Esophageal Varices in Pregnancy Secondary to Hepatic Cirrhosis: A Case Report

INTRODUCTION

Pregnancy associated with liver diseases is a rare condition, as these patients typically experience impaired fertility due to disruptions in the hypothalamic-pituitary axis combined with disturbances in hepatic sex hormone metabolism [1,2]. However, when it occurs, it can lead to complex clinical situations that require careful management. Portal hypertension is one of the liver-related complications that may develop during pregnancy and arises from various underlying causes. In Western countries, cirrhosis is the most common cause of portal hypertension, although non-cirrhotic etiologies such as porto-sinusoidal vascular disease, acute fatty liver of pregnancy, and Budd-Chiari syndrome may also contribute [3].

The incidence of cirrhosis in pregnancy has been reported as approximately 1 in 5,950 pregnancies in previous epidemiological studies [4]. Cirrhosis may worsen during pregnancy as a result of physiological compensations, including the development of a hyperdynamic circulatory state. This progression can lead to poor maternal and fetal outcomes, particularly when complicated by gastrointestinal bleeding. In developing countries, non-cirrhotic portal hypertension is more prevalent and tends to have a better prognosis, with reports indicating the possibility of spontaneous pregnancies and relatively preserved liver function [4].

Esophageal varices represent one of the key manifestations of portal hypertension, resulting from increased blood flow through collateral circulations. Variceal rupture can lead to gastrointestinal bleeding in up to one-third of pregnant women with cirrhosis and poses a serious risk of mortality for both mother and fetus [4]. Therefore, understanding the impact of pregnancy-induced physiological changes on portal hemodynamics, as well as the consequences of portal hypertension and its underlying causes on maternal and fetal health, is crucial to optimizing pregnancy outcomes. This case report discusses a case of esophageal varices during pregnancy and provides a comprehensive review of clinical assessment and management options for pregnant women affected by this condition.

CASE DESCRIPTION

A 22-year-old woman was first referred from the Internal Medicine-Gastroenterology Department to the Obstetrics and Gynecology outpatient clinic in March 2023 with a diagnosis of grade IV esophageal varices and grade IV gastric fundal varices. At the time of referral, the patient was unaware of her pregnancy but had been referred due to amenorrhea for the preceding two months. Transvaginal ultrasonography confirmed an intrauterine pregnancy of 5–6 weeks gestation, consistent with her last menstrual period on January 23, 2023, with an estimated due date of October 30, 2023.

In February 2023, she presented to the emergency department at Dr. Zainoel Abidin Regional General Hospital with complaints of hematemesis — dark red vomiting, occurring once, approximately 1.5 glasses in volume — accompanied by melena with a frequency of once and a characteristic foul odor. On admission, the patient appeared weak, pale, and anorexic, and was subsequently admitted to the internal medicine ward. Laboratory findings revealed severe microcytic hypochromic anemia (Hb 5.12 g/dL; MCV 73 fL; MCH 24 pg; MCHC 32 g/dL), hematocrit 16%, leukocytes 3.49 × 10⁹/L, platelets 79 × 10⁹/L, urea 15 mg/dL, creatinine 0.5 mg/dL, albumin 3.1 g/dL, random blood glucose 107 mg/dL, SGOT 22 U/L, SGPT 25 U/L, total bilirubin 0.42 mg/dL, direct bilirubin 0.12 mg/dL, indirect bilirubin 0.3 mg/dL, PT 6 seconds, and APTT 5.6 seconds. FibroScan confirmed mild hepatic fibrosis with liver stiffness measurement of 8.4 kPa.

Throughout her pregnancy, the patient experienced recurrent episodes of hematemesis, totaling nine times up to the eighth month of gestation. She denied uterine contractions, leakage of fluid, or vaginal spotting, and reported no abnormal vaginal discharge. Urination remained within normal limits, and stools were characteristically dark. She attended regular monthly antenatal care visits at our obstetrics clinic.

