Published online Jul 28, 2026. doi: 10.5528/wjtm.120845
Revised: June 16, 2026
Accepted: July 7, 2026
Published online: July 28, 2026
Processing time: 141 Days and 19.6 Hours
Portal hypertension during pregnancy poses risks for the mother and fetus due to changes in blood flow dynamics, progression of varices, and potential for hepatic failure. Given the limited studies involving pregnant women, current clinical guidelines are largely based on research conducted in non-pregnant populations and from considerable clinical experience. Preconception counseling and early risk assessment are essential, focusing on the severity of liver disease. Ideally, upper gastrointestinal endoscopy should be performed before conception in women with known portal hypertension. If this has not been done, the second trimester is considered the safest time for endoscopy, provided there is a strong clinical reason, minimal sedation is used, and appropriate maternal positioning is maintained. For primary prophylaxis, non-selective beta-blocker (NSBB) is reco
Core Tip: Portal hypertension in pregnancy poses challenges due to physiological changes in blood flow, variceal pro
- Citation: Rajput M, Kumar A. Esophageal varices in pregnancy: Strategies to optimize maternal and fetal outcomes. World J Transl Med 2026; 12(2): 120845
- URL: https://www.wjgnet.com/2220-6132/full/v12/i2/120845.htm
- DOI: https://dx.doi.org/10.5528/wjtm.120845
Portal hypertension in pregnancy poses distinct maternal and fetal risks due to hemodynamics changes, variceal progression, and hepatic decompensation. Owing to limited controlled trials in pregnant women, current guidelines rely mainly on studies in non-pregnant cirrhosis populations and clinical experience[1].
Portal venous pressure is most accurately measured using hepatic venous pressure gradient (HVPG), which is the difference between wedge hepatic pressure and free hepatic pressure and is regarded as the gold standard for assessing portal hypertension[2].
Normal portal pressure ranges from 5 mmHg to 10 mmHg, while portal hypertension is diagnosed when pressure exceeds 10 mmHg. Clinically significant portal hypertension (CSPH), which is associated with a heightened risk of complications like variceal bleeding, is defined by HVPG values greater than 10 mmHg; notably, the risk of bleeding becomes significant once HVPG exceeds 12 mmHg[2]. During pregnancy, non-invasive assessment tools for portal hypertension are preferred for safety reasons. Transient elastography, which measures liver stiffness (LS), is considered safe during pregnancy. Values exceeding 20 kPa indicate the presence of CSPH. When combined with platelet count, as outlined in the Baveno criteria (LS < 20 kPa and platelet count > 150000/μL)[3], it helps identify patients at low risk for variceal bleeding. Although spleen stiffness measurement is less validated in pregnancy, it may provide better predictive value for varices. Doppler ultrasonography (USG) is a safe, non-invasive method that can detect flow reversal and portosystemic collaterals, though its accuracy may depend on the operator’s skill. Magnetic resonance imaging and magnetic resonance elastography may provide additional insights into liver and spleen stiffness[4].
For pregnant women with known or suspected portal hypertension, current guidelines recommend initial evaluation using Doppler USG, transient elastography, and platelet count. If these non-invasive tests are inconclusive, or if there is a clinical suspicion of varices, upper gastrointestinal endoscopy (UGI) may be considered during the second trimester, carefully weighing the diagnostic benefits against the procedural risks[1].
Measurement of HVPG should be avoided unless necessary due to its invasive nature and associated risks during pregnancy[4-6]. The etiology of cirrhosis in pregnancy varies around the world. Viral hepatitis and autoimmune liver disease are the most common causes, while alcoholic cirrhosis is now rare even in developed countries, as per recent studies[7,8].
In developing countries, extrahepatic portal vein obstruction (EHPVO) contributes to non-cirrhotic portal hyper
A literature search was conducted in PubMed, EMBASE, Scopus, and Web of Science from their inception to January 2026. The inclusion criteria comprised guidelines, reviews, original research and case series that addressed prophylaxis and management of variceal bleeding, portal hypertension, and endoscopic interventions in pregnancy as well as the general population. We excluded non-English publications and studies with incomplete data.
