, which is
a
Department of Obstetrics and Gynecology, Blekinge Hospital, Karl-
skrona, Sweden and bDepartment of Obstetrics and Gynecology, Faculty
of Medicine, Albert Szent-Györgyi Medical and Pharmaceutical Center,
University of Szeged, Szeged, Hungary
Correspondence to Zoltan Kozinszky, MD, PhD, Utövägen 10/A,
Karlskrona 37137, Sweden. Tel: +46 0730720835; e-mail: kozinszky@
gmail.com
Curr Opin Obstet Gynecol 2014, 26:67–76
DOI:10.1097/GCO.0000000000000051

1040-872X ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins www.co-obgyn.com
Maternal–fetal medicine
KEY POINTS
 Transabdominal amnioinfusion prolongs the latency
period and is associated with reductions in perinatal
mortality and pulmonary hypoplasia in pregnancies
with oligohydramnios, either with or without PPROM.
No increase in infectious morbidity has been observed.
 The amniopatch treatment protocol for women with
previable iPPROM results in a high neonatal survival
rate, with fewer neonatal skeletal abnormalities and
pulmonary hypoplasia.
 The prognosis of midtrimester oligohydramnios is
still poor.
very low as compared with that of 57.7–85.3%
in the third trimester [4,10]. Moreover, umbilical
cord compression causes fetal heart rate anomalies
and oligohydramnios may also be accompanied by
abruption of the placenta [11].
Oligohydramnios has six possible major causes:
failure of the regulatory mechanisms accompanied
by severe fetal abnormalities; preterm prelabor
rupture of the membranes (PPROM); an isolated/
idiopathic form; an impaired placental function
leading to insufficiency; a complication of multiple
pregnancies; and iatrogenic [12].
CLINICAL FEATURES OF
OLIGOHYDRAMNIOS
A fetal abnormality contributes up to 50% of the
decreased AFV in the second trimester [4], but major
or even lethal malformations generally cause severe
oligohydramnios via fetal anuria. An amnioinfusion
procedure improves the possibility of diagnosis from
the sonographic imaging in 26% of the cases and
may result in an improved identification of the
urinary tract, in consequence of the improvement
in the severe decrement in AFV [13,14]. Additionally,
amnioinfusion may prolong the gestation and
improve the perinatal outcome in nonlethal mal-
formations [15]. A uteroplacental insufficiency may
arise from a maternal hypertensive disease or some
other pathologic condition, which should be treated,
as underperfusion of the placenta generates a reduced
nutrient and oxygen supply. Fetal regulatory mech-
anisms lead to a low level of urination by the fetus,
and this condition may be associated with a growth
restriction or even fetal demise [15,16].
PREVIABLE PROM AND EXPECTANT
MANAGEMENT
Fetal membrane rupture affects less than 1%
of pregnancies before or at the limit of viability
68 www.co-obgyn.com
(22 weeks) [17,18]. PPROM is associated with
clinical signs of chorioamnionitis in 37% of the
cases and with devastatingly adverse neonatal
survival rates, ranging from 22 to 63% at best, due
to the frequently infectious neonatal outcome and
pulmonary hypoplasia [9]. However, for PPROM up
to 25 weeks of pregnancy, these cases have a survival
to discharge of 44.4% [8,10]. The overall perinatal
mortality of previable PROM managed expectantly
has been reported to be 60% [19], and almost one-
third of these deaths occur in utero. The survival
rate for infants born alive increases progressively
from 26% at 23 weeks to 84% at 26 weeks [20],
and prolongation of the pregnancy is therefore
of paramount importance. Pulmonary hypoplasia
occurs in 50% of the cases diagnosed before 19 weeks
[21]. The main reason for the high perinatal
mortality is that the period of 17–26 weeks of
gestation is the canalicular phase of lung develop-
ment, which is most vulnerable to the effects of
oligohydramnios [22].
Iatrogenic PPROM (iPPROM) affords a more
favorable prognosis than spontaneous PPROM
(sPPROM) [23,24]. Despite efforts to reduce the access
diameter, iPPROM remains the most frequent
complication of invasive fetal procedures. It occurs
in 0.5–1.2% of the cases (usually at an early gesta-
tional age) after genetic amniocentesis [24–27],
in 3–5% after diagnostic fetoscopy [28,29], and
approximately 5–8% after operative fetoscopy
[28,29], depending on the operative time and
gestational age. Although the membranes tend to
seal spontaneously with high frequency following
iPPROM [27], amniotic fluid leakage may continue,
leading to the risk of infection and miscarriage.
In contrast, spontaneous ruptures are usually a result
of ascending infection, located near the cervix,
and the membrane defect is much larger [29,30].
Hence, the chance of spontaneous sealing is only
6–11% [31,32], and such defects can rarely be sealed
artificially [33–35].
The traditional obstetric management includes
the administration of antibiotics to prolong latency,
and steroid administration to enhance pulmonary
maturity [36], though the development of pul-
monary hypoplasia often limits survival. The
cornerstone in the conservative management is
broad-spectrum antibiotic therapy. In recent years,
the use of antibiotics has increased up to 97% in
cases with PPROM [10], with reports of a lower
frequency of chorioamnionitis and an improved
fetal survival as compared with patients not
treated with antibiotics [37,38]. Miyazaki et al.
[39] demonstrated amniotic sac inflammation via
histopathology in more than 91% of women with
previable PROM. It is noteworthy that intra-amniotic
Volume 26  Number 2  April 2014

