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\begin{document}

\title{Extreme fetal macrosomia at 42 gestational weeks: a case report and
literature review}



\author[1]{Julia Kummer}%
\author[1]{Anja Jebens}%
\author[1]{Valentin Mihajlov}%
\author[1]{Luisa Maria Pech}%
\author[1]{Lars Hellmeyer}%
\affil[1]{Vivantes Klinikum im Friedrichshain}%


\vspace{-1em}



  
  \date{May 27, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
Excessive neonatal birth weight with its increasing figures complicates
obstetrical management as well as outcome severely and is associated
with gestational diabetes and maternal obesity. The increase in
pregnancies complicated by maternal obesity and gestational diabetes
emphasizes the necessity of evidence-based clinical interventions to
prevent or decelerate these diseases. If prenatal care is not frequented
by mothers-to-be there are no options open for obstetricians to detect
fetal macrosomia and to intervene.%
\end{abstract}%



\sloppy


\emph{Extreme fetal macrosomia at 42 gestational weeks: a case report
and literature review}

authors: Kummer, Julia\textsuperscript{1}, Jebens
Anja\textsuperscript{1}, Mihajlov, Valentin\textsuperscript{1},~Pech,
Luisa Maria \textsuperscript{1}, Hellmeyer, Lars\textsuperscript{1}

\textsuperscript{1} Department of Gynecology and Obstetrics, Vivantes
Klinikum im Friedrichshain, Berlin, Germany

Corresponding author:

Julia Kummer

Landsberger Allee 49

10249 Berlin

julia.kummer@vivantes.de

tel.: 0049 176 31 42 20 12

Abstract: Excessive neonatal birth weight with its increasing figures
complicates obstetrical management as well as outcome severely. It is
associated with gestational diabetes and maternal obesity. The increase
in pregnancies complicated by maternal obesity and gestational diabetes
emphasizes the necessity of evidence-based clinical interventions to
prevent or decelerate these diseases. If prenatal care is not frequented
by mothers-to-be there are no options open for obstetricians to detect
fetal macrosomia and to intervene.

Key words: fetal macrosomia, maternal obesity, gestational diabetes
mellitus, unsupervised pregnancy

Introduction

Fetal macrosomia is a term to describe excessive fetal birth weight.
{[}1{]} Fetal macrosomia is strongly associated with adverse obstetrical
outcome. {[}1, 2{]} The morbidity for infants and women increases
sharply with a birth weight exceeding 4500 g. {[}3{]} Gestational
diabetes mellitus, a high pre-pregnancy body mass index, and excessive
gestational weight gain have been independently associated as risk
factors. {[}4{]} According to the ISUOG Guidelines indispensable
elements of antenatal care include the screening for and management of
fetal growth abnormalities. {[}5{]} Predicting macrosomia correctly and
establishing a therapeutic regimen help optimizing both perinatal and
maternal outcome. {[}6{]}~So far it is still object to ongoing research
to find an accurate way of predicting fetal macrosomia and establish
interventions to prevent it. {[}6{]} We report a case of excessive
neonatal weight in a medically unsupervised pregnancy.

Methods

We report a case of excessive neonatal weight in a medically
unsupervised pregnancy and give a literature review on the subject. The
relevant papers were selected by a PubMed search using appropriate key
words.

Results

A 38-year-old woman (Gravida 8 Para 7) presented herself for the first
time at 42 2/7 weeks of gestation at the labor ward for a check-up. The
patient had a history of seven spontaneous births with natal weight
ranging between 3100 g and 4800 g.

This pregnancy had not been supervised medically except for one check-up
in 32 weeks of gestation. Blood pressure was taken and showed 148/85
mmHg, heart rate 111 bpm, temperature 36.5 \selectlanguage{ngerman}°C. The woman was obese with
a body mass index of 46.8 kg/m². Since the patient had not seeked
medical consultation before pre-existing maternal diseases had not been
diagnosed so far.