We prioritized those from major international and Indian societies, including the American Association for the Study of Liver Diseases (AASLD)[2], European Association for the Study of the Liver (EASL)[3], American Society for Gas
During pregnancy, significant cardiovascular adaptations occur, including a 40%-50% increase in plasma volume, a 30%-50% increase in cardiac output (CO) due to increases in stroke volume and heart rate, and a decrease in systemic vascular resistance (SVR) as a result of the effects of progesterone and the development of the placental vascular bed. These changes can worsen portal hypertension through hyperdynamic circulation, increased splanchnic blood flow, and me
Elevated levels of estrogen and progesterone cause systemic vasodilation and sodium retention. This leads to fluid overload, increased portal venous return, and further dilation of varices[12].
In patients with cirrhosis, the impaired synthetic function (such as low albumin levels and coagulopathy), altered drug metabolism, and portosystemic shunting hinder maternal adaptation to hemodynamic changes. This increases the risk of hepatdecompensation, hepatic encephalopathy, and variceal bleeding[13]. Figure 1 illustrates the physiological changes associated with portal hypertension.
During a normal pregnancy, physiological hemodilution leads to predictable changes in biochemical and hematological parameters. Serum albumin levels decline throughout all trimesters, with a more pronounced decrease as pregnancy progresses. Alkaline phosphatase levels rise in the third trimester, primarily due to placental production and fetal bone development. Similarly, alpha-fetoprotein levels increase as it is produced by the fetal liver. Other liver function tests—including total bile acids, alanine aminotransferase, aspartate aminotransferase (AST), gamma-glutamyl transpeptidase, and bilirubin—generally remain within the normal range during uncomplicated pregnancy[12,14].
However, hemodilution can lower the upper limit of these normal ranges, which should be considered while in
Consequently, elevations in transaminases, bilirubin, fasting total bile acids, or PT above the pregnancy-adjusted normal range are considered abnormal and require evaluation for possible underlying pathology.
It is essential to recognize hemodilution when evaluating hemoglobin, hematocrit, and coagulation parameters, as seemingly “low” values may indicate physiological changes rather than pathology[12]. Transfusion thresholds may need to be individualized due to the risks of fluid overload. Coagulation abnormalities outside the expected pregnancy ranges should prompt targeted correction using blood products such as fresh frozen plasma, cryoprecipitate, or platelets, depending on the specific deficiency. Close multidisciplinary coordination between obstetricians, hepatologists, and hematologists is essential to optimize maternal and fetal outcomes.
Pregnancy outcomes in patients with portal hypertension can vary based on the underlying cause, the severity of liver disease, and the presence of complications.
Cirrhotic Portal Hypertension: This is commonly caused by viral hepatitis, autoimmune hepatitis, or non-alcoholic steatohepatitis. Patients with cirrhotic portal hypertension typically have poor hepatic reserve, an increased risk of bleeding, and worse fetal outcomes[16]. Non-cirrhotic portal hypertension accounts for nearly half of cases in developing countries, primarily due to non-cirrhotic portal fibrosis (NCPF) and EHPVO[17]. NCPF is characterized by a patent spleno-portal axis and an absence of cirrhosis on biopsy. Patients usually present with recurrent hematemesis and massive splenomegaly, but they usually have favorable pregnancy outcomes. EHPVO involves the occlusion of the main portal vein with cavernoma formation, while liver histology remains normal. These conditions are associated with better outcomes[18].
The severity of liver disease plays a crucial role in predicting prognosis: Child-Pugh Score: Class B or higher scores in
These include variceal bleeding, hepatic decompensation, thrombocytopenia or coagulopathy, hepatorenal syndrome, and infections. Table 1 outlines the fetomaternal risks associated with portal hypertension during pregnancy.
| Risk | Mechanism/description |
| Maternal risks | |
| Variceal bleeding | Peak incidence in the 2nd and 3rd trimesters; triggered by increased portal venous flow and intra-abdominal pressure |
| Hepatic decompensation | Higher risk in advanced cirrhosis; manifestations include jaundice, ascites, and hepatic encephalopathy |
| Thrombocytopenia and coagulopathy | Caused by hypersplenism and reduced hepatic synthesis of clotting factors |
| HRS | Rare but potentially fatal; precipitated by fluid shifts, infection, or preeclampsia |
| Infections | Includes SBP and UTIs; risk increased by immune dysregulation |
| PPH | Increased due to varices, coagulopathy, and portal hypertension-related splenic sequestration of platelets |
| Fetal risks | |
| FGR | Due to uteroplacental insufficiency, chronic maternal hypoxia, and hepatic dysfunction |
| Preterm delivery | May result from spontaneous labour or iatrogenic delivery following maternal complications |
| Increased perinatal mortality | Reported rates up to 20% in older studies; currently lower with improved maternal and neonatal care |
Approximately one-third of patients develop new varices during pregnancy, and up to 75% of those with pre-existing varices may experience bleeding at this time[2].