inflammation can merely be controlled, and
not eradicated with antibiotic therapy: subclinical
chorioamnionitis remains despite the treatment
[39,40]. Antenatal corticosteroid administration
seems to improve the neonatal survival rate signifi-
cantly [37] and it is recommended when viability has
been reached. The use of tocolysis is controversial,
though a moderate effect on the latency period is
suspected [37,38]. In the event of conventional
management, the signs of chorioamnionitis, labor
and fetal compromise must be screened.
Expectant management in previable PROM
delays pregnancy by a mean latency of 11.8 days
(73% within 2 weeks), which is related primarily to
the gestational age and the presence of infection
[25,26,41–47]. The occurrence of musculoskeletal
deformities ranges from 0 to 46% [48], and the
rate of pulmonary hypoplasia is up to 63%
[48], the residual AFV and the gestational length
being the most important prognostic factors [9,49].
New therapies may be beneficial to patients without
any regular uterine contractions, vaginal bleeding
or symptoms of clinical chorioamnionitis.
AMNIOINFUSION
Although amnioinfusion has not been studied
&&
effectively in a controlled manner [5,50 ], this is
the method that has been addressed as a technique
for the restoration of a normal AFV, in order to
prolong gestation and to prevent fetal complica-
tions at least until pulmonary maturity is achieved
[39,51,52]. Antepartum amnioinfusion involves
artificially increasing the AFV by injecting a variable
amount of solution via a transabdominal [52] or
transcervical approach [53], from the earliest gesta-
tion time of 16 weeks [54] to prevent lethal pulmon-
ary hypoplasia, but transabdominal amnioinfusions
have rather been performed in midgestation. It is
assumed that augmenting the AFV in the second
trimester may decrease the associated risks of oligo-
hydramnios and increase the perinatal survival [55].
The technical equipment is similar to that
used for amniocentesis; it is performed with [55]
or without local anesthesia [52], usually with a
20–22-gauge 150-mm amniocentesis needle, which
is introduced [52,55,56] transabdominally into
the widest amnion pocket with the assistance of
real-time ultrasound guidance [49,57]. The correct
positioning of the needle tip may be checked
by visualization of the incoming jet by color flow
mapping, or aspiration may be used to avoid
funipuncture [49,57]. It is recommended to direct
the needle away from the umbilical cord loops and
to apply a very slow initial infusion in order to avoid
puncture of the cord. After formation of a small
1040-872X ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins
Severe midtrimester oligohydramnios Kozinszky et al.
amniotic pocket, the infusion velocity may be
increased to a maximum of 25–50 ml/min [55],
applying a 30–50-ml syringe [55,56] or an infusion
set [52] connected to the needle.
The infused crystalloids are 0.9% saline solution
or Ringer’s lactate solution at body temperature,
which are both isotonic and do not induce any
electrolyte imbalance in the fetus [58]. The infused
volume should depend on the gestational age and
the amount of fluid remaining inside the amniotic
cavity, keeping in mind that the injection of 250 ml
of fluid is presumed to increase the AFI by 4 cm [59],
whereas the physiological increase in AFV is 10 ml
per week [49,55]. The aim is to re-establish the
normal AFV (AFI 8 cm) [52,56]. Sonographic
control of the AFV and a fetal morphological
evaluation are required after the procedure for
