2025 PACUPrep BCCCP Preparatory Course Portal Hypertension & Variceal Hemorrhage Diagnostic Evaluation and Risk Stratification in Variceal Hemorrhage
Diagnostic Evaluation and Risk Stratification in Variceal Hemorrhage

Diagnostic Evaluation and Risk Stratification in Variceal Hemorrhage

Objectives Icon A checkmark inside a circle, symbolizing achieved goals.

Learning Objective

Utilize clinical, laboratory, imaging, and hemodynamic data to accurately diagnose portal hypertension, stratify variceal bleeding risk, and guide timely interventions in patients with cirrhosis.

1. Clinical Assessment

Recognize variceal bleeding early through history and physical examination to initiate resuscitation and vasoactive therapy without delay.

Recognition of Acute Bleeding

  • Hematemesis: Vomiting of bright red blood or “coffee-ground” material signifies active or recent upper gastrointestinal bleeding.
  • Melena: The passage of black, tarry stools typically develops 12 to 24 hours after a significant bleed.
  • Hemodynamic Instability: A systolic blood pressure (SBP) below 90 mmHg, heart rate (HR) above 100 bpm, or significant orthostatic changes indicate severe volume loss.

Differential Diagnosis

  • Peptic Ulcer Disease: Often associated with epigastric pain and a history of nonsteroidal anti-inflammatory drug (NSAID) use.
  • Mallory-Weiss Tear: Characterized by linear mucosal lacerations at the gastroesophageal junction following forceful retching or vomiting.
  • Portal Hypertensive Gastropathy: Appears as a mosaic or “snakeskin” mucosal pattern on endoscopy, typically causing slow, chronic oozing rather than acute hemorrhage.

Case Vignette: A 58-year-old with known cirrhosis presents with melena, an SBP of 85 mmHg, and a heart rate of 115 bpm. His hemoglobin is 7.8 g/dL. A variceal bleed should be strongly suspected. Immediate actions include securing the airway if needed, starting octreotide and prophylactic antibiotics, and preparing for endoscopy within 12 hours.

Pearl Icon A shield with an exclamation mark, indicating a clinical pearl. Clinical Pearls
  • In patients with cirrhosis, a drop in hemoglobin greater than 2 g/dL over 24 hours, even without overt hematemesis, suggests occult variceal bleeding.
  • Initiate vasoactive agents (e.g., octreotide, terlipressin) immediately upon clinical suspicion of variceal hemorrhage—do not wait for endoscopic confirmation.

2. Laboratory Investigations

Laboratory studies are crucial to quantify blood loss, assess liver synthetic function, and identify coagulopathy and renal impairment that influence management and prognosis.

Complete Blood Count (CBC)

  • Hemoglobin: A restrictive transfusion strategy is recommended, with a target threshold of hemoglobin < 7 g/dL.
  • Platelets: Thrombocytopenia is common. A count < 50 × 10³/µL increases the risk of procedural bleeding.

Liver Function and Coagulation

  • Bilirubin: A level > 3 mg/dL is a key component of prognostic scores and predicts worse outcomes.
  • Albumin: A level < 3 g/dL signals hepatic decompensation and poor nutritional status.
  • PT/INR: Reflects synthetic failure but is a poor predictor of clinical bleeding risk in cirrhosis.
  • Fibrinogen: A level < 1.0 g/L (100 mg/dL) is a better predictor of bleeding than the INR.

Renal Function & Electrolytes

  • Creatinine/BUN: These are components of the MELD score and are essential for guiding fluid management and detecting hepatorenal syndrome.
  • Sodium: Hyponatremia is a powerful prognostic marker that portends worse outcomes.
Pearl IconA shield with an exclamation mark, indicating a clinical pearl. Clinical Pearls
  • Avoid prophylactic fresh frozen plasma (FFP) transfusion for an elevated INR alone. Instead, correct fibrinogen deficits with cryoprecipitate if levels fall below 1.0 g/L.
  • Viscoelastic testing like thromboelastography (TEG) can provide a more holistic view of coagulation and may help tailor component therapy, but its role remains largely investigational in this setting.

