Esophageal varices: nursing assessment, management, and NCLEX review

Esophageal varices are dilated submucosal veins in the distal esophagus that develop when portal hypertension forces blood through portosystemic collateral pathways. Approximately 30% to 40% of patients with compensated cirrhosis have varices at diagnosis, and without prophylaxis, 25% to 30% of those with medium or large varices will experience a hemorrhagic episode within two years. Each bleeding episode carries a 15% to 25% mortality rate, with 6-week mortality reaching 10% to 20% depending on disease severity. This makes variceal hemorrhage one of the most lethal GI emergencies a nurse will manage. Recognizing the early hemodynamic signs, understanding pharmacologic and endoscopic interventions, and knowing what to prioritize during an active bleed are essential competencies tested on the NCLEX and used daily in ICU, med-surg, and hepatology settings.

Pathophysiology: portal hypertension and variceal formation

Esophageal varices develop through a predictable hemodynamic sequence that begins with increased resistance to portal blood flow and ends with rupture of thin-walled collateral vessels. Understanding this pathway connects directly to the rationale behind every treatment intervention.

Increased intrahepatic resistance. In cirrhosis, fibrotic remodeling and regenerative nodules compress the hepatic sinusoids and increase resistance to portal blood flow. This structural component accounts for approximately 70% of the increased portal pressure. The remaining 30% comes from a functional component — increased intrahepatic vascular tone driven by endothelin-1 overproduction and reduced nitric oxide availability within the liver.

Splanchnic vasodilation. As portal pressure rises, the splanchnic (mesenteric) vascular bed responds by overproducing vasodilators — primarily nitric oxide, prostaglandins, and glucagon. This progressive splanchnic arterial vasodilation increases blood flow into the portal system, further raising portal pressure. The result is a self-amplifying cycle: higher portal pressure causes more vasodilation, which drives more blood into an already congested portal system.

Portosystemic collateral formation. When the hepatic venous pressure gradient (HVPG) exceeds 10 mmHg — defined as clinically significant portal hypertension (CSPH) — blood seeks alternative pathways back to systemic circulation. The most clinically important collaterals form at the gastroesophageal junction, where the left gastric (coronary) vein connects with the esophageal venous plexus draining into the azygos system. These dilated submucosal veins in the distal esophagus are esophageal varices.

Variceal wall tension and rupture. The risk of variceal rupture depends on wall tension, governed by LaPlace’s law: wall tension = (transmural pressure x variceal radius) / wall thickness. As portal pressure increases (raising transmural pressure), varices enlarge (increasing radius), and the vessel wall thins. When wall tension exceeds the elastic limit of the vessel, rupture occurs. This is why bleeding risk correlates with variceal size and HVPG — specifically, varices rarely bleed when HVPG is below 12 mmHg.

Grading and classification

Endoscopy is the gold standard for identifying and grading esophageal varices. The two most widely used classification systems are the Japanese Research Society for Portal Hypertension grading (F1 through F3) and the simplified North Italian Endoscopic Club (NIEC) system (small vs. large). In clinical practice and AASLD/Baveno VII guidelines, the small versus large distinction is most commonly referenced.

Small varices (F1). Straight veins that minimally protrude into the esophageal lumen. These flatten with insufflation during endoscopy. Annual bleeding risk is approximately 5% per year.

Medium varices (F2). Tortuous, slightly enlarged veins occupying less than one-third of the esophageal lumen. They do not flatten with insufflation. Presence of red wale signs elevates bleeding risk significantly.

Large varices (F3). Coiling veins that occupy more than one-third of the esophageal lumen. Annual first-bleed risk is approximately 15% per year. These require primary prophylaxis regardless of other factors.

Red wale signs

Red wale markings are the most important endoscopic risk markers for impending hemorrhage. These appear as longitudinal red streaks on the variceal surface representing microtelangiectasias in the variceal wall. Additional high-risk endoscopic features include cherry red spots (small, discrete red dots), hematocystic spots (blood-filled blisters — the highest-risk finding), and diffuse mucosal redness over the varix. The combination of large variceal size plus red wale signs in a Child-Pugh C patient represents the highest bleeding risk category.