identification of lethal abnormalities or PPROM.
Prophylactic antibiotic therapy is necessary only
in PPROM cases, but patients with a negative Rh-
factor should receive anti-D prophylaxis [52,59]. A
repeat ultrasound examination should be performed
every fourth [49] or seventh day [39,52,55,60] in
order to assess the need for further infusion, and
serial amnioinfusion may be recommended when-
ever the AFI decreases below the limit [39,61,62].
AMNIOPATCH
Another accepted novel technique is use of the
amniopatch in order to achieve artificial membrane
sealing (defects ranging from 0.72 to 3.8 mm)
following iPPROM [29,30]. However, some authors
[33–35,63] succeeded in prolonging gestation sig-
nificantly in cases of sPPROM. Warm isotonic saline
(50–200 ml, optionally mixed with antibiotics) is
infused intra-amniotically under ultrasound moni-
toring without knowledge of the exact site of
rupture of the amniotic membranes. Cross-matched
allogenic platelets [20–40 ml (0.5 units)] are infused,
followed by 0.5 units of cryoprecipitate (including
clotting factors). Another 100 ml of normal saline
is then instilled to achieve the optimal (5 cm)
deepest pocket of the amniotic fluid bag. Theoreti-
cally, the platelet/cryoprecipitate plug may seal the
amniotic membranous defect by artificial platelet
activation and fibrin adhesion at the site of the
rupture, forming a ‘white’ coagulum as a plug.
Although procedure-related complications are infre-
quent, amniopatch predominantly fails [29,34,63],
usually because of infection, chiefly after sPPROM.
However, pregnancies corrected with amniopatch
can continue for even a fairly long time (mean
104 days), suggesting a low neonatal and maternal
risk. Concomitant serial amnioinfusion appears to
be an effective method of flushing out the bacteria
www.co-obgyn.com 69
Maternal–fetal medicine
[39] and may be beneficial in preventing threaten-
ing chorioamnionitis when amniopatch fails [63].
In sPPROM, amniopatch therapy is less likely to
be effective because the defect is large and near
the internal cervical os [23], and amniotic infection
is common.
OUTCOME AFTER AMNIOTIC FLUID
REPARATION INTERVENTIONS
Tables 1 [39,49,52,54,56,60–62,64] and 2 [29,33–
35,63,65–71] present an overview of the outcome
of treated second-trimester oligohydramnios.
Pulmonary hypoplasia developed in 28 out of
120 neonates (23.3%) as a deadly consequence in
pregnancies treated with amnioinfusion apart from
the expectant management, that is, only a slight
reduction relative to the overall rate in the popu-
lation (31.8%) [24,42–44,46]. Chronic lung diseases
were the most critical perinatal complications,
accounting for 34.8% as major morbidity, whereas
the severe maternal complication (infection and
abruption) rate was 22.4% of the 179 amnioinfusion
cases reported so far [39,49,52,56,60–62,64].
The efficacy of the amniopatch varies with the
underlying cause and the risk of infection [72].
Although the population treated with the amnio-
patch was highly mixed, procedure-related compli-
cations were reasonably low: 28.2% among the
71 amniopatch cases performed. Even though
the pooled perinatal survival rate was 61.4%, fatal
pulmonary hypoplasia and chronic lung disease
were minimal (both <1%). Although the procedure
failed in 50.7% due to relapse of the amniotic leak-
age, the achieved duration of gestation at delivery
(median 29.4 weeks) was considerable following use
of the amniopatch [29,33–35,63,65–71]. This is in
line with the idea that subclinical (biochemical)
leakage after iPPROM is significantly more preva-
