Clinical Presentation and Treatment of Hyperemesis Gravidarum in a Lady Carrying Twins in the First Trimester: A Case Reports

ABSTRACT

We report a 12‐week‐old pauci‐geste carrying twins who experienced potentially fatal hyperemesis gravidarum. Clinical and paraclinical investigations revealed severe hypovolemic shock/dehydration, ionic disruption, undernutrition, and acute renal failure (GFR: 36.8 mL/min/1.73 m² according to modified MDRD). The patient spent almost 3 weeks in emergency and critical care at the University Clinics of Bukavu, where her pregnancy was tracked until her twins were born. Hyperemesis gravidarum diagnosis remains clinical, with incomplete etiopathogenesis understanding. Genetic research, including Growth Differentiation factor 15, is promising. Maternal morbidity consensus exists, but fetal effects vary by severity. Early multimodal approaches, psychological support, viral screening, Non‐Invasive Prenatal Testing, nutraceuticals, and long‐term Frozen Embryo Transfer child follow‐up are vital for life‐saving outcomes.

Key Clinical Message

This 12‐week case, which was successfully treated with vigorous rehydration, multimodal antiemetics, and nutritional support, demonstrates how severe hyperemesis gravidarum in twin pregnancies can cause life‐threatening hypovolemic shock, acute renal failure, and malnutrition. To maximize maternal‐fetal outcomes, early intervention, genetic insights (such as GDF‐15), viral screening, NIPT, nutraceuticals, and long‐term FET child follow‐up are crucial.

1. Introduction

The most common gastrointestinal problems during pregnancy are nausea and vomiting, which affect 70% to 80% of expectant mothers, frequently during their first pregnancy [1]. These normally harmless symptoms typically go away around the 20th gestational age and are prevalent during the first trimester of pregnancy [2]. Weight loss, ketonuria, and altered consciousness are all signs of hyperemesis gravidarum, which is characterized by excessive and prolonged vomiting, up to five exonerations per day [3, 4, 5]. The incidence ranges from 0.2% to 10%, depending on the ethnic group [6]. we describe the clinical progression of a potentially fatal case of hyperemesis gravidarum in a second twin pregnancy with an estimated gestational age of 12 years.

2. Analysis of the Case History

With obstetric formula G2, P1, A0 D0 E1, and a last menstrual period on September 20, 2022, the 25‐year‐old pregnant woman was admitted to the Obstetrics Department of the University Clinics of Bukavu on December 8, 2022. Her gestational age was determined to be 12 weeks, and she complained of nausea, incoercible vomiting (approximately 7 episodes per day, evolving approximately a month prior to our consultation), and severe epigastric pain. Her obstetric history includes an early vaginal delivery of a 3000‐g female infant with no obvious physical abnormalities when she was still 16 years old. She didn't use smoke, alcohol, or stimulants, and she didn't have any known chronic ailments. Her mother had experienced severe vomiting during her first pregnancy, according to her family history.

According to the additional history, there was severe thirst, amenorrhea lasting longer than 3 months, and physical asthenia with a score of 4 on the World Health oganization/Karnofski performance scale.

A medical examination revealed that she was severely dehydrated and had lost weight, which had affected her overall health. Vital signs: RF 28 cycles/min, HR 143 beats/min, BP 80/60 mmHg, and temperature 36.6°C.

Anthropometric measurements: height 1.57 m, weight 35 kg, and body mass index 15 kg/m², which indicates a 30% decrease of about 17 kg from her prior weight of 52 kg, which was recorded around the time of her last weight gain.

The bulbar anicteric with hypotonic sunken eyeballs and hypersialorrhea was stained, as were the palpebral conjunctivae. The heart beat regularly and tachycardically at 143 beats/min. Palpation revealed a slightly enlarged belly, an ovoid mass two fingerbreadths below the umbilicus, and diffuse pain that was emphasized in the epigastrium with minor effacement of the skin folds.

The remainder of the clinical evaluation went without incident.

3. Methods

First, we evaluated malnutrition that exacerbated severe pregnant vomiting and hypovolemic shock, also known as severe dehydration. and to rule out dyspeptic syndrome or a painful epigastrium.