3. Imaging Modalities

Noninvasive imaging confirms the presence of portal hypertension, evaluates vascular anatomy, and may obviate the need for invasive measurements in select patients.

Doppler Ultrasound

This is the initial imaging modality of choice. Key findings supporting portal hypertension include:

  • Portal vein diameter > 13 mm
  • Reduced portal vein flow velocity < 15 cm/s
  • Hepatofugal (reversed) portal vein flow
  • Splenomegaly (> 12 cm in longitudinal axis)
  • Exclusion of portal vein thrombosis as a cause of bleeding

Transient Elastography (TE) and Platelet Count

Liver stiffness measurement (LSM) by TE, combined with platelet count, provides a validated noninvasive method to rule in or rule out clinically significant portal hypertension (CSPH).

Baveno VI Criteria for Diagnosing CSPH
LSM Threshold (kPa) Platelets (×10³/µL) Interpretation
≥ 25 Any Rule-in CSPH
20–25 < 150 Rule-in CSPH
< 15 > 150 Rule-out CSPH

4. Invasive Hemodynamic Measurements

The hepatic venous pressure gradient (HVPG) is the gold standard for quantifying the severity of portal pressure and prognosticating variceal risk, though its use is limited by its invasive nature.

HVPG Technique

  1. A catheter is inserted via the jugular or femoral vein and advanced into a hepatic vein under fluoroscopic guidance.
  2. The free hepatic vein pressure (FHVP) is measured.
  3. A balloon at the catheter tip is inflated to occlude the vein, measuring the wedged hepatic vein pressure (WHVP), which reflects sinusoidal pressure.
  4. The HVPG is calculated as the difference: HVPG = WHVP – FHVP.

Interpretation and Prognostic Value

  • HVPG > 5 mmHg: Defines portal hypertension.
  • HVPG ≥ 10 mmHg: Defines clinically significant portal hypertension (CSPH), the threshold at which varices may develop.
  • HVPG ≥ 12 mmHg: Marks a high risk of variceal bleeding.

A baseline HVPG and its reduction in response to non-selective beta-blocker (NSBB) therapy are strongly correlated with the risk of future clinical decompensation.

Pearl IconA shield with an exclamation mark, indicating a clinical pearl. Clinical Pearl: The Evolving Role of HVPG

While HVPG remains the reference standard, its routine use for risk stratification is declining due to the validation of noninvasive surrogates like transient elastography. Its use is now largely reserved for clinical trials, complex cases, and selected pre-TIPS assessments where precise pressure measurements are critical.

5. Classification and Severity Scoring Systems

Standardized grading and scoring systems are essential to predict bleeding risk and mortality, thereby informing the urgency of intervention and discussions about prognosis.

Endoscopic Variceal Grading

  • Esophageal Varices: Classified by size as small (< 5 mm) or large (> 5 mm).
  • High-Risk Stigmata: The presence of red wale marks or cherry red spots on a varix indicates a very high imminent risk of rupture.
  • Gastric Varices (Sarin Classification): Categorized based on their location relative to the esophagus and cardia (e.g., GOV1, GOV2, IGV1, IGV2).

Child-Pugh (CTP) Score

This score assesses the severity of chronic liver disease based on five clinical and laboratory parameters.

Child-Pugh Score Components
Parameter 1 Point 2 Points 3 Points
Bilirubin (mg/dL)< 22–3> 3
Albumin (g/dL)> 3.52.8–3.5< 2.8
INR< 1.71.7–2.3> 2.3
AscitesNoneMild/ModerateSevere/Refractory
EncephalopathyNoneGrade I–IIGrade III–IV

Scoring: Class A (5–6 points), Class B (7–9 points), Class C (10–15 points).

MELD Score

The Model for End-Stage Liver Disease (MELD) score is a robust predictor of short-term mortality and is used for organ allocation in liver transplantation. The formula is: 3.78 × ln[Bilirubin] + 11.2 × ln[INR] + 9.57 × ln[Creatinine] + 6.43. Scores ≥ 15 denote a poor prognosis.