lent, but usually without clinical consequences [23].
The overall perinatal survival rate following
expectant management in severe second-trimester
oligohydramnios was 29.3% [24,26,41–46], signifi-
cantly higher at 49.1% after treatment with amnio-
infusion [39,49,52,56,60–62,64] and 57.3% after the
amniopatch [29,33–35,65–71].
The perinatal survival rate after previable
iatrogenic membrane rupture (59.3%) [24,26,44]
was considerably higher as compared with that after
spontaneous rupture (20.1%) [24,26,41–43,45] with
traditional treatment, but iPPROM is usually treated
with the amniopatch [30,72,73], whereas sPPROM
is rather a therapeutic target for amnioinfusion
[74]. The weighted mean difference in latency was
increased after patching (44 days, P < 0.001) follow-
ing iPPROM, and the latency was also significantly
70 www.co-obgyn.com
prolonged after amnioinfusion (37.4 days, P < 0.001)
following PPROM compared with expectant treat-
ment (mean 11.8 days, range 0–163) [24,26,41–46].
Deformation defects may occur in up to 53%
in oligohydramnios [24,42,43], whereas amnio-
infusion results in a 16.5% reduction in the risk
(P < 0.05) of a postural deformity and it was
not recorded among amniopatch survivors. When
amnioinfusion was repeated frequently and com-
plemented with tocolytic and antibiotic therapy as
aggressive treatment to suppress uterine contrac-
tions and emergency cerclage to arrest cervical dila-
tation in sPPROM, a 60% survival rate was attained,
with nearly two-thirds of the surviving infants not
suffering serious sequelae [39].
In line with the reports demonstrating the
critical role played by the AFV in oligohydramnios
as concerns the pregnancy outcome [9,49],
Kozinszky et al. [52] found a direct correlation
between the volume instilled during serial amnio-
infusion procedures and the length of the latency
period in idiopathic cases. Conversely, there was an
indirect correlation between the amount infused
volume and latency after PPROM [60], suggesting
that a better equilibrated initial uterine environ-
ment is beneficial in PPROM-related oligohydram-
nios. It is of note that the delay between the sPPROM
and the intervention is 4–7 days [49,60,61], which is
questionable when it is considered that the rate of
spontaneous resealing is 6–11% [31,32], and the risk
of infection is high.
Patients require accurate information as regards
the neonatal outcome and the risk of the inter-
ventions; 25.8% opted for termination instead
of amnioinfusion [39,49,56,62] and 15% preferred
termination in the amniopatch group [29,35,68]
after counseling.
OTHER THERAPIES
A variety of closure techniques have been proposed
earlier, including in-situ cerclage [75], intra/trans-
cervical instillation of coagulation factors combined
or without cerclage [76–78], which could even be
employed via a catheter or fetoscopy [35], fetoscopic
closure of the defect (amniograft) [79], or fixation of
the PPROM with a transcervical double balloon
catheter [80] or with gelatin sponge [81]. However,
there are as yet no data establishing their efficacy
in preventing pulmonary hypoplasia or delaying
delivery, and these interventions have not gained
ground in clinical practice.
A correction of the reduced maternal intra-
vascular volume by hydration [82] or vasopressin
[83] has also been demonstrated, which may increase
the AFI significantly.
Volume 26  Number 2  April 2014
1040-872X ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Table 1. Amnioinfusion (AI) for treatment in severe midtrimester (between 16 þ 0 and 25 þ 6 weeks) oligohydramnios