The patient was put on emergency rehydration treatment, which included 6 L of physiological serum (NaCl) and 3 L of balanced solution (Ringer's lactate) every 4 h for 24 h. Antiemetics Ondasetron 2 mg intravenously (IV) every 6 h, vitamin B/pyridoxine 300 mg every 12 h, ranitidine 50 mg IV for 8 h, and an antispasmodic (Spasfon) 40 mg every 12 h were also administered.

At the same time, the following tests were conducted (Appendix A).

An evolutive twin pregnancy, bichorionic, biamniotic, with a gestational age at ultrasonography estimated at 12 SA, was discovered during an abdomino‐pelvic ultrasound (Appendix B). The ultrasound of the abdomen revealed nothing unusual.

Based on these investigations, we determined that the patient had severe dehydration and hypovolaemic shock, along with ionic disturbance, malnourishment, and acute renal failure (GFR: 36.8 mL/min/1.73 m² according to the modified MDRD). The ultrasound and the date of the last menstrual period in the second gestational/skin test also indicated that the patient had complicated hyperemesis gravidarum in a twin pregnancy of 12 SA.

We supplemented our initial treatment with central venous potassium at a rate of 1 g/h by continuous infusion.

Small quantities of hemorrhage were added to the basic symptoms on the second day of hospitalization.

The patient had mild Mallory syndrome, we determined.

This made it possible for us to add Primperan 10 mg daily to his original treatment, which included treating the remainder of his digestive tract.

Although the physical asthenia and epigastric pain continued, there was a noticeable clinical improvement in the haematemesis and vomiting on the third day of hospitalization.

In addition to replacing the ranitidine with omeprasole 40 mg IV every 12 h and polygel syrup 10 mL every 8 h for gastric dressing, we also added Largactif 25 mg daily by infusion to her treatment. Additionally, we recommend a vitamin and amino acid supplement every 12 h, metoclopramide 10 mg every 8 h, and a light, fractionated diet high in protein and carbs, consisting of minced meats, eggs, fruit, and juices every 4 h.

On his fourth day of hospitalization, we observed a positive clinical evolution, characterized by the cessation of vomiting and epigastric pain as well as an improvement in his overall health and hydration.

We were able to cease the potassium chloride and change the hydration plan to three liters per day with 1 L of 0.9% NaCl, 1 L of Ringer's lactate, and 1 L of 5% glucose serum because the examination revealed a good correction of the ionic disorder. Ketonuria was negative on the urine dipstick (Appendix C).

The patient, who weighed 37 kg and was in good overall health with a few mild episodes of nausea and vomiting, was released from the hospital after 2 weeks. She received treatment with Polygel 10cl syrup every 8 h, Ondansetron 4 mg tablets every 12 h, and Metoclopramide 5 mg tablets every 12 h. Water consumption averaged two liters each day, and nutrition was promoted.

4. Conclusion and Findings

The pregnant woman arrived for a one‐week appointment in good health, still experiencing nausea but without vomiting or epigastric pain. She attended the prenatal consultations, and at 37 weeks, a caesarean section was planned, which is recommended for twin pregnancies with D1 in breech presentation and D2 in cephalic presentation.

The respective weights of these babies were 3005 and 2010 g. With their AGPGARs at delivery being 6 at the first minute, 8 at the fifth minute, and 10 at the tenth minute for J1 and 5 at the first minute, 7 at the fifth minute, and 9 at the tenth minute for J2, respectively, J1 and J2 demonstrated a good adaptation to life outside the womb.

5. Discussion

We observed a case of hyperemesis gravidarum (HG) that was made worse by malnourishment and hypovolemic shock in a twin pregnancy at the University Clinics of Bukavu. The characteristic of HG is excessive nausea and vomiting, which are frequently harmless symptoms throughout the first trimester. They usually peak during the ninth week of amenorrhea and end by the twentieth [7, 8, 9] However, symptoms might continue until birth, at which point they might worsen and even be fatal [10] Since multiple pregnancies frequently result in more severe nausea and vomiting than singletons, this was demonstrated in our patient, where twin gestation exacerbated symptoms [11].

The gastrointestinal, hormonal, genetic, and psychological components of HG's etiology are still unknown [5]. Genome‐wide association studies (GWAS) link HG to growth differentiation factor 15 (GDF‐15), a placental hormone that influences appetite and nausea through brain pathways, but show no direct connection to β‐HCG [12] Hormones such as estrogen, progesterone, β‐HCG, and serotonin are linked to intestinal motility through 5‐HT3 receptor activation; familial patterns indicate hereditary predisposition [13] Helicobacter pylori infection is common in HG cases, and approximately 18% of affected women have post‐traumatic stress disorder [3, 13, 14, 15, 16]. The history of HG and H. pylori in our case suggests complex origins, including possible viral effects.