Fetal heart rate patterns were monitored and showed a normal pattern
with a normal oscillation, sporadic accelerations and no decelerations.
The ultrasound examination revealed a vital macrosomic singleton
pregnancy with an estimated weight of 4100 g (estimation formula
generated by Hadlock). However, assessibility was extremely limited due
to maternal obesity.

Labor induction was initiated with oxytocin under close supervision of
the maternal blood pressure. There was a spontaneous rupture of the
membranes with clear amniotic fluid running in the early stage of labor.
Due to her obesity an epidural could not be performed so the patient
received analgesia with an opioid. In the second stage of labor there
was a failure to progress due to fetal malposition with persistent
occiput posterior position and suspicion of a disproportion of the fetal
head and maternal pelvis. An urgent caesarean section was performed in
general anesthesia and a vital macrosomic male infant was delivered
(birth weight: 6760 g {[}\textgreater{}99. percentile{]}, length: 60 cm
{[}\textgreater{}99. percentile{]}, APGAR 4-8-9, NA-pH: 7.15, BE -5.3
mmol/l). (figure 1)

The patient received cefuroxime as a single shot and carbetocin for
uterus contraction initially. Due to an atonic uterus medication was
switched to sulprostone. Blood loss in total during the caesarean
section was 1500 ml. The patient's vital parameters were stable at all
times.

Due to tachydyspnea the baby boy required face mask-delivered
non-invasive ventilation from birth until 24h of life. The neonate was
transferred to the neonatal intensive care unit where a chest x-ray was
performed and showed only minor regional ventilation dysfunction. Blood
was drawn and yielded a normal white cell count and an elevated
C-reactive protein level (results presented in table 1) so that
intravenous antibiotic treatment with ampicillin and gentamicin was
initiated. Since blood cultures were negative for bacteria and
infectious parameters were dropping the antibiotic treatment was
terminated after five days.

The neonate initially developed hypoglycemia with a blood sugar level of
33 g/dl. He needed oral glucose supplementation once and in addition to
breast-feeding supplementary formula-feeding.

An extensive diagnostic regimen was initiated due to neonatal
macrosomia. Clinically the baby boy presented no signs of a syndromal
disorder. Blood was drawn to examine the function of the neonate's
hypothalamic-pituitary-thyroid axis. The results are demonstrated in
table 1. Except for elevated thyroxine (fT4) and low thyroid-stimulating
hormone (TSH) there were no pathological findings.

Echocardiography was performed and showed a generalized myocardial
hypertrophy, a patent ductus arteriosus and a small patent foramen ovale
(figure 2).

Apart from excessive abdominal fat abdominal ultrasound yielded no signs
of congenital malformations or tumorous alterations. Cerebral ultrasound
showed normal results (figure 3).

At maternal urging the neonate was discharged on the 11th day of living
against medical advise. The neonate was scheduled for a postdischarge
follow-up to which mother and child did not appear.

The maternal postoperative course included a detailed blood check-up
which showed an anemia and elevated HbA1c of 7.2 \% (results presented
in table 2). Blood sugar levels were monitored closely and demonstrated
elevated values. However blood sugar levels did not make insulin
treatment necessary. Oral iron supplementation was initiated.

The maternal blood pressure was monitored closely and showed elevated
results. An antihypertensive medication with alpha-methyldopa was
started which helped to achieve normal blood pressure.

The patient underwent a neurosurgical examination which ruled out
acromegaly clinically. Additionally laboratory results showed no
overproduction of insulin-like growth factor 1 (IGF-1) (results shown in
table 2).

In summary of all findings the neonate's excessive weight was led back
to either a preexisting or gestational maternal unsupervised diabetes
mellitus and extreme maternal adiposity.