Complications among perinatal survivors

GA at Type of
diagnosis Initial infused Pulmonary
of PROM gestation solution hypoplasia, Abnormal
Type of Additional (weeks, at AI (weeks, Latency (volume ml: Perinatal broncho- neurologic
oligo- pregnancy Intervention median median and (days, mean, mean and survival Maternal Postural pulmonary outcome
hydramnios management type and range) range) range) range) rate (%) complications deformities (%) dysplasia (%) (%)

Locatelli et al. 32 sPPROM; Waiting 4 days Single ¼ 11 16.5 20.3 89 (48–139) Isotonic sodium 73 0 n.g. (1 case n.g. (2 cases 1 PH case among 0/8
(2000) [49] 4 iPPROM with AI after (14.0–21.0) (16.5-; 24.2) chloride (n.g.) among among 10 neonates
diagnosing pregnancies) pregnancies) led to neonatal
oligohydramnios, deaths
bed rest,
prophylactic
antibiotics,
corticosteroid,
tocolysis if
necessary
Serial ¼ 25 19.3 20.2 22 (9–105) 20 32% n.g. (2 cases n.g. (4 cases 13 PH cases among 3/5 : 60%
(14.0–25.2) (16–25.6) chorioamnionitis; among among 21 neonates led
16% abruption pregnancies) pregnancies) to neonatal
deaths
Ogunyemi and 11 PPROM Bed rest, Single ¼ 4; 21 21.2 35.4 (3–83) Isotonic sodium 63.6 36% chorioamnitis; 9% 3/7 : 43 1 PH and 1 BPD 0
Thompson prophylactic serial ¼ 7 (15.0–24.0) (17–24) chloride (n.g.) 9% abruption cases among
(2002) [64] intravenous 7 neonates
antibiotics þ (28.6%)
antibiotics in the
instilled solution,

Severe midtrimester oligohydramnios Kozinszky et al.

corticosteroid,
tocolysis if
necessary
Tan et al. 6 PPROM Bed rest, Single ¼ 4; 19.3 (16–25) n.g. 67.7 (14–126) Isotonic sodium 66.7 16.7% abruption; 1/4 : 25 0 3/4 : 75; chronic 0
(2003) [56] corticosteroid serial ¼ 2 chloride (n.g.) 16.7 lung disease
chorioamnionitis
De Santis et al. 29 sPPROM; Waiting 7 days Serial ¼ 32; Mean  SD: Mean  SD: Mean  SD: Isotonic sodium 27 Unsuccessful: 50% 0 5/24 : 20.8 led 2/10 : 20%
(2005) [60] 8 iPPROM with AI after single ¼ 5 20.1  2.8 22.3  2.9 41.6  29.7 chloride; 10.8% (repeat); to death;
diagnosing (mean  SD: 46% lost some of among survivors:
oligohydramnios, 208  89) the infused fluid; 2/10 : 20%
bed rest, 2.7% cord
www.co-obgyn.com

corticosteroid, prolapse; 2.7%

tocolysis, abruption; 16.2%
antibiotics chorioamnionitis
Stefos et al. 2 iPPROM No delay with AI Serial ¼ 2 16.3 and 16.4 and 140 Isotonic sodium 100 No No No No No
(2005) [54] after diagnosing 16.4 17.0 chloride (167,
oligohydramnios, 100–200)
n.g.