Her medical history included a two-year history of esophageal varices. She denied any use of over-the-counter medications or alcohol consumption, but reported regular use of traditional herbal remedies aimed at weight gain. There was no history of hepatitis or similar familial conditions. Her medications included propranolol, vitamin K, cefixime, ferrous sulfate, octreotide, and curcumin supplements. The patient’s menarche was at 15 years of age, with regular menstrual cycles lasting seven days, and no dysmenorrhea. She married at 20 years old and was gravida 1 para 0 abortus 0, with no history of contraception use. She is a housewife, and her husband is self-employed. Her pre-pregnancy BMI indicated underweight status (16 kg/m²), with a pre-pregnancy weight of 36 kg and height of 150 cm. She gained approximately 8 kg during pregnancy. Vital signs were within normal limits: blood pressure 90/60 mmHg, pulse 90 bpm, respiratory rate 20 breaths per minute, and body temperature 36.5°C. General examination revealed anemic conjunctivae and icteric sclerae, with otherwise unremarkable findings. Obstetric examination showed a calm vulva and urethra. Speculum examination demonstrated a smooth cervix with a closed external os, no bleeding, and no abnormal discharge. Vaginal examination was not performed.

The latest laboratory tests prior to delivery revealed persistent microcytic hypochromic anemia (Hb 8.4 g/dL), improved coagulation profile (APTT 30.3 seconds, PT 14.4 seconds), decreased fibrinogen (243 mg/dL), elevated D-dimer (3010 ng/mL), and persistent thrombocytopenia (61 × 10³/μL). Renal function tests showed low serum creatinine (0.48 mg/dL) and urea (5.0 mg/dL). Electrolytes were within normal range (Na⁺ 138 mmol/L, K⁺ 3.7 mmol/L). Ferritin level was 9.12 ng/mL. Fetomaternal ultrasound at 34 weeks revealed a singleton cephalic presentation fetus with positive fetal heart rate, BPD 8.29 cm, HC 32.2 cm, AC 26.80 cm, FL 6.25 cm, and an estimated fetal weight of 1840 g, suggestive of intrauterine growth restriction (IUGR). Abdominal ultrasound performed in March 2023 indicated features consistent with hepatic cirrhosis, portal vein thrombosis, splenomegaly, and gravid uterus.

Figure 2. Abdominal ultrasound on March 13, 2023.

The diagnosis was established as G1P0A0, 34 weeks and 1 day gestation, cephalic presentation, suspected fetal IUGR, and maternal complications of grade III–IV esophageal varices, grade IV gastric fundal varices, and microcytic hypochromic anemia secondary to iron deficiency. Gastroscopy findings in March and September 2023 confirmed progression of the esophageal and gastric varices.

Figure 3. Gastroscopy images from March [left] and September [right] 2023.

The patient received antenatal corticosteroids for fetal lung maturation and was referred to the maternal-fetal medicine, pediatrics, internal medicine-gastroenterology, and anesthesiology departments for multidisciplinary planning. Maternal-fetal medicine recommended elective delivery prior to 37 weeks as the fetus was deemed viable (>34 weeks) following lung maturation therapy. The pediatrics team agreed with early delivery, anticipating NICU care at level IIB. The gastroenterology team concurred, with emphasis on optimizing beta-blocker therapy and future contraceptive counseling due to high hemorrhage risk in subsequent pregnancies. The anesthesiology team approved spinal anesthesia for delivery.

An elective cesarean section was performed, delivering a female infant weighing 1900 g, length 43 cm, Apgar scores 8/9, and Ballard score consistent with 34–36 weeks. The amniotic fluid was clear with adequate volume, and the placenta was delivered intact. The neonate was admitted to a level 2A NICU with diagnoses of respiratory distress syndrome, very low birth weight, and preterm small-for-gestational-age neonate.

DISCUSSION

Gastrointestinal bleeding, ascites, hepatic encephalopathy, and hepatorenal syndrome are some of the potential complications associated with portal hypertension. The primary manifestations of portal hypertension include esophageal varices, splenomegaly, and hypersplenism [5]. In this case, we report a pregnant woman at 34 weeks of gestation, presenting with grade IV esophageal varices and grade IV gastric fundal varices, as confirmed by gastroscopy. The presence of splenomegaly, confirmed through abdominal ultrasound, further indicated portal hypertension in this patient. Portal hypertension represents a hyperdynamic circulatory state, characterized by decreased peripheral vascular resistance and elevated portal vein pressure (>10 mmHg). This condition can progress significantly during pregnancy due to the physiological changes associated with gestation [5]

Numerous hemodynamic and physiological changes occur during pregnancy to accommodate the growing fetus. These changes begin around six weeks of gestation and peak at approximately 32 weeks. One of the earliest changes is an increase in plasma volume by about 40–50%, accompanied by a rise in maternal cardiac output by 30–50%, driven by increased stroke volume and heart rate. Systemic vascular resistance also decreases due to the effects of progesterone and the development of the placental vasculature. Collectively, these changes contribute to a hyperdynamic state. While these adaptations support fetal growth, they can exacerbate portal hypertension in pregnant women and elevate the risk of variceal bleeding [6,-8].

