Ascites And Liver Disease: Understanding The Fluid Imbalance

Pathophysiology, clinical recognition, management options, complications, and the role of TIPS

Introduction

Ascites—the abnormal accumulation of intraperitoneal fluid—is a frequent consequence of advanced liver disease, most commonly cirrhosis. Recognizing how ascites develops, how it is diagnosed, and how it is treated helps clinicians and patients navigate care and improve outcomes.

Pathophysiology

Portal hypertension from cirrhosis increases splanchnic hydrostatic pressure, while systemic vasodilation and neurohormonal activation (RAAS, SNS, ADH) drive renal sodium and water retention. Reduced oncotic pressure and impaired hepatic handling of fluids further promote peritoneal fluid accumulation.

References: Ginès & Arroyo (1999); Rukunuzzaman (2018).

Clinical Presentation & Diagnosis

Physical Examination

Progressive abdominal distension; shifting dullness; fluid wave; umbilical hernia; peripheral edema in advanced cases.

Imaging & Procedures

Ultrasound confirms fluid and estimates volume; CT for complications or alternative causes. Diagnostic paracentesis assesses cell count, albumin (to calculate SAAG), total protein, and culture to rule out infection.

Reference: Moore & Aithal (2006).

Management & Treatment

Medical Therapy

  • Diet: Sodium restriction (e.g., ~2 g/day).
  • Diuretics: Spironolactone ± furosemide to promote natriuresis and reduce fluid.

Therapeutic Paracentesis

Large-volume paracentesis (e.g., >5 L) relieves tense ascites; albumin infusion reduces circulatory dysfunction risk.

Definitive Therapy

For refractory ascites or end-stage disease, liver transplantation provides the only curative option.

Reference: EASL Guidelines (2018).

Complications

Spontaneous Bacterial Peritonitis (SBP)

Infection of ascitic fluid without evident source; presents with fever, abdominal pain, encephalopathy, or may be subtle. Requires prompt antibiotics and albumin in select patients.

Hepatorenal Syndrome (HRS)

Functional renal failure due to severe circulatory dysfunction. Overdiuresis can contribute; treat precipitating factors and follow protocolized therapy.

Reference: Piano et al. (2018).

Prevention & Future Prospects

Optimize underlying liver disease management, abstain from alcohol, maintain a low-sodium diet, address metabolic risk factors, and ensure vaccinations and early infection control.

Reference: Tsochatzis, Bosch & Burroughs (2014).

Transjugular Intrahepatic Portosystemic Shunt (TIPS) in Ascites

TIPS decompresses the portal system by creating a low-resistance channel between the portal and hepatic veins. It is considered for:

  • Refractory ascites: Unresponsive to maximal diuretics or rapidly recurrent after paracentesis.
  • Recurrent variceal bleeding despite standard therapy.

Candidate considerations: Favorable MELD (often <~15), no advanced cardiopulmonary disease, no uncontrolled infection, and no severe/recurrent encephalopathy. Recognize risks such as post-TIPS hepatic encephalopathy and shunt dysfunction. TIPS frequently serves as a bridge to transplant.

References: Garcia-Tsao & Lim (2009); Boyer & Haskal (2010); Kamath et al. (2001); Sanyal et al. (2006); Riggio et al. (2005).

Conclusion

Ascites is a hallmark of decompensated cirrhosis driven by portal hypertension and sodium retention. Accurate diagnosis, stepwise therapy, attention to complications, and judicious use of TIPS—alongside transplant evaluation—form the backbone of care to improve quality of life and outcomes.

References

  1. Ginès P, Arroyo V. Ascites and hepatorenal syndrome in cirrhosis. Gastroenterol Clin North Am. 1999;28(4):801–818.
  2. Rukunuzzaman M. Pathogenesis of ascites in cirrhosis. Indian J Med Res. 2018;148(6):647–656.
  3. Moore KP, Aithal GP. Guidelines on the management of ascites in cirrhosis. Gut. 2006;55(Suppl 6):vi1–vi12.
  4. European Association for the Study of the Liver (EASL). Decompensated cirrhosis: clinical practice guidelines. J Hepatol. 2018;69(2):406–460.
  5. Piano S, Brocca A, Mareso S, Angeli P. Infections complicating cirrhosis. Liver Int. 2018;38:126–133.
  6. Tsochatzis EA, Bosch J, Burroughs AK. Liver cirrhosis. Lancet. 2014;383(9930):1749–1761.
  7. Garcia-Tsao G, Lim JK. Management of cirrhosis and portal hypertension. Am J Gastroenterol. 2009;104(7):1802–1829.
  8. Boyer TD, Haskal ZJ. Role of TIPS in portal hypertension (update 2009). Hepatology. 2010;51(1):306.
  9. Kamath PS, Wiesner RH, Malinchoc M, et al. Model to predict survival (MELD). Hepatology. 2001;33(2):464–470.
  10. Sanyal AJ, Genning C, Reddy KR, et al. Treatment of refractory ascites: North American study. Gastroenterology. 2006;130(3):657–666.
  11. Riggio O, Efrati C, Catalano C, et al. Portal-systemic shunts and persistent encephalopathy. Hepatology. 2005;42(5):1158–1165.

Note: For online publishing, add DOIs or PubMed links to each citation.

Medical Disclaimer: Educational content only; not a substitute for professional medical advice, diagnosis, or treatment.