(Continued )
71
72

Maternal–fetal medicine
Table 1 (Continued)
www.co-obgyn.com

Complications among perinatal survivors

GA at Type of
diagnosis Initial infused Pulmonary
of PROM gestation solution hypoplasia, Abnormal
Type of Additional (weeks, at AI (weeks, Latency (volume ml: Perinatal broncho- neurologic
oligo- pregnancy Intervention median median and (days, mean, mean and survival Maternal Postural pulmonary outcome
hydramnios management type and range) range) range) range) rate (%) complications deformities (%) dysplasia (%) (%)

Hsu et al. 3 sPPROM Waiting 7 days Single ¼ 11; 21 (19–25) n.g. 9.3 (7–14) Isotonic sodium 0 7.1% n.g. n.g. n.g. n.g.
(2007) [61] with AI after serial ¼ 3 chloride; (n.g., chorioamnionitis
diagnosing 250–600)
oligohydramnios,
bed rest,
prophylactic
antibiotics,
corticosteroid
1 iPPROM 16 n.g. 168 100 n.g. n.g. n.g. n.g.
10 idiopathic 20.2 (15–25) n.g. 59.5 (7–147) 50 n.g. n.g. n.g. n.g.
Kozinszky et al. 17 idiopathic No delay with AI Single ¼ 11; 21.6 21.6 28.4 (0–121) Isotonic sodium 35.3 23.6% retroamnial 1/: 16.7 1: intrauterine 1 PH case among 0
(2013) [52] after diagnosing serial ¼ 6 (16.0–25.0) (16.0–25.0) chloride (398, filling that led to death 1 intrauterine
oligohydramnios, 200–750) spontaneous deaths
corticosteroid abortion shortly
after AI, 5.9%
abruption; 5.9%
chorioamnionitis
Agressive
management
Chen et al. 4 sPPROM; No delay with AI Serial ¼ 11; 23.3 n.g. 34 (11–59) Ringer’s lactate or 72.7 18.2% n.g. n.g. n.g. n.g.
(2005) [62] 7 idiopathic after diagnosing additional (17.4–26.0) isotonic sodium chorioamnionitis
oligohydramnios, amniopatch ¼ 1 chloride;
prophylactic (200–500);
antibiotics,
tocolytics; PPROM
cases: AI þ
cerclage
Miyazaki et al. 45 sPPROM AI for ‘flushing the Serial ¼ 45 22 (12–22) n.g. 24 (0–103) Isotonic sodium 60 Histological n.g. 0 5/45 led to 7/26 : 26.9%
Volume 26  Number 2  April 2014

(2011) [39] cavity’ þ cerclage chloride; n.g. chorioamnionitis: neonatal death;

þ tocoly- (500–1500) 90.7%; clinical among survivors:
ticsþantibiotics chorioamnionitis: bronchopulmonary
(sometimes 8.9% dysplasia: 17/27
steroid)

GA, gestational age; iPPROM, iatrogenic preterm prelabor rupture of the membranes; n.g., not given; PH, pulmonary hypoplasia; sPPROM, spontaneous preterm prelabor rupture of the membranes.
1040-872X ß 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins

Table 2. Amniopatch (AP) for treatment in severe midtrimester (between 16 þ 0 and 25 þ 6 weeks) oligohydramnios

Complications among perinatal survivors

Intervention Pulmonary
Additional GA at diagnosis Gestation at AP (volume ml: Perinatal Postural hypoplasia, Abnormal
Type of management of PROM (weeks, (weeks, median Latency (days, mean and survival Maternal deformities bronchopulmonary neurologic
oligohydramnios of pregnancy mean and range) and range) mean, range) range) rate (%) complications (%) dysplasia (%) outcome (%)

