The goal of this program is to improve the management of ascites and spontaneous bacterial peritonitis. After hearing and assimilating this program, the clinician will be better able to:
Ascites: refers to the accumulation of fluid within the abdomen; grade 1 is mild and detectable only by ultrasonography, grade 2 involves moderate abdominal distention with positive shifting dullness, and grade 3 is severe gross ascites and fluid thrill; causes include presinusoidal issues below the level of the liver, postsinusoidal issues at the level of the vena cava, and sinusoidal issues (most common type) associated with cirrhosis-induced portal hypertension (PH); the hallmark diagnostic measurement is the hepatic vein pressure gradient (HVPG), defined as the difference between hepatic vein wedge pressure and free hepatic vein pressure; normal is 1 to 5 mm Hg; >5 mm Hg is PH; >12 mm Hg is clinically significant PH; patients with pre- or postsinusoidal ascites typically have normal HVPG, while those with sinusoidal ascites exhibit elevated HVPG; in cirrhosis, PH and splanchnic vasodilation contribute to the development of ascites; mechanism — arterial underfilling, driven by PH and splanchnic vasodilation, contributes to ascites in the early phase; arterial overflow (common in late phase and hypervolemic patients) stimulates various systems, including the renin-angiotensin system and antidiuretic hormone axis, promoting fluid retention and ascites formation
Key indicators and clinical implications of ascites: ascites is a common sign of decompensated liver disease and should prompt paracentesis for fluid analysis; serum-ascites albumin gradient (SAAG) is crucial; a SAAG ≥1.1 g/dL indicates transudative ascites, often liver- or heart-related; ascitic fluid total protein (TP) <2.5 g/dL suggests PH-related ascites; cardiac ascites is indicated by TP >2.5 g/dL and SAAG ≥1.1 g/dL; antibiotic prophylaxis for spontaneous bacterial peritonitis is recommended for patients with SAAG ≥1.1 g/dL and TP <1.5 g/dL; consider nephrogenic or serous ascites for SAAG <1.1 g/dL and TP <2.5 g/dL; SAAG <1.1 g/dL and TP ≥2.5 indicates exudative ascites, primarily related to tuberculosis, peritoneal carcinomatosis, pancreatitis, and other infections; for the first paracentesis, analyze ascitic fluid albumin, total albumin, and cell count; consider amylase and triglyceride levels if pancreatic fluid or chylous ascites is suspected; cytology is usually unhelpful
Compensated cirrhosis: development of ascites is associated with decreased survival; subtle sodium retention occurs, progressing with worsening PH to cause responsive ascites; with further advancement, avid sodium retention leads to refractory ascites and dilutional hyponatremia, culminating in functional renal failure; patients presenting with acute kidney injury (AKI) without ascites likely do not have hepatorenal syndrome; patients with hepatorenal syndrome typically have refractory ascites and hypotension
Management of ascites: involves sodium restriction and diuretic therapy, with large volume paracentesis (LVP) if symptoms are uncontrolled; liver transplantation (LT) is recommended for patients with ascites as their first complication regardless of alcohol consumption; sodium intake should ideally be limited to 78 mmol/day; aim for urinary sodium excretion >78 mmol/day; only 10% to 15% of patients achieve spontaneous natriuresis; a urine sodium-to-potassium ratio >1 without fluid weight loss suggests dietary noncompliance; a ratio <1 suggests need for increased diuretics; a single morning dose of oral spironolactone (SPL) 100 mg and furosemide (FRS) 40 mg is a typical starting dose; dose adjustments should be made using the same ratio every 3 to 5 days; usual maximum doses are 400 mg for SPL and 160 mg for FRS per day; ≈90% of patients respond to this combination therapy; common side effects of diuretics include dehydration, hyper- or hypokalemia, hyponatremia, alkalosis, hepatic encephalopathy (HE), AKI, orthostatic hypotension, leg cramps, gynecomastia, and ototoxicity
