Obstetric and gynecological management in a patient with abnormal invasion of the placenta (placenta percreta)
- Authors: Ishchenko A.I.1, Gorbenko O.Y.1, Khokhlova I.D.1, Zuev V.M.1, Dzhibladze T.A.1, Baburin D.V.1
-
Affiliations:
- I.M. Sechenov First Moscow State Medical University
- Issue: Vol 11, No 3 (2024)
- Pages: 350-359
- Section: Clinical case reports
- Submitted: 02.02.2024
- Accepted: 14.06.2024
- Published: 07.10.2024
- URL: https://archivog.com/2313-8726/article/view/626389
- DOI: https://doi.org/10.17816/aog626389
- ID: 626389
Cite item
Abstract
Pathological placental invasion is a dangerous anomaly during pregnancy, which causes increased maternal morbidity and mortality. Patients with abnormal placental invasion may experience life-threatening uterine bleeding during delivery, particularly in cases of placenta percreta. This often requires surgical intervention, specifically a hysterectomy, which some researchers refer to as the “gold standard” treatment for pathological placental invasion, with rates ranging from 47% to 77.8%. Conversely, other researchers recommend a conservative approach, involving the complete removal of the placenta percreta, excision of damaged areas on the uterine walls and bladder, and metroplasty and restoration of the integrity of the.
This article presents a clinical case of a 40-year-old patient with a complicated obstetric history, including abnormal placental invasion (placenta percreta) involving the anterior wall of the uterus and the bladder.
Delayed diagnosis of such pathology leads to inappropriate treatment and, consequently, acute massive bleeding, posing a risk to the patient’s health and life. The applied comprehensive diagnostic and therapeutic measures facilitated the preservation of the pelvic organs and restoration of the patient’s reproductive function.
Keywords
Full Text
INTRODUCTION
The incidence of thyroid diseases (autoimmune thyroiditis and diffuse toxic goiter) tends to increase worldwide [1–4]. Endocrine changes associated with thyroid dysfunction are more common in women than in men [1, 5].
It should be noted that during pregnancy a woman’s body is exposed to increased endocrine organs stress due to hormonal changes and formation of fetoplacental complex [1, 3, 5].
Thyroid hormones such as thyroxine (T4) and triiodothyronine (T3) are pivotal for both intrauterine fetal development and the child’s subsequent extrauterine life [2, 4, 6].
Both low and high levels of thyroid hormones are known to be capable of triggering spontaneous abortion, premature birth, low birth weight, hypoxic and ischemic changes in the brain, etc. [1, 3–6]. Therefore, it is important to continue studying the influence of thyroid function on intrauterine fetal status [2–4].
AIM
The aim of the study was to evaluate the functional status of a fetus in pregnant women with certain thyroid disorders.
MATERIALS AND METHODS
The results of functional fetal assessment were evaluated in 118 pregnant women, who were divided into 3 groups: group 1 (n=44) included patients with autoimmune thyroiditis; group 2 (n=52) patients with diffuse toxic goiter; control group 3 (n=22) patients without physical diseases and gestational complications. Thyroid disease was diagnosed by an endocrinologist during a third trimester consultation based on laboratory and instrumental data. It should be noted that all patients with thyroid diseases first consulted a gynecologist for pregnancy only in the third trimester. Until then, patients with these thyroid disorders had not been followed by an obstetrician/gynecologist or a specialist.
For functional assessment of the fetal status, cardiotocographic curves and ultrasound results obtained at 32–40 weeks of gestation were evaluated.
Cardiotocography (CTG) was performed using a Partecust cardiomonitor (Siemens, Germany) to determine the fetal heart rate, rate variability, fetal movement count, and maximum change in heart rate during movement. CTG data were used for integrated assessment of the fetal status. Computer analysis of CTG was performed using a Fisher score. An International Federation of Gynecology and Obstetrics (FIGO) scale was used for grading.
A fetal biophysical profile was determined using a 6-parameter approach including a non-stress test and ultrasound parameters obtained using an Aloka-1700 system (Hitachi, Japan), such as fetal breathing movements, motor activity and tone, amniotic fluid volume, and placental maturity. Each parameter was scored from 0 to 2.
StatSoft (Russia) was used for statistical processing of the evaluated clinical material. Means and standard deviations were calculated. Student’s t-test was used to determine the reliability of the values between the groups compared.
RESULTS AND DISCUSSION
As shown in Table 1, basal fetal heart rate was not significantly different between groups and averaged 140–147 beats/min. In pregnant women with autoimmune thyroiditis and diffuse toxic goiter, fetal basal heart rate variability was significantly (p <0.05) reduced compared to normal pregnant women.