Sener et al. 1 iPPROM after Waiting 2 days with 16.1 16.7 147 4 ml fresh maternal 100 0 0 0 0
(1997) [65] TAAC AP after diagnosing blood
oligohydramnios,
bed rest, antibiotic
therapy
Quintero 26 iPPROM Waiting 7 days with 18.7 (13.1–23.3) 19.3 (n.g.) 75.6 (2–178) Autologous platelets 64.1 Not successful: 0 0 0
(2003) [29] (39 fetuses) AP after diagnosing (22–80 ml) and 31%; (relapse of
oligohydramnios, cryoprecipitate amniotic fluid
1 week bed rest and leakage); 3.9%
antibiotics chorioamnionitis
(ended with
hysterectomy)
10 iPPROM: 18.3 (13.1–22.2) n.g. 81.1 (2–178) 50 0 0 0
9 TAAC and
1 CVS (14 fetuses)
16 cases iPPROM 19 (16.1–23.3) n.g. 71.5 (4–140) 68 0 0 0
after fetoscopy
(25 fetuses)
Young et al. 4 sPPROM Waiting 14 days 16.4 (14.4–20.7) 18.3 (16.4–23.4) 21.5 (0–83) Endoscopic 15 ml 25 100% not successful 0 1 0
(2004) [35] after PPROM; platelets, 2–5 ml (continuing fluid
antibiotics, fibrin sealant and leakage); 25%
prophylactic collagen slurry for chorioamnionitis

Severe midtrimester oligohydramnios Kozinszky et al.

tocolysis; cerclage all membrane
for 1 sPPROM defects
4 iPPROM (after 17.3 (15.4–20.7) 21.1 (18.1–24.0) 46.0 (2–89) 75 Not successful: 50%
TAAC) (relapse of amniotic
fluid leakage); 25%
abruption
Contino et al. 3 iPPROM, 2 sPPROM Waiting 3 days with 17–23 19 (17–23) 68.6 (21–168) 30 ml platelets, 20 80 Not successful: 60% n.g. 0 25
(2004) [34] AP after diagnosing ml cryoprecipitate (relapse of amniotic
oligohydramnios, fluid leakage)
steroid, prophylactic
antibiotics, tocolytics
if necessary
www.co-obgyn.com

Lewi et al. 2 iPPROM: Waiting 7 days with 19.6 (17.2–22.0) 20.75 (18.5–23.0) 77 days and 100 ml Hartmann’s 66.6 Not successful: 100% 0 0 0
(2004) [66] 1 monoamniotic AP after diagnosing 56 days solution, 25–50 (relapse of amniotic
acardiac twin oligohydramnios, ml platelets, fluid leakage); 50%
pregnancy; laser bed rest, antibiotic 15–30 ml chorioamnionits
ablation of vascular therapy, 1 week cryoprecipitate
anastomoses for waiting, 1 AP
1 severe twin–twin
transfusion
syndrome

(Continued )
73
74

Maternal–fetal medicine
Table 2 (Continued)
www.co-obgyn.com

Complications among perinatal survivors

Intervention Pulmonary
Additional GA at diagnosis Gestation at AP (volume ml: Perinatal Postural hypoplasia, Abnormal
Type of management of PROM (weeks, (weeks, median Latency (days, mean and survival Maternal deformities bronchopulmonary neurologic
oligohydramnios of pregnancy mean and range) and range) mean, range) range) rate (%) complications (%) dysplasia (%) outcome (%)

Sipurzynski- 1 iPPROM after Waiting 42 days with 20 26 70 30 ml platelets, 100 0 0 0 0

Budrass et al. TAAC AP after diagnosing 20 ml
(2006) [67] oligohydramnios, cryoprecipitate
bed rest, antibiotic
therapy,