Factors that increase the risk of bleeding include large varices, the presence of endoscopic red signs, a history of variceal bleeding, and undiagnosed or untreated varices[21].
The highest risk for bleeding occurs during the late second to third trimester and during the second stage of labor[22].
Small, straight varices.
Moderate, tortuous varices that occupy less than one-third of the lumen.
Large, coiled varices that occupy more than one-third of the lumen.
High-risk stigmata include cherry red spots, red wale marks, hematocystic spots, and diffuse erythema.
Non-cirrhotic portal hypertension with no varices, Child-Pugh A → routine antenatal care with periodic hepatology reviews.
Small varices, Child-Pugh A/B, no prior bleeding → monthly reviews and consideration for endoscopy.
Child-Pugh B/C, prior gastrointestinal bleeding, ascites → multidisciplinary care, inpatient monitoring, and early delivery planning. Table 2 summarizes predictors of adverse maternal and fetal outcomes.
| Category | Predictor | Implication |
| Maternal | History of variceal bleeding | Strongest predictor of peripartum hemorrhage |
| Maternal | Large esophageal varices | > 30% risk of bleeding in late 2nd or 3rd trimester |
| Maternal | Thrombocytopenia (< 50000/mm³) | Indicates hypersplenism and coagulopathy |
| Maternal | Coagulopathy (INR > 1.5) | Increases hemorrhagic risk during delivery |
| Maternal | Ascites | Marker of hepatic decompensation; predicts poor maternal outcomes |
| Maternal | Hepatic encephalopathy | Sign of end-stage liver disease |
| Maternal | Portal vein thrombosis | May worsen hepatic congestion and complicate delivery |
| Fetal | Maternal cirrhosis | Associated with placental insufficiency, preterm labour, and fetal loss |
| Fetal | Hypoalbuminemia | Indicates poor hepatic reserve and suboptimal nutritional status |
| Fetal | Beta-blocker therapy | Potential for FGR and bradycardia |
| Fetal | Acute variceal bleeding episodes | May cause fetal distress and hypoxia |
| Fetal | Preterm delivery | Often iatrogenic due to maternal decompensation |
Key predictors of bleeding include large varices (greater than 5 mm), the presence of red wale marks, advanced liver disease (Child-Pugh B/C), platelet count less than 100000/mm³, splenomegaly, and previous episodes of variceal bleeding. Non-invasive predictors, such as the AST-to-platelet ratio index (APRI), fibrosis-4 (FIB-4) index, and transient elastography, may be useful for pre-pregnancy risk assessment but have not been validated in pregnancy-specific cohorts[23].
A platelet count of less than 110000/mm³ may indicate the presence of varices with reasonable sensitivity. However, non-invasive tests like FIB-4 can miss up to 25% of small varices, which may enlarge during pregnancy and require treatment. Therefore, AASLD guidelines recommend against using non-invasive tests for variceal screening in pregnancy; upper endoscopy remains the gold standard for evaluating varices in pregnant patients[4].
Women with known cirrhosis or portal hypertension should undergo a preconception endoscopy to evaluate for esophageal varices[4]. Pregnancy-induced physiological changes, such as increased plasma volume, elevated CO, decreased SVR, and increased intra-abdominal pressure, can exacerbate portal pressure and elevate the risk of variceal rupture[24].
