ascites
Jump to navigation
Jump to search
Introduction
The accumulation of excess fluid within the peritoneal cavity.
Etiology
- transudates
- pathophysiology
- increased portal venous pressure (portal hypertension)
- increased lymph production
- decreased oncotic pressure
- impaired renal excretion of Na+ & H2O
- disorders associated with transudative ascites
- pathophysiology
- exudates
- pathophysiology
- inflammation disrupts capillaries & lymphatics
- protein leak into peritoneal cavity
- inflammation superimposed on exudative ascites
- disorders associated with exudative ascites
- abdominal tumor
- abdominal infection
- peritonitis
- pancreatitis
- intestinal perforation
- lymphatic obstruction
- trauma, tumor, tuberculosis
- pathophysiology
* ascites develops in 50% of patients with cirrhosis within 10 years[2]
Pathology
- in ascites due to portal hypertension, blood pressure falls resulting in reduced renal blood flow & glomerular filtration
- compensatory upregulation of renin-angiotensin system supports blood pressure & renal function
Clinical manifestations
- mild ascites is frequently asymptomatic
- several hundred mL of ascitic fluid required for detectable ascites
- anorexia, nausea, early satiety, heartburn
- protruding flanks
- fluid wave
- shifting dullness (> 1.5 liters of ascitic fluid)
- puddle sign
- severe ascites
Laboratory
- general
- complete blood count (CBC)
- liver function tests
- basic metabolic panel
- serum amylase
- serum triglycerides
- serum BNP may help distinguish heart failure from cirrhosis as a cause of new-onset ascites[4]
- paracentesis (see ascitic fluid analysis)
- indications
- all patients with new onset ascites
- all patients with cirrhosis admitted to hospital[9]
- paracentesis takes priority over upper GI endoscopy if no GI bleeding[10]
- tests
- cell count
- differential total protein & albumin (to enable calculation of serum albumin - ascites albumin gradient
- gram stain, culture & sensitivity
- acid fast stain, culture for Mycobacterium tuberculosis
- cytology
- specific gravity
- serum amylase, serum triglycerides, serum bilirubin
- transudates
- clear or straw-colored fluid
- [[[A13149|serum albumin]]] - [ascites albumin] >= 1.1 g/dL
- protein in peritoneal fluid < 1.5 g/dL may indicate need for prophylaxis for spontaneous bacterial peritonitis
- ascitic fluid protein > 2.5 g/dL suggests right heart disease or Budd Chiari syndrome
- ascitic fluid protein < 2.5 g/dL suggests cirrhosis
- [[[A13149|serum albumin]]] - [ascites albumin] < 1.1 g/dL &
- ascitic fluid protein > 2.5 g/dL suggests infection, malignancy or pancreatic ascites[2]
- ascitic fluid protein < 2.5 g/dL suggests nephrotic syndrome or myxedema
- specific gravity < 1.016
- further ascites workup generally uneccessary
- exudates
- [[[A13149|serum albumin]]] - [ascites albumin] < 1.1 g/dL
- chylous or turbid milky fluid with lymphatic obstruction
- WBC > 500/mm3 or neutrophils > 250/mm3 indicates infection (spontaneous bacterial peritonitis)[2]
- indications
Diagnostic procedures
- laparoscopy with biopsy of peritoneum & liver
Radiology
(as indicated)
- abdominal ultrasound (US) is imaging modality of choice[2]
- can detect > 100 mL of ascitic fluid
- US of ovaries for suspected Meigs' syndrome
- US of liver & spleen
- abdominal CT
- liver-spleen scan
Complications
- massive ascites may result in abdominal compartment syndrome
Differential diagnosis
Management
- minimal ascites detected only by ultrasound does not require treatment[9]
- moderate ascites
- salt restriction (< 2 g of Na+/day)
- bedrest
- spironolactone (Aldactone) with furosemide
- furosemide (Lasix) 40 mg QD
- paracentesis
- large volume ascites
- all patients with new-onset ascites & all patients with cirrhosis & pre-existing ascites admitted to the hospital[9]
- removal of up to 5 liters of fluid is safe
- administration of albumin if > 5 L of ascitic fluid removed