Cobo et al. 5 iPPROM after Waiting 5 days with 13.3 (11.2–15.0) 15.5 (12.3–18) 19.4 (1–98.7) Saline infusion, 50 20 Not successful: 20% 0 0 0
(2007) [68] TC-CVS AP after diagnosing ml donor platelets, (relapse of amniotic
oligohydramnios, 15 ml fluid leakage)
bed rest, antibiotic cryoprecipitate
therapy
Mandelbrot 1 iPPROM after Waiting 21 days with 15.3 18.3 140 30 ml platelets, 20 100 0 n.g. n.g. n.g.
et al. (2009) TAAC AP after diagnosing ml cryoprecipitate
[69] oligohydramnios,
bed rest, antibiotic
therapy,
progesterone
Pathak et al. 3 iPPROM (twin Waiting 1 day with AP 21.7 (18.3–23.7) 21.8 (18.4–23.8); 95 (45–139) 30 ml donor platelets 83.3 Not successful: 25% 0 0 0
(2010) [70] pregnancies) after diagnosing and 30 ml (relapse of amniotic
after SLPCV oligohydramnios, cryoprecipitate fluid leakage);
antibiotic therapy, repeated procedure
1AP, 2 AP in one
case
Ferianec et al. 1 sPPROM Bed rest, antibiotic 19.14 21.14 84 30 ml platelets, 20 100 0 0 0 0
(2011) [33] therapy ml cryoprecipitate
Kwak et al. 7 sPPROM: 3 Waiting 7 days with 21.0 (17.3–23.0) 22.3 (21.1–23.7) 46.5 (4–152) 20–40 ml platelets, 71.4 not successful: 85.7% 0 1 neonatal death: 20
(2011) [63] incompetent cervix AP after diagnosing 20–40 ml (relapse of fluid bronchopulmonary
and 4 competent oligohydramnios, cryoprecipitate leakage) dysplasia and sepsis
cervix, 1 twin corticosteroid,
pregnancy prophylactic
antibiotics, tocolytics
Volume 26  Number 2  April 2014

if necessary, and
serial AI if necessary
Richter et al. 13 iPPROM: after Waiting 7 days with 16.3 (15.2–19.0) 20.1 (16.6–23.1) 38.5 (0–101) 100 ml Hartmann’s 50 Not successful: 61% 0 7.7% 15.4
(2013) [71] needle-based (NP) AP after diagnosing solution, 25–50 (relapse of fluid bronchopulmonary
procedure; 2 twin oligohydramnios, 6 ml platelets, FFP leakage); 12.5% dysplasia
pregnancies repeat AP in 17 up to each chorioamnionitis
cases with ongoing platelet; 15–30 (1 case ended with
leakage: 4 cases in ml FFP; 15–30 ml hysterectomy)
NP and 2 cases in platelets
the FI group
11 iPPROM after (FI) 20.2 (15.6–25.3) 21.0 (16.4–25.5) 58.8 (8–120)
fetoscopy; 8 twin
pregnancies

iPPROM, iatrogenic preterm prelabor rupture of the membranes; IUGR, intrauterine growth retardation; n.g., not given; SLPCV, selective laser photocoagulation of communicating vessels (for twin–twin transfusion syndrome); sPPROM,
spontaneous preterm prelabor rupture of the membranes; TAAC, transabdominal amniocentesis; TACVS, transabdominal chorionvillus sampling; TOP, termination of pregnancy.

CONCLUSION
Amnioinfusion may be considered an effective
treatment option both for PPROM-related and for
idiopathic oligohydramnios in terms of successful
prolongation of the gestation and reduction of the
risk of infectious fetal and maternal complications.
IPPROM seems to be more amenable to correction
by the amniopatch technique, doubling the peri-
natal survival rate as compared with controls, with
more infants reaching viability and with a reduced
risk of infection. However, discussions with the
patient are critical, providing information concern-
ing the risk of the interventional clinical manage-
ment, because the prognosis is still questionable,
particularly in cases of spontaneous rupture of
the membranes. However, definitive conclusions
cannot be drawn from case series, and multicenter
randomized controlled trials are necessary, con-
trolled by the cause of oligohydramnios and other
procedure-related factors, in order to establish the
clinical value of these amniotic fluid correction
techniques.
Acknowledgements
None.
Conflicts of interest
No funding support from any of the following
organizations: National Institutes of Health (NIH);
Wellcome Trust; Howard Hughes Medical Institute
(HHMI); and other(s).
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