Discussion

Excessive neonatal birth weight with its increasing figures complicates
obstetrical management and outcome severely. The proportion of fetal
macrosomia ranges from 5 \% to 20 \% in high income countries according
to studies world wide with a tendency of increase over the last decades.
{[}6 -- 10{]}

Predicting fetal macrosomia correctly and establishing a therapeutic
regimen could help to optimize both perinatal and maternal outcome.
{[}6{]} Strategies of predicting fetal macrosomia consist of three major
aspects: assessing clinical risk factors, performing Leopold's maneuvers
and using ultrasound. {[}6{]}

According to Gaudet et al. risk factors for excessive fetal birth weight
include maternal pre-existing and gestational diabetes mellitus,
previous macrosomic birth, postterm gestation over 42 weeks of gestation
and male infant gender. {[}1{]} Of the aformentioned maternal diabetes
mellitus is the strongest risk factor. {[}6{]} Gestational diabetes
defined as a glucose intolerance with an onset or first recognition
during pregnancy increases the risk for fetal macrosomia to a 2-3-fold.
{[}6, 11{]} Gestational diabetes is characterized by maternal
hyperglycemia resulting from progressive insulin resistance. {[}12{]}
Elevated maternal blood sugar levels seem to cause to some extend fetal
hyperglycemia which leads to fetal islet tissue hypertrophy, stimulation
of fetal insulin and insulin-like growth factor I production and results
in excessive fetal growth. {[}13, 14, 15{]} International guidelines
recommend the use of the 75-g 2-hour oral glucose tolerance test to test
for gestational diabetes in women with risk factors and to establish
early interventions to prevent gestational diabetes mellitus related
complications. {[}29{]} In 1991 the \selectlanguage{english},Diabetes in early pregnancy` study
showed that monitoring of nonfasting elevated glucose levels in the
third trimester is the strongest predictor of fetal macrosomia in
diabetic pregnancies. {[}16{]}

The meta-analysis of Gaudet et al. additionally states a strong
association between fetal macrosomia and maternal obesity. {[}1{]} The
underlying mechanisms are not yet understood completely but seem to be
associated with a dysregulation of glucosis, insulin, lipid and amino
acid metabolism, both maternal and fetal. {[}17{]} This implicates the
necessity of preventing maternal overnutrition and monitoring maternal
weight during pregnancy strictly. {[}18{]} Pre-pregnancy obesity is
associated with a 1.6-fold increase in risk for neonatal macrosomia.
{[}18{]} Optimization of the maternal weight prior to the pregnancy
through the encouragement of lifestyle modifications including diet
control and exercise seem essential in managing gestational weight gain
and abnormal glucosis metabolism. {[}1, 18, 19{]} Excessive weight gain
during pregnancy increases the risk for neonatal macrosomia 3.6 times
compared to women with normal weight gain during pregnancy. {[}18{]}

In our case two major risk factors contributed to fetal macrosomia. On
the one hand the patient was extremely obese with a body mass index of
46.8 kg/m2. On the other hand advanced maternal insulin resistence had
to be acknowledged. A pre-existing diabetes mellitus can be suspected.

Most common biometric ultrasound measurements to estimate fetal weight
involve biparietal diameter, head circumference, abdominal circumference
and femur diaphysis length. {[}5, 20{]} In order to improve prenatal
fetal growth evaluation it is suggested that ultrasound estimated growth
curves should be adjusted for maternal ethnicity and individual
characteristics. {[}3{]}

Nevertheless, the accurate detection of fetal macrosomia via ultrasound
is limited. {[}5,20{]} A recent cochrane review stated that there is
insufficient evidence that the use of fetal biometry in pregnancies
affected by gestational diabetes mellitus could in addition to
monitoring maternal blood glucose levels help to optimize medical
management of gestational diabetes mellitus. {[}28{]} Clinical
decisions~concerning fetal macrosomia based on ultrasound prediction
only need to be questioned. {[}20, 21{]}