The second trimester is particularly high-risk due to the peak in portal pressure and splanchnic blood flow. Women with moderate to large varices may benefit from primary prophylaxis before conception[25]. Optimal management for patients with esophageal varices due to cirrhosis and portal hypertension requires highly individualized care[26]. An overview of guideline recommendations is provided in Table 3.
| Guideline | Key recommendations | Relevance to pregnancy |
| AASLD 2017 | All cirrhotic patients should undergo upper GI endoscopy at diagnosis | Preconception or early pregnancy |
| EASL 2022 | Screening endoscopy in all cirrhotics; repeat every 2-3 years or sooner if decompensated | Encourages evaluation before or early in pregnancy |
| Baveno VII Consensus | Use non-invasive markers (platelets < 150000/mm³ + liver stiffness measurement > 20-25 kPa) to decide need for endoscopy | Limited validation in pregnancy; underutilized |
| WGO 2014 | EVL preferred in high-risk varices; NSBB first line | Safe use of carvedilol or propranolol in selected cases |
Women with cirrhosis or EHPVO should undergo esophagogastroduodenoscopy (EGD) before pregnancy to assess their risk of bleeding, according to AASLD and EASL guidelines. Prophylaxis with non-selective beta-blocker (NSBB) or endoscopic variceal ligation (EVL) should be considered for those with large varices, a history of variceal bleeding, or signs such as red wale marks.
If preconception screening has not been performed, Baveno VII permits the use of non-invasive tools like LS mea
No guidelines recommend routine repeat endoscopy later in pregnancy unless clinically indicated. Indications for repeat endoscopy include symptoms such as hematemesis or melena, signs of decompensated liver disease (e.g., ascites, encephalopathy), and significant drop in hemoglobin or platelet counts.
The primary fetal risk during endoscopic procedures in pregnancy stems from maternal hypoxia or hypotension. While sedative and analgesic agents can cross the placenta, the most commonly used medications—such as a single low dose of midazolam, propofol, and short-acting opioids—have not consistently demonstrated teratogenic effects. There is no evidence that in utero human exposure to anesthetic or sedative drugs has any effect on the developing fetal brain, and there are no animal data to support such an effect with limited exposures of less than 3 hours’ duration. Nevertheless, data on this subject are limited, and the risk-benefit ratio should be carefully evaluated on a case-by-case basis[27]. The fetal heartbeat should be assessed before sedation and again after the endoscopic procedure.
When endoscopy can be postponed, the second trimester is generally preferred because it poses a lower risk of teratogenesis than the first trimester and reduces the likelihood of triggering preterm labor compared to the third trimester[27]. However, in urgent situations, such as variceal bleeding, the procedure should not be delayed, as stabilizing the mother takes precedence over fetal concerns[28].
In a multicenter retrospective study of 83 pregnant women concerning the safety and clinical efficacy of EGD in pregnant patients, indications for endoscopy included UGI bleeding, abdominal pain and vomiting. The diagnostic yield for UGI bleeding was 95% and there were no patients who had premature labor or congenital fetal malformation[29].
Although adverse pregnancy outcomes related to GI endoscopy seem to be extremely rare, gastroenterologists should take a methodical approach during preprocedural, procedural, and postprocedural management for GI endoscopy in the pregnant patient and require careful risk-benefit assessments and informed consent[9]. Emphasizing the ethical principle of maternal primacy, which prioritizes optimizing maternal health, often provides the best chance for fetal survival. Patients should receive clear and comprehensive information regarding the risks of the procedure, available alternatives, and existing uncertainties[30]. Shared decision-making is crucial; it should incorporate the mother’s preferences, fetal considerations, and input from a multidisciplinary team that includes specialists in hepatology, obstetrics, anesthesiology, and neonatology. Endoscopy is contraindicated in placental abruption, imminent delivery, ruptured membranes, or uncontrolled eclampsia.
The measurement of the HVPG is considered the gold standard for diagnosing CSPH. However, this method is invasive, costly, operator-dependent, and not widely available, which limits its practical use—especially during pregnancy. As a result, non-invasive diagnostic modalities for portal hypertension and CSPH are increasingly relevant in clinical practice. Clinically, signs such as spider veins, splenomegaly (enlarged spleen), and visible abdominal portosystemic collaterals can suggest the presence of CSPH. Imaging that shows portosystemic collaterals or a reversal of portal venous flow is considered diagnostic, although their absence does not rule out the condition.
