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Ascites

Ascites is a topic covered in the 5-Minute Clinical Consult.

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Basics

Description

  • Accumulation of fluid in the peritoneal cavity; may occur in conditions that cause generalized edema
  • Men generally have no fluid in peritoneal cavity; women may have up to 20 mL depending on menstrual phase.

Epidemiology

  • Children: most commonly associated with nephrotic syndrome and malignancy
  • Adults: cirrhosis (81%), cancer (10%), heart failure (3%), other (6%)

Incidence
~50–60% of cirrhotic patients develop ascites within 10 years (1).

Prevalence
10% of patients with cirrhosis have ascites.

Etiology and Pathophysiology

  • Portal hypertension versus nonportal hypertension causes
    • Cannot reliably establish/confirm etiology without paracentesis
    • Serum-ascites albumin gradient (SAAG): (serum albumin level: ascites albumin level) helps to differentiate causes
  • High portal pressure (SAAG ≥1.1)
    • Cirrhosis
    • Hepatitis (alcoholic, viral, autoimmune, medications)
    • Acute liver failure
    • Liver malignancy (primary or metastatic)
    • Elevated right-sided filling pressures from heart failure or constrictive pericarditis
    • Hepatic venous thrombosis (Budd-Chiari syndrome)
    • Portal vein thrombosis
  • Normal portal pressure (SAAG <1.1)
    • Peritoneal carcinomatosis
    • Tuberculosis
    • Severe hypoalbuminemia (nephrotic syndrome; severe enteropathy with protein loss)
    • Meigs syndrome (ovarian cancer)
    • Lymphatic leak (chylous ascites)
    • Pancreatitis
    • Inflammatory (vasculitis, lupus serositis, sarcoidosis)
    • Other infections (parasitic, fungal)
    • Hemoperitoneum (trauma or ectopic pregnancy)
  • Pathophysiology is best described for portal hypertensive (typically cirrhotic) ascites.
    • Reduced renal and carotid perfusion activates systemic vasoconstrictors and antinatriuretic mechanisms. This stimulates the sympathetic nervous system and renin-angiotensin-aldosterone system to retain sodium and water.
    • Most ascites is due to portal hypertension, with preferentially dilated splanchnic vasculature causing systemic hypotension.

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Citation

Stephens, Mark B., et al., editors. "Ascites." 5-Minute Clinical Consult, 27th ed., Wolters Kluwer, 2019. Medicine Central, im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116056/all/Ascites.
Ascites. In: Stephens MB, Golding J, Baldor RA, et al, eds. 5-Minute Clinical Consult. 27th ed. Wolters Kluwer; 2019. https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116056/all/Ascites. Accessed August 21, 2019.
Ascites. (2019). In Stephens, M. B., Golding, J., Baldor, R. A., & Domino, F. J. (Eds.), 5-Minute Clinical Consult. Available from https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116056/all/Ascites
Ascites [Internet]. In: Stephens MB, Golding J, Baldor RA, Domino FJ, editors. 5-Minute Clinical Consult. Wolters Kluwer; 2019. [cited 2019 August 21]. Available from: https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116056/all/Ascites.
* Article titles in AMA citation format should be in sentence-case
TY - ELEC T1 - Ascites ID - 116056 ED - Stephens,Mark B, ED - Golding,Jeremy, ED - Baldor,Robert A, ED - Domino,Frank J, BT - 5-Minute Clinical Consult, Updating UR - https://im.unboundmedicine.com/medicine/view/5-Minute-Clinical-Consult/116056/all/Ascites PB - Wolters Kluwer ET - 27 DB - Medicine Central DP - Unbound Medicine ER -