Screening recommendations

Per Baveno VII consensus, patients with compensated advanced chronic liver disease (cACLD) who have liver stiffness below 20 kPa and platelet count above 150,000/microL have a very low risk of high-risk varices and can avoid screening endoscopy. These patients are monitored with annual transient elastography and platelet counts instead. All other patients with cirrhosis require screening upper endoscopy, repeated every two to three years for compensated disease and annually for decompensated disease.

Nursing assessment

Assessment priorities for a patient with known or suspected esophageal varices depend on whether the patient is stable (surveillance phase) or actively bleeding.

Stable patient assessment

For patients with known varices who are not bleeding, nursing assessment focuses on identifying risk factors for decompensation and monitoring for early signs of hemorrhage:

• History: Etiology of liver disease (alcohol, hepatitis B or C, NAFLD), prior variceal bleeding episodes, current medications (beta-blocker adherence, NSAIDs — which increase bleeding risk), alcohol use status
• Hepatic function indicators: Ascites presence and severity, hepatic encephalopathy grade, jaundice, Spider angiomata — these contribute to Child-Pugh scoring (A, B, or C) which directly predicts bleeding risk and mortality
• Baseline labs: Platelets (thrombocytopenia below 150,000 suggests portal hypertension), INR (coagulopathy), albumin (synthetic function), creatinine (renal function — relevant for hepatorenal syndrome risk), hemoglobin baseline
• MELD score awareness: The Model for End-Stage Liver Disease uses bilirubin, INR, and creatinine to predict 90-day mortality. A MELD score above 18 significantly increases post-bleed mortality

Active bleeding assessment

When a patient with esophageal varices presents with hematemesis (bright red or coffee-ground emesis) or melena, the assessment shifts to rapid hemodynamic evaluation:

• Airway first. Massive upper GI hemorrhage carries a high aspiration risk. Assess level of consciousness, gag reflex, and airway patency. Patients with altered mental status (from hepatic encephalopathy or hemorrhagic shock) or massive hematemesis often require emergent intubation before any other intervention.
• Hemodynamic status. Heart rate (tachycardia above 100 bpm is often the earliest sign), blood pressure (systolic below 90 mmHg indicates class III or IV shock), mean arterial pressure (target above 65 mmHg), orthostatic vital signs if the patient can sit safely, capillary refill, and skin color/temperature.
• Hemorrhage volume estimation. Serial hemoglobin and hematocrit (note: initial values may be falsely normal in acute hemorrhage before equilibration), urine output (goal above 0.5 mL/kg/hr), and lactate level.
• Two large-bore IVs (16-gauge or larger) immediately. Send type and crossmatch, CBC, CMP, coagulation studies, and lactate with the initial draw.

Primary prophylaxis

Primary prophylaxis aims to prevent the first variceal bleed in patients with medium or large varices. The Baveno VII consensus (2021) and AASLD practice guidance both recommend two first-line options.

Non-selective beta-blockers

NSBBs reduce portal pressure by decreasing cardiac output (beta-1 blockade) and causing splanchnic vasoconstriction (beta-2 blockade). They reduce first-bleed risk from approximately 25% to 15% over two years.

• Carvedilol (6.25 mg daily, may titrate to 12.5 mg daily) is the preferred NSBB per Baveno VII due to its additional alpha-1 blocking activity, which reduces intrahepatic vascular resistance. Carvedilol produces a greater reduction in HVPG than propranolol or nadolol. Baveno VII recommends carvedilol for all compensated patients with clinically significant portal hypertension.
• Propranolol (20 mg twice daily, titrated to a resting heart rate of 55 to 60 bpm, maximum 320 mg/day) remains an alternative.
• Nadolol (40 mg daily, titrated similarly to heart rate target) is used when propranolol is not tolerated.

Nursing considerations for NSBB therapy: Monitor heart rate (hold if below 55 bpm), blood pressure (hold if systolic below 90 mmHg or MAP below 65 mmHg), and for signs of bronchospasm in patients with reactive airway disease. NSBBs are contraindicated in refractory ascites with severe hypotension, as they may worsen renal perfusion — this is the so-called “NSBB window” where beta-blockers help portal hypertension but harm systemic hemodynamics.

Endoscopic variceal ligation

EVL (banding) is recommended for patients with medium or large varices who have contraindications or intolerance to NSBBs. Bands are placed on the varices to necrose and obliterate them. Sessions are repeated every 2 to 4 weeks until variceal eradication, then surveillance endoscopy every 3 to 6 months. Post-banding, patients receive a proton pump inhibitor (such as lansoprazole 30 mg daily) until varices are obliterated to reduce band ulcer complications.