The etiology of portal hypertension is generally divided into two categories: cirrhotic and non-cirrhotic portal hypertension. Cirrhosis-related portal hypertension is more commonly encountered and strongly associated with complications, while non-cirrhotic portal hypertension can result from conditions such as portal vein obstruction, malignancies, or Budd-Chiari syndrome [9]. Hepatotoxic substances or alcoholism are among the known triggers of cirrhosis. Certain medications (such as amiodarone, methotrexate, and steroids) and chemicals can cause acute or chronic liver injury. Acute liver damage results in necrosis or steatosis, whereas chronic injury leads to cirrhosis. Compared to non-cirrhotic portal hypertension, patients with cirrhosis tend to experience reduced fertility due to hypothalamic-pituitary axis disruption, hepatic metabolism impairment of sex hormones, portosystemic shunting of weak androgens, and peripheral aromatization of androgens. Consequently, menstrual irregularities are common among cirrhotic patients [10]. In this case, the patient’s abdominal ultrasound confirmed cirrhosis, yet she displayed atypical characteristics, such as a regular menstrual cycle, possibly due to the relatively recent onset of cirrhosis (within two years) or her young age.

Gastrointestinal bleeding is a major complication in pregnant women with portal hypertension. Previous literature reports an incidence of 18–32% among pregnant patients with cirrhosis and approximately 75% among those with esophageal varices. This arises from the increased flow and pressure within collateral circulations in the hyperdynamic state of pregnancy. Bleeding from esophageal varices can occur at any stage of pregnancy, although the highest risk periods are during the second and third trimesters and the second stage of labor. Major predictors of variceal bleeding in pregnancy include large variceal size, the presence of high-risk endoscopic signs, and a history of gastrointestinal bleeding prior to conception [4,5]

In this case, the patient experienced gastrointestinal bleeding during the first trimester (10–11 weeks gestation). Her principal risk factors were portal hypertension secondary to cirrhosis and large varices, classified as grade III–IV on gastroscopy. The management of portal hypertension during pregnancy encompasses emergency management (for acute gastrointestinal bleeding), peripartum management, and postpartum care. In the event of active gastrointestinal bleeding, immediate maternal resuscitation and stabilization are critical, accompanied by intensive monitoring and emergent variceal management. Upper gastrointestinal endoscopy is considered safe during pregnancy, with minimal risk of fetal hypoxia from sedation and appropriate maternal positioning. The primary treatment modality is endoscopic variceal ligation (EVL), preferred over sclerotherapy to avoid the potential placental transfer of sclerosant toxins [5].

Pharmacologic therapy with vasopressors plays a role in managing acute variceal bleeding. Terlipressin, a category D drug in pregnancy, should be avoided. Octreotide, a category B medication, may be considered, although its safety profile in pregnancy has not been fully established. Third-generation cephalosporins such as cefazolin can be used as prophylaxis against spontaneous bacterial peritonitis (SBP) in variceal bleeding, while fluoroquinolones should be avoided [4,5].

Pregnant patients at risk of variceal bleeding should receive primary prophylaxis, either through EVL or beta-blockers. Beta-blockers are generally considered safe in pregnancy, although propranolol and nadolol (both category C drugs) carry risks of fetal bradycardia, growth retardation, and neonatal hypoglycemia. Ascites is a relatively uncommon finding in pregnant women with portal hypertension (7–11%), and its management with diuretics and paracentesis should be cautiously considered based on risk-benefit analysis[11]. In this case, the patient was previously hospitalized for gastrointestinal bleeding and treated with octreotide. She later received propranolol as prophylactic therapy. The occurrence of intrauterine growth restriction (IUGR) in this case is likely associated with propranolol use, a category C medication known to cause fetal IUGR, bradycardia, and hypoglycemia.