6. Integrated Risk Stratification Algorithm

A modern approach combines clinical, laboratory, imaging, and endoscopic data to categorize a patient’s bleeding risk and tailor the timing of interventions.

Variceal Hemorrhage Risk Stratification Algorithm A flowchart showing how clinical, lab, and endoscopic findings are used to classify patients into low-risk and high-risk profiles for variceal bleeding, leading to different management pathways such as elective versus urgent intervention. Initial Patient Assessment Clinical signs, Labs (CTP/MELD), Endoscopy, Imaging Low-Risk Profile • Small varices, no red stigmata • CTP Class A, MELD < 15 • HVPG < 10 mmHg (if measured) High-Risk Profile • Large varices OR red stigmata • CTP Class B/C, MELD ≥ 15 • HVPG ≥ 12 mmHg (if measured) Management Elective EVL + NSBB Therapy Management Urgent Endoscopy; Consider Early TIPS
Figure 1: Integrated Risk Stratification. This algorithm demonstrates how patient data is synthesized to determine risk. High-risk patients (large varices, high-risk stigmata, advanced liver disease) require urgent intervention, including consideration for early/preemptive TIPS within 72 hours to reduce rebleeding and mortality.

7. Controversies and Future Directions

The field continues to evolve, balancing noninvasive and invasive diagnostics while exploring novel biomarkers and imaging to refine risk stratification.

Controversy IconA chat bubble with a question mark, indicating a point of controversy or debate. Controversy: Noninvasive vs. Invasive Testing

The primary debate centers on the replacement of the invasive HVPG with noninvasive tests. While transient elastography combined with platelet count is widely adopted for ruling CSPH in or out, HVPG remains the undisputed reference standard for quantifying portal pressure and response to therapy. A key limitation of noninvasive tests is the lack of universal LSM thresholds that apply across all etiologies of liver disease (e.g., viral, alcohol, NAFLD).

Emerging Tools and Future Directions

  • Advanced Imaging: MR elastography offers higher accuracy than TE, especially in obesity, while spleen stiffness measurement is being explored as a complementary marker of portal hypertension.
  • Serum Biomarkers: Markers of endothelial dysfunction, such as von Willebrand factor (VWF) and soluble CD163, are being investigated as potential liquid biopsies for portal hypertension severity.
  • Artificial Intelligence: AI-driven analysis of endoscopic and cross-sectional imaging may soon provide automated, objective risk stratification. The integration of these multimodal noninvasive tests may eventually replace the need for routine HVPG measurement.

References

  1. Kaplan DE et al. AASLD Practice Guidance on risk stratification and management of portal hypertension and varices in cirrhosis. Hepatology. 2024;79(4):1180–1211.
  2. Diaz-Soto MP, Garcia-Tsao G. Management of varices and variceal hemorrhage in liver cirrhosis: a recent update. Ther Adv Gastroenterol. 2022;15:1–12.
  3. Garcia-Tsao G et al. Portal hypertensive bleeding in cirrhosis: risk stratification, diagnosis, and management: AASLD guidance. Hepatology. 2017;65(1):310–335.
  4. Ripoll C et al. Hepatic venous pressure gradient predicts clinical decompensation in compensated cirrhosis. Gastroenterology. 2007;133(2):481–488.
  5. Kamath PS et al. A model to predict survival in patients with end-stage liver disease. Hepatology. 2001;33(2):464–470.
  6. Sterling RK et al. AASLD guidance: noninvasive liver disease assessments of portal hypertension. Hepatology. 2023.
  7. Garcia-Pagan JC et al. Early use of TIPS in cirrhosis with variceal bleeding. N Engl J Med. 2010;362(25):2370–2379.
  8. de Franchis R; Baveno VI Faculty. Expanding consensus in portal hypertension: Baveno VI workshop. J Hepatol. 2015;63(3):743–752.
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