Maternal complications caused by fetal macrosomia include emergency
caesarean section, peripartum hemorrhage and anal sphincter injury.
{[}22{]} In our case the patient received an urgent caesarean section
due to failure to progress in the second stage of labor with a
persistent occiput posterior position of the fetus. Even though the
patient quickly received uterotonic agents we experienced a postpartum
hemorrhage with a total blood loss of 1500 ml and a consecutive maternal
anemia. The systemic review of eight studies by Beta et al. showed a
2,5-fold increase in the performance of emergency caesarean sections in
pregnancies with a neonatal birth weight of \textgreater{} 4500 g
compared to those without macrosomic neonates. {[}22{]}

Beta et al. were able to show that pregnancies with a neonatal birth
weight of \textgreater{} 4000 g had a 2-fold increased risk of
peripartal hemorrhage and pregnancies with a neonatal birth weight of
\textgreater{} 4500 g a 3-fold increased risk compared to pregnancies
with non-macrosomic neonates. {[}22{]}

Compared to non-macrosomic pregnancies there is a significant increase
in obstetric anal sphincter injury in pregnancies with a neonatal weight
\textgreater{} 4000 g, especially when complicated by shoulder dystocia.
{[}22, 23{]}

So far there exist no established guidelines on how to inform and advise
women when fetal macrosomia is suspected. {[}22{]}

Neonatal outcome is severely impaired due to macrosomic birth weight as
well. {[}22{]} Macrosomic newborns form a heterogenous patient group in
regard to body constitution and metabolism. {[}2{]} An increased birth
weight is however associated with a 2-3-fold increase in risk of
intrauterine death. {[}2{]} Mondestin et al. showed a significantly
increased rate of fetal death in non-diabetic pregnancies with a birth
weight \selectlanguage{english}[?]4250 g and a significantly increased rate of fetal death in
diabetic pregnancies with a birth weight \selectlanguage{english}[?]4000 g. {[}24{]}

Macrosomic newborns present an increased risk of a prolonged neonatal
intensive care, especially in the presence of maternal diabetes mellitus
as well as when weighing more than 5000 g, having shown fetal distress
or when suspecting a cephalopelvic disproportion. {[}25{]} All of the
aformentioned applied in our case.

Macrosomic birth weight furthermore augments the risk of shoulder
dystocia, obstetric brachial plexus injury and clavicular fracture in
newborns after vaginal delivery significantly. {[}22, 23{]}

Lately more attention has been drawn to the longterm consequences on
childrens' health due to maternal obesity. {[}26, 27{]} Animal models
were able to show unambiguously that maternal obesity promotes insulin
resistance in the offspring as well as the development of cardiovascular
disease risk factors later on in life. {[}27{]} However, human
observational studies have not yet distinguished causality from
association concerning maternal obesity and childhood diseases due to
the complexity of influential factors and confounder data. {[}27{]}

The increase in pregnancies complicated by maternal obesity and
gestational diabetes emphasizes the necessity of evidence-based clinical
interventions to prevent or decelerate these diseases. {[}4{]} However,
if prenatal care is not frequented by mothers-to-be there are no options
open to intervene for obstetricians. A variety of studies show that
fetal macrosomia complicates pregnancies and labor which we demonstrated
with this case report as well.

Competing interests: The authors declare that they have no competing
interests.

Consent: Informed consent was obtained from the patient for publication
of this case report and any accompanying images.

Authors' contributions: JK wrote the article. AJ, LH, LP, VM and JK were
the leading clinicians in charge of the patient's care. All authors read
and approved the final manuscript.

Ethics approval: Ethics approval was not needed due to the retrospective
character and anonymized theoretical treatment of patient information.

Funding: Funding played no role in the making of this article.