LS measurement using transient elastography (FibroScan) has become a reliable non-invasive alternative. An LS value of less than 15 kPa, combined with a platelet count greater than 150000/µL, can confidently rule out CSPH. Conversely, an LS value greater than 25 kPa, or an LS value between 20-25 kPa with platelets less than 150000/µL, can rule in CSPH with high specificity. Advanced techniques, such as two-dimensional shear wave elastography, show promising diagnostic accuracy, though the lack of standardized cutoff values currently limits their clinical use.
Spleen stiffness measurement (SSM) is another valuable tool, demonstrating a strong correlation with esophageal varices and CSPH. An SSM reading less than 21 kPa effectively rules out CSPH, while values greater than 50 kPa indicate its presence. Notably, SSM offers additional diagnostic advantages when LS is in the intermediate range of 15-20 kPa. A platelet count below 100000/µL is also strongly associated with CSPH, although a normal count does not exclude it.
Several serum-based indices, such as the APRI, FIB-4 score, and FibroTest, provide additional non-invasive insights, but they lack specificity for portal hypertension. Emerging artificial intelligence -based tools represent a promising frontier, utilizing models derived from platelet count, portal vein diameter, and splenic width to predict esophageal varices. Some even use computational fluid dynamics from computed tomography -based three dimensional portal vein reconstructions to generate estimates of “virtual HVPG”. These innovative techniques require further validation before becoming standard clinical practice[31]. In summary, while HVPG remains the reference standard for diagnosis, liver stiffness measurement and platelet count are the most practical and accessible non-invasive surrogates for CSPH in routine clinical settings.
This condition is more prevalent in developing countries. Portal hypertension can occur without the presence of cirrhosis. Although liver function may be preserved, there is often a higher burden of varices[32]. EVL is the preferred treatment for this condition.
This condition is often linked to autoimmune disorders and thrombophilias. The surveillance guidelines for non-cirrhotic portal hypertension are similar to those for cirrhosis; however, the long-term risk of bleeding is generally lower[17].
Worsening portal hypertension may occur due to increased circulating blood volume and the direct compression of the gravid uterus on the inferior vena cava, which can impair venous return. Consequently, variceal bleeding most co
In settings where endoscopy is not available, management strategies must be tailored to the available infrastructure and resources. In such contexts, empirical use of NSBB is recommended for patients with cirrhosis and CSPH to provide primary prophylaxis against variceal bleeding[4,6]. For secondary prophylaxis following an initial variceal bleed, the combination of NSBB and EVL is ideal. However, when endoscopic intervention is not accessible, long-term NSBB monotherapy remains a practical alternative.
In cases of active variceal bleeding where UGI is unavailable, vasoactive agents such as terlipressin or octreotide should be administered promptly. If the bleeding remains uncontrolled, balloon tamponade (e.g., Sengstaken-Blakemore tube) can serve as a temporary, life-saving measure until transfer to a higher-level facility for definitive management is possible. Sclerotherapy has a limited but critical role during pregnancy, serving mainly as a last-resort option. Fur
For small varices, guidelines recommend initiating NSBBs, such as propranolol, in patients who have red wale marks or have Child-Pugh class B or C cirrhosis. The AASLD[4] recommends using NSBBs for primary prophylaxis in non-pregnant patients with medium to large varices. In pregnant patients, propranolol can be continued if it was already prescribed, but regular fetal monitoring is necessary.
As per Baveno VII Consensus (2022)[6] UGI endoscopy is advised before or early in pregnancy for women with cirr
Propranolol is the most commonly used NSBB during pregnancy. It helps reduce portal pressure by decreasing cardiac output and promoting splanchnic vasodilation. Previous studies indicate that NSBBs may lower the rates of variceal bleeding during pregnancy[37]. NSBBs were well tolerated, with no significant effect on fetal outcomes, birth weight, or intrauterine growth restriction[38]. A study conducted by Aggarwal et al[1] involving 62 pregnancies in women with cirrhosis showed that the use of NSBBs was associated with a reduced risk of bleeding without increasing perinatal mortality or the occurrence of congenital anomalies. As there is a probable risk of hypoglycemia and bradycardia in neonates following in utero exposure to beta-blockers (less commonly with propranolol and metoprolol), monitoring of blood glucose levels and heart rate is recommended in beta-blocker-exposed neonates for up to 24 hours after birth, irrespective of the type of beta-blocker used. The dose is typically initiated at a low level and gradually titrated upward to the maximum tolerated dose or until a target heart rate of 50-55 beats per minute is achieved.