Acute variceal hemorrhage management

Acute variceal bleeding is a medical emergency requiring simultaneous resuscitation, pharmacotherapy, and endoscopic intervention. The sequence below reflects current AASLD and Baveno VII guidance.

Step 1: Airway and hemodynamic stabilization

Airway protection is the first priority. Patients with massive hematemesis, altered mental status, or hemodynamic instability should be intubated before endoscopy. Establish two large-bore peripheral IVs and begin crystalloid resuscitation. Blood transfusion follows a restrictive threshold — target hemoglobin of 7 g/dL, transfusing only to 7 to 9 g/dL. Over-transfusion raises portal pressure and increases rebleeding risk. Avoid aggressive volume resuscitation for the same reason.

Step 2: Vasoactive drug therapy

Vasoactive agents should be started as soon as variceal hemorrhage is suspected — before endoscopy, before lab confirmation, and ideally in the emergency department.

• Octreotide (most commonly used in the United States): 50 mcg IV bolus followed by a continuous infusion of 50 mcg/hr for 2 to 5 days. Octreotide inhibits splanchnic vasodilation and reduces portal blood flow.
• Terlipressin (a vasopressin analog, available internationally and FDA-approved in the US): 2 mg IV every 4 hours for the first 24 to 48 hours, then reduced to 1 mg IV every 4 hours. Terlipressin directly constricts splanchnic arterioles, reducing portal inflow. It is the only vasoactive agent shown to reduce mortality in variceal bleeding. Monitor for ischemic complications (mesenteric, cardiac, peripheral) and hyponatremia.
• Somatostatin (used in some European centers): 250 mcg IV bolus followed by 250 mcg/hr infusion.

Step 3: Prophylactic antibiotics

Antibiotics are started immediately — ideally before endoscopy — because bacterial infections occur in up to 50% of cirrhotic patients with GI bleeding and are an independent predictor of rebleeding and mortality. A 7-day course reduces the incidence of spontaneous bacterial peritonitis, bacteremia, and pneumonia.

• Ceftriaxone 1 g IV every 24 hours is the preferred agent for patients with advanced cirrhosis (Child-Pugh B or C) or in settings with high quinolone resistance.
• Norfloxacin 400 mg orally twice daily (or ciprofloxacin 500 mg IV twice daily for patients who cannot take oral medications) is an alternative for Child-Pugh A patients.

Step 4: Emergent endoscopy with EVL

Upper endoscopy should be performed within 12 hours of presentation. Erythromycin (250 mg IV, given 30 to 120 minutes before endoscopy) improves gastric visualization by promoting gastric emptying. EVL is the endoscopic treatment of choice — it has lower rebleeding rates, fewer complications, and faster variceal eradication than sclerotherapy. Successful hemostasis is achieved in approximately 90% of cases.

NG tube precaution: Nasogastric tube insertion is avoided in patients with known unligated esophageal varices due to the risk of mechanical trauma and hemorrhage provocation. If gastric decompression is required before endoscopy, the decision should be made by the endoscopy or critical care team with full awareness of the variceal status.

Step 5: Rescue therapies for refractory bleeding

Approximately 10% to 20% of variceal hemorrhages are refractory to standard pharmacologic and endoscopic therapy. Rescue options include:

• Balloon tamponade (Sengstaken-Blakemore tube or Minnesota tube). A temporary bridge measure that achieves hemostasis in approximately 90% of cases by direct compression of varices. It is a temporizing measure only — placement is limited to a maximum of 24 hours due to a high complication rate (20% to 60%), including esophageal necrosis, perforation, and aspiration. The patient must be intubated before insertion. Gastric balloon is inflated first (250 to 300 mL air), confirmed by X-ray, then traction is applied. The esophageal balloon is inflated only if gastric balloon tamponade fails. Continuous monitoring of balloon pressures and respiratory status is mandatory.
• Transjugular intrahepatic portosystemic shunt (TIPS). TIPS creates a low-resistance channel between the portal vein and the hepatic vein, decompressing the portal system. Preemptive (early) TIPS — placed within 24 to 72 hours — is recommended for high-risk patients (Child-Pugh B with active bleeding at endoscopy, or Child-Pugh C with a score of 10 to 13) and has been shown to improve survival and reduce treatment failure. Rescue TIPS is used when EVL and pharmacotherapy fail. The primary complication of TIPS is hepatic encephalopathy (occurring in 25% to 45% of patients) and shunt occlusion or stenosis, requiring surveillance Doppler studies.