Table 1. Features of fetal cardiotocograms in pregnant women studied (М±m)
Indicator | Group 1 (n=44) | Group 2 (n=52) | Group 3 (n=22) |
Basal rhythm (bpm) | 145.0±7.0 | 148.0±2.0 | 142.0±7.0 |
Variability (bpm) | 6.3±1.4* | 7.1±0.8* | 11.7±0.9 |
Accelerations (per 1 hour) | 6.6±0.8* | 8.2±0.2* | 10.4±0.7 |
Cardiotocogram assessment (points) | 6.3±0.4* | 7.3±0.1* | 8.3±0.4 |
* Significance (р <0.05) of differences in indicators compared with values in pregnant women from group 3 (control).
In addition, the control group had a significantly (p < 0.05) higher acceleration amplitude (10.4±0.7 per hour) than pregnant women with autoimmune thyroiditis and diffuse toxic goiter. It should be noted that in 4 patients with autoimmune thyroiditis (9.1%), fetal cardiotocography patterns had a monotonous basal rhythm.
In general, the mean fetal CTG score was significantly (p <0.05) lower in pregnant women with autoimmune thyroiditis and diffuse toxic goiter compared to controls. This suggests chronic fetal hypoxia in patients with thyroid disease.
The instrumental study of fetal reactivity (mobility) during exercise testing in pregnant women is important for a comprehensive assessment of the adaptive fetal capacity. Non-stress testing records a response of the fetal cardiovascular system in response to fetal movements [7]. A good outcome is defined as a positive reactive test with at least 2 fetal heart rate increases of 15 beats/min lasting at least 15 seconds associated with fetal movements [7].
The studies conducted showed that during pregnancy, patients with thyroid dysfunction were significantly (p < 0.05) less likely to have a reactive positive non-stress test compared to pregnant women in the control group (Table 2).
Table 2. Results of non-stress test in pregnant women studied, n (%)
Non-stress test | Group 1 (n=44) | Group 2 (n=52) | Group 3 (n=22) |
Reactive | 32 (72.2*) | 38 (73.1*) | 21 (95.5) |
Questionable | 10 (23.8) | 10 (19.2) | 1 (9.1) |
Areactive | 2 (4.0) | 4 (7.7) | — |
* Significance (р <0.05) of differences in indicators compared with values in pregnant women from group 3 (control).
Table 3 shows results of assessment of fetal biophysical profile in pregnant women from different groups.
Table 3. Assessment of the biophysical profile of the fetus in compared groups, n (%)
Indicators | Points | Group 1 (n=44) | Group 2 (n=52) | Group 3 (n=22) |
Fetal breathing movements | 2 | 12 (27.3) | 29 (57.7) | 21 (95.5) |
1 | 10 (22.7) | 4 (7.7) | 1 (4.5) | |
0 | 22 (50.0) | 15 (26.9) | — | |
Fetal tone | 2 | 19 (45.5) | 41 (80.8) | 21 (95.5) |
1 | 4 (9.1) | 5 (11.5) | 1 (4.5) | |
0 | 19 (45.5) | 4 (7.7) | — | |
Fetal motor activity | 2 | 30 (68.2*) | 41 (80.8) | 21 (95.5) |
1 | 12 (27.3) | 10 (19.2) | 1 (4.5) | |
0 | 2 (4.5) | — | — | |
Stages of placental maturity | 2 | 21 (50.0*) | 29 (57.7) | 17 (77.3) |
1 | 16 (36.4) | 13 (23.1) | 4 (18.2) | |
0 | 6 (13.6) | 9 (19.2) | 1 (4.5) | |
Amniotic fluid | 2 | 24 (54.5) | 37 (73.1) | 21 (95.5) |
1 | 10 (22.7) | 8 (15.4) | 1 (4.5) | |
0 | 10 (22.7) | 5 (11.5) | — | |
Non-stress test | 2 | 32 (72.7) | 36 (69.2) | 19 (86.3) |
1 | 8 (18.2) | 6 (23.1) | 2 (9.1) | |
0 | 4 (9.1) | 4 (7.7) | 1 (4.5) |
* Significance (р <0.05) of differences in indicators compared with values in pregnant women from group 3 (control).
A fetal score of 10–12 was observed in only 6 (13.6%) pregnant women with autoimmune thyroiditis, whereas a high score indicating normal fetal condition was 4 times more common in 54.5% of clinical cases in controls.
In patients with diffuse toxic goiter, a fetal biophysical profile with a high score of 10–12 was recorded in 7 (15.9%) cases, which was also significantly less (3.4 times) than in the control group (p <0.05).