EVL is a safe and effective method for both primary and secondary prophylaxis, particularly during the second trimester. This approach avoids systemic drug exposure, making it ideal for women who cannot tolerate NSBBs or have contraindications to their use.
Combining EVL with NSBBs provides enhanced protection for women with a history of variceal bleeding. A meta-analysis by de Franchis and Baveno VI Faculty[3] reviewed three randomized controlled trials and concluded that combined therapy offers the best long-term outcomes, although more pregnancy-specific trials are needed[3,39]. In summary, NSBBs, particularly propranolol, are the preferred first-line treatment for primary prophylaxis. EVL is a suitable alternative when NSBBs are contraindicated or not tolerated. Additionally, the second trimester is generally considered the safest period for elective endoscopy during pregnancy.
AASLD and EASL guidelines support early UGI endoscopy in high-risk patients. The ASGE and the BSG recommend performing endoscopy in the early second trimester. The second trimester spans from 13 weeks to 28 weeks, with the ideal timeframe for procedures being between 13 weeks and 20 weeks. During this period, organogenesis is complete, and the risk of preterm labor is minimal. Additionally, the risk of procedure-related hypotension is lower before 20 weeks. Endoscopy should ideally be carried out preconception to evaluate and manage varices in women with known portal hypertension. If endoscopy has not been performed before pregnancy, the ASGE advises that the procedure should only be undertaken for strong clinical indications, preferably during the second trimester. Minimal sedation should be used, and appropriate maternal positioning should be implemented to avoid aortocaval compression. Table 4 presents a comparative summary of guideline recommendations on esophageal varices in pregnancy.
| Guideline | Timing of endoscopy | Primary prophylaxis (NSBB vs EVL) |
| AASLD (2023) | Preconception; if not done, perform in the second trimester for high-risk cases | Recommends NSBB for small varices with high-risk features. For medium to large varices, either NSBB or EVL may be used. EVL preferred if NSBB contraindicated or not tolerated |
| EASL (2022) | Not specified | Both NSBB and EVL are first-line options. NSBB preferred as they improve long-term outcomes (reduce ascites, decompensation, and mortality) compared with EVL |
| Baveno VII (2022) | Does not specify timing in pregnancy | NSBB preferred in all patients with CSPH irrespective of variceal size; EVL only if NSBB contraindicated or not tolerated |
| ASGE (2021) | Second trimester preferred for safety of endoscopy | Not specified |
| BSGE (2021) | Second trimester preferred | Not specified |
| INASL (2019) | Not specified | Small high-risk varices: NSBB prophylaxis. Medium/Large varices: NSBB or EVL can be used |
Known cirrhosis or portal hypertension without prior endoscopic screening. History of variceal bleeding. Advanced liver disease (Child-Pugh class B or C). Clinical or radiological evidence of CSPH — such as splenomegaly, thrombocytopenia, ascites, or significant collateral circulation.
When screening is necessary, the second trimester represents the safest period for elective endoscopy. However, in emergency situations (e.g., variceal bleeding), maternal stabilization and urgent endoscopic intervention should take priority, regardless of gestational age. On endoscopy, if no varices are detected, only surveillance is required. For small varices without high-risk features, either surveillance or non-selective NSBB may be used if clinically CSPH is confirmed. Small varices with high-risk features should be treated with NSBB. In medium to large varices, NSBB are preferred, while EVL is reserved for patients who cannot tolerate or have contraindications to NSBB.
According to the AASLD guidelines[4], the initial management of acute variceal bleeding involves prompt hemodynamic stabilization, early initiation of vasoactive drugs in combination with prophylactic antibiotics, and urgent EVL. The Baveno consensus[6] similarly recommends that vasoactive agents be started immediately, before endoscopy, with the endoscopic intervention performed within 12 hours of presentation.
The EASL guidelines[5] emphasize the safety and efficacy of EVL as the preferred modality during pregnancy. In cases of refractory bleeding that do not respond to standard therapy, a trans-jugular intrahepatic portosystemic shunt (TIPS) may be considered; however, its use during pregnancy should involve a multidisciplinary evaluation.