Current research emphasizes how viral infections can exacerbate HG, especially in susceptible groups. Previous or concomitant COVID‐19 infection can worsen HG symptoms, as seen in instances when SARS‐CoV‐2 worsened nausea, increasing hospitalizations or consequences like preeclampsia [17].

Lockdowns during the COVID‐19 pandemic decreased total HG hospitalizations, either as a result of reduced exposure or changed access to healthcare; however, pregnant women who were infected were more likely to experience severe symptoms and metabolic disorders [18] Similarly, Zika virus (ZIKV) infection during pregnancy may indirectly affect HG through systemic inflammation or placental disruption, although direct causal links require more research. ZIKV infection during pregnancy is primarily associated with congenital Zika syndrome (CZS), which involves microcephaly and neurodevelopmental issues [17, 19].

In patients who have previously had infertility or thyroid dysfunction, these viral variables are particularly important since autoimmune or metabolic vulnerabilities (such as thyroid autoimmunity) increase the risk [20, 21, 22].

In these situations, cell and gene treatments have the potential to improve reproductive outcomes and treat infertility associated with thyroid autoimmunity by modifying immune responses [21].

Furthermore, factors including perceived safety and past medical conditions affect high‐risk pregnant women's acceptance of the anti‐SARS‐CoV‐2 vaccine, highlighting the necessity of customized counseling to reduce viral consequences on HG [7, 23].

Thorough anamnesis is necessary for the diagnosis of HG in order to rule out differentials such as gastrointestinal disorders (such as peptic ulcers, cholecystitis, …), metabolic/endocrine problems (such as hyperthyroidism, diabetic ketoacidosis, …), neurological abnormalities, trophoblastic disorders, or vomiting brought on by drugs [5, 15].

The PUQE‐24 questionnaire is used to evaluate severity [3, 5, 24]. Although newer analyses have questioned the diagnostic utility of ketonuria monitoring in HG, it still helps with hospitalization and rehydration decisions [25]. Non‐invasive prenatal testing (NIPT) with cell‐free fetal DNA (cffDNA) is advised at the beginning of pregnancy to improve early risk stratification, particularly in HG with infertility or viral background.

NIPT provides vital medicolegal and prognostic insights by screening for chromosomopathies and monogenic disorders. It is especially useful in high‐risk cases to identify fetal abnormalities that may be connected to maternal problems such as HG or viral exposures [26].

HG affects the fetus as well as the mother. Electrolyte imbalances (hyponatremia, hypokalemia) that cause arrhythmias and thiamine deficiency that causes Wernicke's encephalopathy are examples of maternal complications. Recent reviews have highlighted contributing factors including as malnutrition and possible malpractice in delayed diagnosis [27, 28] Autoimmune, thyroid, and breast disorders continue to be linked [11, 21]. There is disagreement over fetal dangers, such as low miscarriage rates but the possibility of preterm birth and problems in cases of severe malnutrition [2]. Long‐term neonatal follow‐up is crucial for patients with a history of infertility, especially those using assisted reproductive technologies (ART) like frozen embryo transfer (FET) [29]. Compared to fresh transfers, children from FET have similar or better perinatal outcomes (e.g., lower low birth weight), but there are certain concerns, such as large for gestational age (LGA) and modest neurological changes that need to be monitored until adulthood [20].

Based on the PUQE‐24, treatment is based on symptoms: routine care for scores below 7, antiemetics for scores 7–12, hospitalization for scores 13 or higher, and rehydration for all [15] Patients with moderate HG can get better with electrolyte drinks and meals high in fractionated protein. Patients with severe cases need more [14]. Ginger works better than pyridoxine and placebo. First‐line treatments for refractory HG include antihistamines, metoclopramide (no teratogenicity), ondansetron (risk of deformities), and corticosteroids. There is no better antiemetic [3, 10, 14, 15, 30]. Nutraceutical supplementation has been shown to improve mother and fetal health, particularly in HG with metabolic or reproductive comorbidities like infertility or polycystic ovarian syndrome (PCOS) [31]. Alpha‐lipoic acid (ALA), vitamin D, betaine, and inositols (including myo‐inositol) have anti‐inflammatory, antioxidant, and insulin‐sensitizing properties that improve oocyte quality, lower the risk of premature birth, and lessen metabolic disorders [32, 33].