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21 Delpapa EH, Mueller-Heubach E. Pregnancy outcome following ultrasound
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27 Patel N, Pasupathy D, Poston L. Determining the consequences of
maternal obesity for offspring health. Exp Physiol. 2015; 100(12):1421-8

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29 NICE Guideline. Diabetes in pregnancy: management from preconception
to the postnatal period. Published date: 25 February 2015 Last updated:
16 December 2020

Table 1 -- neonatal laboratory values\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\textbf{parameter} & \textbf{value} & \textbf{reference range} &
\textbf{unit}\tabularnewline
\midrule
\endhead
leucozytes & 10.45 & 7.20 -- 21.60 & /nl\tabularnewline
hemoglobin & 19.1 & 13.2 -- 21.7 & g/dl\tabularnewline
platelets & 183 & 220 -- 520 & /nl\tabularnewline
sodium & 140 & 131 -- 144 & mmol/l\tabularnewline
potassium & 5.5 & 3.2 -- 5.5 & mmol/l\tabularnewline
interleukin-6 & 172.7 & \textless{} 30.4 & ng/l\tabularnewline
c-reactive protein & 30.4 & \textless{} 5.0 & mg/l\tabularnewline
glucose & 33 & & mg/dl\tabularnewline
thyroid stimulating hormone & 1.97 & 2.12 -- 13.50 & mU/l\tabularnewline
free thyroxine & 25.90 & 10.60 -- 23.00 & ng/l\tabularnewline
total triiodothyronine & 3.90 & 2.16 -- 5.88 & ng/l\tabularnewline
insulin-like growth factor 1 & 50.9 & 19.0 -- 130.0 &
ng/ml\tabularnewline
adrenocorticotropic hormone & 35.7 & 10.0 -- 185.0 &
pg/ml\tabularnewline
cortisol & 71.6 & 80.0 -- 300.0 & nmol/l\tabularnewline
\bottomrule
\end{longtable}

Table 2 -- postoperative maternal laboratory values\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\textbf{parameter} & \textbf{value} & \textbf{reference range} &
\textbf{unit}\tabularnewline
\midrule
\endhead
leucozytes & 15.15 & 3.90 -- 10.50 & /nl\tabularnewline
hemoglobin & 7.3 & 12.0 -- 15.6 & g/dl\tabularnewline
platelets & 268 & 150 -- 370 & /nl\tabularnewline
sodium & 139 & 136 -- 145 & mmol/l\tabularnewline
potassium & 4.1 & 3.4 -- 4.5 & mmol/l\tabularnewline
creatinine & 0.79 & 0.50 -- 0.90 & mg/dl\tabularnewline
glutamate oxaloacetate transaminase & 29 & \textless{} 35 &
U/l\tabularnewline
glutamate pyruvate transaminase & 16 & \textless{}31 &
U/l\tabularnewline
c-reactive protein & 21.7 & \textless{} 5.0 & mg/l\tabularnewline
lactate dehydrogenase & 422 & 135 -- 250 & U/l\tabularnewline
glycated hemoglobin & 7.2 & \textless{} 6.0 & \%\tabularnewline
glucose & 167 & 74 - 106 & mg/dl\tabularnewline
thyroid stimulating hormone & 3.22 & 0.27 -- 4.20 & mU/l\tabularnewline
prolactin & 309.00 & 4.79 -- 23.30 & \selectlanguage{greek}µ\selectlanguage{english}g/l\tabularnewline
human growth hormone & 0.09 & \textless{} 5.00 & ng/ml\tabularnewline
insulin-like growth factor 1 & 175.2 & 72.0 -- 237.0 &
ng/ml\tabularnewline
cortisol & 579.0 & & nmol/l\tabularnewline
estradiol & 206.0 & 46.0 -- 1828.0 & pmol/l\tabularnewline
\bottomrule
\end{longtable}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

Figure 1 -- macrosomic male neonate\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}

Figure 2 -- neonatal echocardiography\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image3/image3}

\end{center}
\end{figure}

Figure 3 -- neonatal abdominal ultrasound showing excessive abdominal
fat

\selectlanguage{english}
\FloatBarrier
\end{document}