- amount of albumin = 6-8 g/L of ascitic fluid removed
- albumin may be appropriate if lesser amounts of ascitic fluid removed
- fluid restriction for hyponatremia (1.5-2 L/day)
- monitor blood pressure with portal hypertension
- decrease or discontinue antihypertensives, especially ACE inhibitors, ARBs[2]
- discontinue NSAIDs
- ascites resistant to diuretic therapy
- discontinue diuretics
- presumptive bacterial peritonitis
- peritoneal fluid neutrophils > 250/uL regardless of symptoms[9]
- serum creatinine > 1.0 mg/dL, serum urea nitrogen > 30 mg/dL, or serum bilirubin (total) > 4.0 mg/dL[2][10]
- 3rd generation cephalosporin[9]
- coverage for gram-negative coliform & Streptococcus
- consider IV albumin infusion[11]
- prophylaxis
- daily norfloxacin or ciprofloxacin for all patients who recover[9]
- ascites & GI hemorrhage: IV ceftriaxone for as long as 7 days[9]
- high-risk patients with cirrhosis & ascites may not benefit from antibiotic prophylaxis[8]
- acute kidney injury
- albumin is the volume expander of choice[11]
- surgery
- peritoneovenous (LeVeen) shunt
- fewer hospital admissions for management of ascites relative to therapeutic paracentesis, but no difference in survival
- transjugular intrahepatic portosystemic shunts (TIPS)
- liver transplantation
- peritoneovenous (LeVeen) shunt
More general terms
More specific terms
Additional terms
References
- ↑ Saunders Manual of Medical Practice, Rakel (ed), WB Saunders, Philadelphia, 1996, pg 363-64
- ↑ 2.0 2.1 2.2 2.3 2.4 2.5 2.6 Medical Knowledge Self Assessment Program (MKSAP) 11, 15, 16, 17, 18, 19. American College of Physicians, Philadelphia 1998, 2009, 2012, 2015, 2018, 2021.
Medical Knowledge Self Assessment Program (MKSAP) 19 Board Basics. An Enhancement to MKSAP19. American College of Physicians, Philadelphia 2022 - ↑ Runyon BA; AASLD Practice Guidelines Committee. Management of adult patients with ascites due to cirrhosis: an update. Hepatology. 2009 Jun;49(6):2087-107 PMID: https://www.ncbi.nlm.nih.gov/pubmed/19475696
- ↑ 4.0 4.1 Farias AQ et al. Serum B-type natriuretic peptide in the initial workup of patients with new onset ascites: A diagnostic accuracy study. Hepatology 2014 Mar; 59:1043 <PubMed> PMID: https://www.ncbi.nlm.nih.gov/pubmed/23907731 <Internet> http://onlinelibrary.wiley.com/doi/10.1002/hep.26643/abstract
- ↑ Gordon FD Ascites. Clin Liver Dis. 2012 May;16(2):285-99 PMID: https://www.ncbi.nlm.nih.gov/pubmed/22541699
- ↑ European Association for the Study of the Liver. EASL Clinical Practice Guidelines for the management of patients with decompensated cirrhosis. J Hepatol. 2018 Apr 10. PMID: https://www.ncbi.nlm.nih.gov/pubmed/29653741 https://www.journal-of-hepatology.eu/article/S0168-8278(18)31966-4/fulltext
- ↑ Sola E, Sole C, Gines P. Management of uninfected and infected ascites in cirrhosis. Liver Int. 2016 Jan;36 Suppl 1:109-15. Review. PMID: https://www.ncbi.nlm.nih.gov/pubmed/26725907
- ↑ 8.0 8.1 Komolafe O, Roberts D, Freemasn SC et al. Antibiotic prophylaxis to prevent spontaneous bacterial peritonitis in people with liver cirrhosis: A network meta-analysis. Cochrane Database Syst Rev 2020 Jan 16; 1:CD013125 PMID: https://www.ncbi.nlm.nih.gov/pubmed/31978256 https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD013125.pub2/ful
- ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 9.7 9.8 Biggins SW 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 Aug; 74:1014 PMID: https://www.ncbi.nlm.nih.gov/pubmed/33942342 https://aasldpubs.onlinelibrary.wiley.com/doi/10.1002/hep.31884
- ↑ 10.0 10.1 10.2 NEJM Knowledge+ Gastroenterology
- ↑ 11.0 11.1 11.2 11.3 Garcia-Tsao G et al. AGA clinical practice update on the use of vasoactive drugs and intravenous albumin in cirrhosis: Expert review. Gastroenterology 2024 Jan; 166:202. PMID: https://www.ncbi.nlm.nih.gov/pubmed/37978969 https://www.gastrojournal.org/article/S0016-5085(23)05143-0/fulltext