In pregnant women with autoimmune thyroiditis and diffuse toxic goiter, 14 (31.8%) and 20 (38.5%) fetuses in groups 1 and 2, respectively, had a satisfactory score. In 10 (45.5%) cases in the control group, such a fetal score was reported according to the biophysical profile.
A controversial fetal biophysical profile was obtained in 18 (40.9%) and 21 (40.4%) pregnant women with autoimmune thyroiditis and diffuse toxic goiter, respectively. In addition, newborns were more likely (90%) to have Apgar scores of 7/7 or 7/8 and various types of postnatal adjustment disorders in the early neonatal period.
An abnormal fetal biophysical profile was reported in 6 (13.6%) pregnant women with autoimmune thyroiditis and in 4 (7.7%) pregnant women with diffuse toxic goiter. In these clinical situations, pregnant women had premature deliveries and neonates were born with moderate asphyxia and required intensive care in the early neonatal period.
It should be noted that changes in CTG parameters and fetal biophysical profile are objective criteria for assessing intrauterine status [7].
Our data confirm the findings of other authors [1–6] that thyroid disease significantly contributes to fetoplacental insufficiency with chronic fetal hypoxia.
In pregnant women with autoimmune thyroiditis and diffuse toxic goiter, changes in respiration, motor function, and muscle tone during fetal instrumental assessment serve as crucial prognostic factors. Non-stress testing is also important in assessing intrauterine fetal status and predicting perinatal outcomes.
CONCLUSION
Our study showed that thyroid dysfunction in pregnant women can negatively affect fetal development. Again, it should be noted that the patients included in this study were not followed by an obstetrician-gynecologist and, for various reasons, did not undergo comprehensive examination until the third trimester. It is possible that early detection of endocrine disorders and timely initiation of treatment to normalize thyroid function may be beneficial to a fetoplacental complex and may prevent chronic fetal hypoxia. This study may serve as a theoretical basis for the development of preventive and therapeutic options to improve perinatal outcomes in pregnant women with thyroid disease.
ADDITIONAL INFO
Authors’ contribution. All authors confirm that their authorship meets the international ICMJE criteria (all authors made a substantial contribution to the conception of the work, acquisition, analysis, interpretation of data for the work, drafting and revising the work, final approval of the version to be published and agree to be accountable for all aspects of the work).
Funding source. The authors declare that there is no external funding for the exploration and analysis work.
Competing interests. The authors declares that there are no obvious and potential conflicts of interest associated with the publication of this article.
Ethical approval. The study was carried out as part of a comprehensive work at the Department of Obstetrics and Gynecology of the Faculty of Medicine of the Astrakhan State Medical University of the Ministry of Health of the Russian Federation and its implementation was agreed upon by the expert commission of this higher educational institution (extract from the protocol dated 07/26/2021 No. 130).
Consent for publication. All patients participating in the study signed the necessary documents on voluntary informed consent to participate in the study and the publication of their medical data.
About the authors
Anatoliy I. Ishchenko
I.M. Sechenov First Moscow State Medical University
Email: 7205502@mail.ru
ORCID iD: 0000-0001-5733-953X
SPIN-code: 3294-3251
MD, Dr. Sci. (Medicine), Professor
Russian Federation, MoscowOksana Y. Gorbenko
I.M. Sechenov First Moscow State Medical University
Email: go2601@mail.ru
ORCID iD: 0000-0002-3435-4590
SPIN-code: 8725-1419
MD, Cand. Sci. (Medicine)
Russian Federation, MoscowIrina D. Khokhlova
I.M. Sechenov First Moscow State Medical University
Author for correspondence.
Email: irhohlova5@gmail.com
ORCID iD: 0000-0001-8547-6750
SPIN-code: 6858-5235
MD, Cand. Sci. (Medicine), Assistant Professor
Russian Federation, MoscowVladimir M. Zuev
I.M. Sechenov First Moscow State Medical University
Email: vlzuev@bk.ru
ORCID iD: 0000-0001-8715-2020
SPIN-code: 2857-0309
MD, Dr. Sci. (Medicine), Professor
Russian Federation, MoscowTea A. Dzhibladze
I.M. Sechenov First Moscow State Medical University
Email: djiba@bk.ru
ORCID iD: 0000-0003-1540-5628
SPIN-code: 5688-1084
MD, Dr. Sci. (Medicine), Professor
Russian Federation, MoscowDmitrii V. Baburin
I.M. Sechenov First Moscow State Medical University
Email: baburin_d_v@staff.sechenov.ru
ORCID iD: 0000-0003-2398-3348
SPIN-code: 3264-0730
Scopus Author ID: 57211347487
ResearcherId: AAQ-3984-2021
MD, Cand. Sci. (Medicine)
Russian Federation, MoscowReferences
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