Step 1 - resuscitation and hemodynamic stabilization: Administer intravenous fluids (crystalloids) and packed red blood cells to restore volume. The target hemoglobin level should be 7-8 g/dL, as higher levels can worsen portal hypertension[6]. A study by Villanueva et al[40] demonstrated that a restrictive transfusion strategy (Hb around 7 g/dL) reduces rebleeding and mortality in non-pregnant patients. This principle should be applied cautiously in pregnancy, with continuous fetal monitoring. Insert large-bore IV lines, initiate oxygen therapy, keep the patient fasting, and monitor vital signs and urine output. Fetal monitoring is critical throughout gestation in viable pregnancies.
Step 2 - therapy for acute variceal bleeding in pregnancy: Octreotide: Administer an initial bolus of 50 μg IV, followed by a continuous infusion of 25-50 μg/hour for 2-5 days. Octreotide induces splanchnic vasoconstriction, reducing portal pressure, and is preferred due to no known teratogenicity or uterine vasoconstriction. Animal studies and case reports suggest it is safe for use in pregnant patients[41]. Terlipressin induces V1 receptor vasoconstriction to reduce portal flow but is contraindicated as it has been associated with fetal hypoxia and stillbirth. There is no role for tranexamic acid in the management of acute variceal bleeding. Antibiotic prophylaxis: Infection can complicate up to 30% of acute variceal bleeding (AVB) cases and increase mortality. The recommended regimen is ceftriaxone 1 g IV every 12 hours for 7 days. Alternatives include ampicillin-sulbactam or cefotaxime. Both AASLD and Baveno VII guidelines recommend empiric antibiotics for all AVB patients, including pregnant women, to reduce the risk of spontaneous bacterial peritonitis and rebleeding.
Step 3 - urgent endoscopic intervention: Timing: Intervention should occur within 12 hours after stabilization. Sclerotherapy is avoided due to systemic effects and safety concerns for the fetus. EVL is considered the standard of care in pregnancy when expertise is available. Anesthetic considerations include the use of conscious sedation with minimal midazolam or fentanyl; avoid propofol in unstable patients. Position the patient in a lateral decubitus position to prevent vena cava compression.
Step 4 - management of refractory cases and rescue therapies: (1) Balloon tamponade: This temporary measure utilizes the Sengstaken-Blakemore tube if EVL fails. It carries a risk of aspiration and requires intensive care unit care with immediate endoscopic backup. Its use in pregnancy is supported only by case reports and is intended as a bridge to definitive therapy such as TIPS[42]; (2) TIPS: This option should be considered in cases of persistent or recurrent bleeding after pharmacotherapy and EVL. It involves deliberate radiation exposure and should only be used if the benefits outweigh the risks. TIPS can be safely performed during pregnancy with proper shielding, and no fetal harm has been reported[43]. However, it requires a multidisciplinary team, fluoroscopy shielding, and tertiary care expertise; and (3) Role of endoscopic sclerotherapy (EST) in pregnancy: EST involves the injection of sclerosants—such as ethanolamine oleate, polidocanol, or sodium tetradecyl sulfate—into or around esophageal varices. This procedure induces thrombosis and fibrosis. However, EST is not recommended for routine prophylaxis during pregnancy and is generally less preferred than EVL due to higher complication rates, including esophageal ulceration, stricture formation, and rebleeding.
The fetal risks associated with EST are primarily indirect. These risks arise from maternal conditions such as hypoxemia, anesthesia, or hemodynamic instability, rather than from direct toxicity of the sclerosants. Therefore, sclerotherapy has a limited but critical role during pregnancy, serving mainly as a last-resort option.
Step 5 - obstetric considerations and delivery planning: AVB is not an indication for immediate delivery unless the gestational age is greater than 37 weeks, there is ongoing bleeding, fetal distress, or fetal demise. Vaginal delivery is preferred if there are no obstetric contraindications. Administer antenatal corticosteroids if delivery is anticipated before 34 weeks.
Delivery planning for women with portal hypertension and esophageal varices: Planning for delivery in women with portal hypertension and esophageal varices requires a multidisciplinary approach. This plan should take into account the mother’s liver condition, obstetric indications, and the well-being of the fetus. Timing of Delivery: Elective delivery between 37-39 weeks is recommended for stable women with well-compensated liver function and controlled varices. Earlier delivery (between 34-36 weeks) may be necessary in the following situations: Hepatic decompensation (e.g., ascites, encephalopathy); persistent or recent variceal bleeding.