In addition to lowering breast density, combinations such as boswellia, betaine, and myo‐inositol (such as Eumast) may also aid pregnant women by reducing inflammation [34]. Inositols improve insulin resistance and ovarian function, whereas vitamin D treats deficiencies in PCOS‐related reproductive problems [35]. These supplements are safe and may help with fetal development and HG symptoms [27].

The diagnosis of HG is still clinical, and the etiopathogenesis is not fully understood. GDF‐15 and other genetic research show promise. There is agreement on maternal morbidity, although the severity of the effects on the fetus varies [30]. For life‐saving results, early multimodal interventions, psychosocial support, viral screening, NIPT, nutraceuticals, and long‐term FET child follow‐up are essential [20].

Author Contributions

Kesheni Banyanga David: conceptualization, methodology, validation, writing – original draft. Carmel Mbalo Walemba: methodology, writing – original draft, writing – review and editing. Vanessa Ndamuso Nshombo: conceptualization, data curation, resources, software, validation. Marc Burume: investigation, methodology, writing – review and editing. Bushambale Rudeha Agath: data curation, validation, visualization. Laurent Kasongo: data curation, formal analysis, funding acquisition. Germain Mugisho Matabaro: conceptualization, funding acquisition, methodology, visualization. Gaston Masimango: data curation, resources, software, validation. Trésor Okamba Alangi: data curation, funding acquisition, validation. Philémon Matabishi: supervision, validation, writing – review and editing. Patient Wimba Mijiriro: project administration, supervision, writing – review and editing.

Funding

The authors have nothing to report.

Consent

A written informed consent was obtained from patient to publish this report in accordance with the journal's patient consent policy.

Conflicts of Interest

The authors declare no conflicts of interest.

Appendix A. Laboratory Profile at the Initial Presentation

Parameter	Patient's value	Reference range
Bilan hormonal
Thyroid stimulating hormone	0.46	0.25–4.00 (IU/mL)
Liver function
Aspartate aminotransferase	41.16	15–41 (IU/L)
Alanine aminotransferase	45.29	14–40 (IU/L)
Hematology
Hemoglobin	12.3	11–16 (g/dL)
Hematocrit	33%	36%–48%
Total white blood cell	6.390	4000–10,000 (mL)
Red blood cells	3.99	×10e6/mm3
Plaquettes	410,000	150–450,000/mm3
Biochimy
Glucose	140	70–99 (mg/dL)
Albumin	3	3.5–5.0 (g/dL)
Total bilirubin	1.5	0.3–1.2 (mg/dL)
Kidney function
Blood urea nitrogen	29	8–20 (mg/dL)
Creatinine	2	0.4–1.2 (mg/dL)
Ionogram
Sodium	12’	135–144 (mEq/L)
Potassium	2.13	3.5–5.1 (mEq/L)
Chloride	98	101–111 (mEq/L)
Magnesium	1.6	1.8–2.5 (mg/L)
Calcium	10.5	8.6–10.2 (mEq/L)
Phosphore	1 0.0	0.81–1.62 (mEq/L)
Inflammatory bilan
C reactive protein	3	< 10 (mg/dL)
The selles' serological test for Helicobacter pylori	Positive
Urine dipstick
Ketouria	Positive
Glycosuria	Negative
Pregnancy test in urine test	Positive

Appendix B. Obstetrical Ultrasound Findings

Twin pregnancy, bichorionic, biamniotic, with a gestational age at ultrasonography estimated at 12 SA

Appendix C. Ionograms and Other Control Tests

Parameter	Patient's value	Reference range
Kidney function
Creatinine	1.0	0.3–1.2 (mg/dL)
Urea	30.3	15–45 (g/L)
Ionogram
Sodium	138	135–144 (mEq/L)
Potassium	3.87	3.5–5.1 (mEq/L)
Chloride	98.8	101–111 (mEq/L)
Biochemistry
Serique albumin	3.4	3.5–5.0 g/dL
Urine dipstick
Ketonuria	Negative

Data Availability Statement

The whole text contains all the knowledge required from these articles.