The choice of delivery method remains controversial in pregnant women with portal hypertension. A major concern with vaginal delivery is the risk of excessive straining, which may elevate intra-abdominal and portal pressures, potentially triggering variceal rupture. To date, no definitive studies have evaluated the impact of vaginal delivery on the risk of variceal bleeding. Consequently, many experts recommend elective cesarean delivery. Cesarean section rates among pregnant women with cirrhosis vary widely (12–81%), influenced by patient and institutional preferences and evolving obstetric practices. Cesarean delivery also carries risks in this population, including poor wound healing and infection. Some institutions advocate for cesarean section only for obstetric indications, while others favor vaginal delivery with a shortened second stage of labor to minimize intra-abdominal pressure increases [5,6,13]. In this case, elective cesarean delivery was performed based on multiple considerations: gestational age, large variceal size with high bleeding risk, and asymmetric IUGR. Asymmetric IUGR, often caused by maternal anemia, hypertension, cardiac disease, or bleeding, typically arises between 28 and 40 weeks of gestation due to impaired cellular hypertrophy. The prognosis for asymmetrical IUGR is generally favorable [13].

Postpartum management aims to detect and treat postpartum hemorrhage, which occurs in 5–45% of women with cirrhosis. This complication results from factors such as thrombocytopenia, coagulopathy, and aberrant variceal formation. Management strategies include administration of coagulation factors, uterotonic agents, vascular ligation, and, if necessary, hysterectomy. Antibiotics should be administered postpartum to prevent SBP, particularly in the presence of ascites [4,14].

Postpartum fever must be promptly investigated and treated with appropriate antibiotics. In cases of cirrhosis related to infectious etiologies such as chronic hepatitis B, vertical transmission should be prevented by administering immunoglobulin and hepatitis B vaccination to the neonate at birth. Breastfeeding is generally not contraindicated unless the mother is using FDA category D or X medications. The American College of Obstetricians and Gynecologists (ACOG) recommends breastfeeding for mothers with hepatitis C or B, provided that for hepatitis B, breastfeeding is initiated after immunoglobulin administration to the newborn [4].

Contraception should be strongly advised for this patient population, with options including barrier methods, intrauterine devices (IUDs), or permanent sterilization. However, permanent sterilization may be contraindicated due to coagulopathy, and hormonal contraceptives are generally avoided due to the risk of cholestasis (Curtis et al., 2016). In this case, the patient was provided with an IUD for contraception.

Live birth rates in pregnant women with cirrhosis vary between 58% and 100%, while neonatal mortality rates range from 0% to 8.3%, higher than in the general population. Some neonatal deaths are attributed to prematurity and low birth weight. The stillbirth rate is reported between 1% and 8%, and congenital anomalies occur in 0.4–2%, similar to the general population (Aggarwal et al., 2014; Rahim et al., 2021; Puljic et al., 2016; Shaheen & Myers, 2010; Tolunay et al., 2020; Hagström et al., 2018). Among women with cirrhosis, the spontaneous abortion rate is approximately 20% in the first trimester. Patients with non-cirrhotic portal hypertension have a spontaneous abortion rate comparable to the general population (3–6%). Prematurity is common in pregnancies complicated by cirrhosis, with reported rates ranging from 19% to 67%. In this case, the infant was delivered alive, weighing 1900 g, classified as very low birth weight and preterm small-for-gestational-age. The neonate was admitted to the NICU with respiratory distress syndrome.

In this case, the patient had grade IV esophageal varices, indicating large-diameter esophageal veins. Gastric varices are classified according to Mathur: type I involves esophageal varices with lesser curvature varices; type II includes esophageal varices with fundal varices (2a subcardial and 2b diffuse fundal); type III refers to isolated fundal varices (3a secondary to splenic vein thrombosis, 3b secondary to generalized portal hypertension); type IV involves lesser curvature gastric varices with esophageal and fundal varices; and type V includes antral varices [15]

DECLARATIONS

None

CONSENT FOR PUBLICATION

The Authors agree to be published in the Journal of Society Medicine.

FUNDING

None

COMPETING INTERESTS

The authors declare no conflicts of interest in this case report.

AUTHORS’ CONTRIBUTIONS

All authors made substantial contributions to the case report. SRD was responsible for patient management, data collection, and the initial drafting of the manuscript. All authors reviewed and approved the final version of the manuscript, ensuring its accuracy and integrity and being accountable for all aspects of the work.

ACKNOWLEDGMENTS

None

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