Refractory ascites: occurs in 10% of patients; defined as fluid overload nonresponsive to sodium restriction and high-dose diuretics; can be diuretic-resistant (ascites persists at maximum doses of SPL and FRS) or diuretic-intractable (side effects develop with every increase of diuretics); first step in treatment is LVP and albumin; for minimal liver dysfunction (Model for End-Stage Liver Disease [MELD] score <18), consider transjugular intrahepatic portosystemic shunt (TIPS) and referral for LT; TIPS can be a bridge to LT; medical options include 7.5 mg midodrine 2 to 3 times daily; angiotensin-converting enzyme inhibitors, angiotensin 2 receptor blockers, and nonsteroidal anti-inflammatory drugs should not be used; consider holding nonselective β-blockers, especially in those with hypotension or AKI; LVP is defined as >5 L; albumin replacement with 6 to 8 g/L of fluid removed is recommended; low platelets and high international normalized ratio do not contraindicate paracentesis; obtain echocardiography to assess cardiac function before TIPS is planned; controlled HE is not a contraindication for TIPS, but TIPS should not be performed if the patient has refractory HE; LT is a definitive therapy; a study showed a survival benefit for TIPS over LVP; younger patients with low MELD scores are most likely to benefit from TIPS
Hepatic hydrothorax: fluid is pushed into the right side of the chest, requiring serial thoracentesis; TIPS is indicated for these patients; do not use a chest tube; refer the patient for LT
Spontaneous bacterial peritonitis: can occur at any point in the development of ascites; diagnostic criteria include polymorphonuclear (PMN) cell count >250 cells/μL; patients with PMN <250 cells/μL plus fever and abdominal pain should be considered for treatment, which includes intravenous antibiotics, 1.5 g/kg albumin on the day of diagnosis, and 1 g/kg albumin on day 3
Biggins SW, Angeli P, Garcia-Tsao G, et al. Diagnosis, evaluation, and management of ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: 2021 Practice Guidance by the American Association for the Study of Liver Diseases. Hepatology. 2021;74(2):1014-1048. doi:10.1002/hep.31884; Caraceni P, O'Brien A, Gines P. Long-term albumin treatment in patients with cirrhosis and ascites. J Hepatol. 2022;76(6):1306-1317. doi:10.1016/j.jhep.2022.03.005; Gallo A, Dedionigi C, Civitelli C, et al. Optimal management of cirrhotic ascites: A review for internal medicine physicians. J Transl Int Med. 2020;8(4):220-236. Published 2020 Dec 31. doi:10.2478/jtim-2020-0035; Khan S, Linganna M. Diagnosis and management of ascites, spontaneous bacterial peritonitis, and hepatorenal syndrome. Cleve Clin J Med. 2023;90(4):209-213. Published 2023 Apr 3. doi:10.3949/ccjm.90a.22028; Popoiag RE, Fierbințeanu-Braticevici C. Spontaneous bacterial peritonitis: update on diagnosis and treatment. Rom J Intern Med. 2021;59(4):345-350. Published 2021 Nov 20. doi:10.2478/rjim-2021-0024; Salgia RJ, Brown K. Diagnosis and management of hereditary hemochromatosis. Clin Liver Dis. 2015 Feb;19(1):187-98. doi: 10.1016/j.cld.2014.09.011. Epub 2014 Oct 23. PMID: 25454304.
For this program, members of the faculty and planning committee reported nothing relevant to disclose.
Dr. Sharma was recorded at 24th Annual Liver Disease Wrap-Up, held October 27, 2023, in Grand Rapids, MI, and presented by University of Michigan Health. For information about upcoming CME activities from this presenter, please visit Medicine.umich.edu. Audio Digest thanks the speakers and presenters for their cooperation in the production of this program.
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The Audio- Digest Foundation designates this enduring material for a maximum of 0.75 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.
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GE381403
This CME course qualifies for AMA PRA Category 1 Credits™ for 3 years from the date of publication.
To earn CME/CE credit for this course, you must complete all the following components in the order recommended: (1) Review introductory course content, including Educational Objectives and Faculty/Planner Disclosures; (2) Listen to the audio program and review accompanying learning materials; (3) Complete posttest (only after completing Step 2) and earn a passing score of at least 80%. Taking the course Pretest and completing the Evaluation Survey are strongly recommended (but not mandatory) components of completing this CME/CE course.
Approximately 2x the length of the recorded lecture to account for time spent studying accompanying learning materials and completing tests.
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