Secondary prophylaxis

After surviving a first variceal bleed, patients face up to a 70% risk of rebleeding within one year if no secondary prophylaxis is instituted. The standard of care per Baveno VII and AASLD is combination therapy.

EVL plus NSBBs together. Combination therapy is superior to either intervention alone for preventing rebleeding. EVL sessions are repeated every 2 to 4 weeks until variceal eradication, with the first session typically performed 1 to 2 weeks after the acute bleed resolves. NSBBs (propranolol, nadolol, or carvedilol) are initiated as soon as the patient is hemodynamically stable, typically before hospital discharge.

Monitoring. After variceal eradication, surveillance endoscopy is performed every 3 to 6 months for the first year, then every 6 to 12 months. NSBB dosing is titrated to a resting heart rate of 55 to 60 bpm with systolic BP maintained above 90 mmHg. Patients should be evaluated for liver transplant candidacy, which is the definitive treatment for the underlying portal hypertension.

TIPS for secondary prophylaxis. TIPS is reserved for patients who rebleed despite combination EVL plus NSBB therapy. An HVPG reduction below 12 mmHg (or a decrease of more than 20% from baseline) after TIPS is associated with near-complete protection from rebleeding.

NCLEX priorities and clinical decision scenarios

The following decision points reflect the high-yield testing concepts for esophageal varices nursing care.

1. Airway before bleeding control. A patient with massive hematemesis and altered mental status requires intubation before endoscopy or any other intervention. Airway protection is always the first priority — the leading cause of death in the first hours of variceal hemorrhage is aspiration, not exsanguination.

2. Restrictive transfusion in variceal bleeding. The target hemoglobin is 7 g/dL. Transfusing to higher levels raises portal pressure and increases rebleeding risk. If an NCLEX question asks about transfusion threshold in a patient with GI bleeding from varices, the answer is lower than a typical surgical patient.

3. Start vasoactive drugs before endoscopy. Octreotide (or terlipressin) is started on clinical suspicion of variceal hemorrhage — do not wait for endoscopic confirmation. If a question presents a patient with known cirrhosis and hematemesis, the immediate nursing action after airway and IV access is to initiate the vasoactive infusion.

4. Beta-blocker parameters. Hold propranolol, nadolol, or carvedilol if heart rate is below 55 bpm or systolic BP is below 90 mmHg. Report these findings to the provider. NSBBs should never be initiated during an active bleed — they are for prophylaxis only.

5. Sengstaken-Blakemore tube complications. The two most tested complications are esophageal rupture (from over-inflation or prolonged placement beyond 24 hours) and airway obstruction (if the gastric balloon deflates and the tube migrates upward). The patient must be intubated. Scissors must be kept at the bedside to cut and deflate the balloon immediately if airway obstruction occurs.

6. Antibiotics are mandatory in variceal bleeding. Prophylactic antibiotics are given to every cirrhotic patient with GI bleeding — this is a standard of care, not an optional add-on. They reduce mortality, rebleeding, and bacterial peritonitis rates. If a question asks which orders to clarify on a variceal bleed patient, the absence of antibiotic orders should be questioned.

7. TIPS and encephalopathy risk. A patient who underwent TIPS placement should be monitored for new or worsening hepatic encephalopathy. Post-TIPS encephalopathy develops in 25% to 45% of patients. The nursing assessment includes orientation checks, asterixis evaluation, and lactulose/rifaximin administration.

8. Avoid NSAIDs in cirrhotic patients. Non-steroidal anti-inflammatory drugs impair platelet function and increase the risk of variceal and non-variceal bleeding in patients with cirrhosis. Acetaminophen (limited to 2 g/day in cirrhosis) is the preferred analgesic.

Related pages

• Cirrhosis nursing: pathophysiology, complications, and care
• Hepatic encephalopathy nursing reference
• Hepatorenal syndrome nursing reference
• GI bleed nursing reference: assessment and interventions
• Nursing lab values cheat sheet
• Electrolyte imbalances nursing reference