Emergency delivery Indications: Refractory variceal bleeding near term; severe hepatic failure; fetal distress or demise. Aggarwal et al[1] reported that term delivery (at 37-38 weeks) was well tolerated by patients with compensated portal hypertension. However, earlier delivery may be required for those with a history of bleeding or fetal growth restriction.
Vaginal delivery is preferred in most cases. It is essential to avoid the Valsalva maneuver; using epidural analgesia can help reduce intra-abdominal pressure. Assisted second-stage delivery (using vacuum or forceps) can shorten the expulsive phase. Active management of the third stage of labor is recommended. Careful monitoring and management of postpartum hemorrhage are crucial. A senior obstetrician should supervise the delivery.
Vaginal delivery is considered safe for women with controlled varices and stable portal pressures. However, pregnancies complicated by portal hypertension carry a high risk of fetomaternal morbidity and mortality, warranting a referral to tertiary care centers[44].
A cesarean section is indicated for uncontrolled variceal bleeding near term or in cases of massive splenomegaly. Risks associated with cesarean delivery include increased blood loss due to thrombocytopenia or coagulopathy, and the potential for postoperative hepatic decompensation[45]. A vascular surgeon may be required to manage bleeding from ectopic varices during the operation.
Monitor patients for any delayed variceal bleeding, especially considering the hemodynamic shifts that can occur after delivery. If non-selective beta-blockers were temporarily stopped during labor, they should be resumed after childbirth. Avoid the use of NSAIDs due to the risk of renal or hepatic injury. Continue endoscopic surveillance 3 months to 6 months postpartum[46].
The safety of drugs used in the context of portal hypertension during lactation remains largely unstudied, although existing evidence suggests varying degrees of compatibility. Propranolol is the best-studied medication and is considered compatible with breastfeeding. Carvedilol appears acceptable with caution, given its likely low milk transfer, but there is limited human data. Octreotide has documented milk transfer, and its use during lactation should be avoided if possible. Terlipressin is contraindicated due to the lack of safety data and the potential for serious adverse effects in infants. Comprehensive contraceptive counseling is essential for women with cirrhosis or portal hypertension, as hormonal and surgical methods can carry unique risks. According to the World Health Organization Medical Eligibility Criteria for Contraceptive Use, 5th Edition (2015)[47], the appropriateness of contraceptive methods varies based on the severity of hepatic disease and the presence of varices, as summarized in Table 5.
| Method | WHO MEC category (compensated liver disease) | WHO MEC category (decompensated cirrhosis/portal hypertension with varices) | Key recommendations |
| Barrier method | 1 | 1 | Less effective alone; encourage for dual protection |
| Combined oral contraceptives | 3 | 4 | Avoid due to estrogenic effects; may worsen cholestasis and increase thrombosis risk |
| Injectable medroxyprogesterone acetate | 2 | 3 | Effective, but caution due to risk of bone loss; osteoporosis is common in cirrhosis |
| Progestin implant/LNG-IUS | 1 | 2 | Highly effective; preferred long-acting reversible options |
| Copper IUCD | 1 | 2-3 (if severe anemia) | Acceptable if anemia is controlled; monitor for bleeding |
| Female sterilization | 1 (if medically fit) | 2-3 | Surgical risk increased by collaterals and coagulopathy; laparotomy may be safer than laparoscopy |
Most available evidence on portal hypertension and variceal management during pregnancy originates from retro
During pregnancy the presence of splenomegaly and thrombocytopenia should prompt an abdominal ultrasound to confirm the diagnosis of portal hypertension. Pregnancy complicated by portal hypertension poses significant risks for both maternal and fetal morbidity and mortality, making it necessary to refer affected patients to specialized tertiary care centers. Regular monitoring for esophageal varices is essential. Although specific guidelines for managing portal hypertension during pregnancy are limited, recommendations from hepatology consensus bodies, such as the AASLD, EASL, and Baveno VII, suggest conducting an UGI endoscopy pre-pregnancy or in the early second trimester, im
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