Episode 200: All About Ascites.
Jesica Mendoza explains the pathophysiology, diagnosis and management of ascites. Dr. Arreaza adds input about early detection and prevention of spontaneous bacterial peritonitis.
Written by Jesica Mendoza, OMS IV, Western University, College of Osteopathic Medicine of the Pacific. Edits and comments by Hector Arreaza, MD.
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Welcome to our episode 200! It is an honor to welcome back a wonderful medical student, her name is Jesica, and she has prepared this topic, and she is excited to share this information with us. Jesica presented in June this year an episode about gestational diabetes (episode 193) and today she will talk about ascites. Jesica, please tell us who you are again.
What is ascites?
Ascites is the buildup of fluid in between the visceral peritoneum and the parietal peritoneum in the abdomen. This is often caused by cirrhosis of the liver due to the increased portal HTN which leads to increased nitrous oxide (NO) and prostaglandins which then causes splanchnic vasodilation and decreased effective arterial volume. The decrease in arterial volume then causes an increase in the renin–angiotensin–aldosterone system (RAAS) and antidiuretic hormone (ADH) from the renal system which leads to sodium and water retention. This then causes a net reabsorption of fluids and ascites.
Evaluation of ascites.
Once someone has been found to have ascites the next step will be a diagnostic paracentesis. This includes removing fluid from the peritoneal cavity in order to determine the SAAG (Serum Ascites Albumin Gradient) score.
SAAG : (serum albumin) − (albumin level of ascitic fluid). The two values should be measured at the same time.
This score helps determine the cause of the ascites with a score >1.1 g/dL indicating portal hypertension usually due to liver disease such as cirrhosis. A SAAG score of <1.1 g/dL will suggest causes such as tuberculosis, malignancy, pancreatitis, nephrotic syndrome, or inflammatory conditions.
A paracentesis can be done for diagnostic purposes in a new-onset ascites or if a patient with known ascites has clinical deterioration (such as fever, abdominal pain, hepatic encephalopathy, renal dysfunction, or leukocytosis). In cases of tense or refractory ascites, the paracentesis can be done for both diagnostic and therapeutic purposes. Tell us more about the serum ascites albumin gradient (SAAG).
If the SAAG is greater than 1.1 (portal hypertension) you then use the serum protein levels for further management. For a low serum protein (<2.5) you proceed with an abdominal US with doppler. The ultrasound will tell you whether the liver is cirrhotic and if the hepatic vessels are patent. Once cirrhosis is identified in the patient, the workup for chronic liver disease management can be started. Another cause of low protein is Budd-Chiari syndrome. In this case anticoagulation is used.
Budd-Chiari syndrome is caused by obstruction of the hepatic venous outflow tract, most commonly the hepatic veins or the intra-/suprahepatic inferior vena cava, in the absence of cardiac or pericardial disease. This causes hepatic congestion, which can present with acute or chronic abdominal pain, hepatomegaly, ascites, and, in some cases, progressive liver dysfunction or portal hypertension; but up to 20% of cases may be asymptomatic. The most frequent underlying cause is a prothrombotic state, particularly cancer (Jes: myeloproliferative neoplasm). That’s why you mention the treatment: anticoagulation.
A SAAG greater than 1.1 with a high serum protein level (>2.5) the cause points towards right sided heart failure or constrictive pericarditis. In both cases a referral to cardiology should be placed for management of the underlying cause of the ascites. Another cause of elevated protein levels is portal or splenic vein thrombosis. If this is the case, the patient is managed with anticoagulation again.
Treating the underlying cause.
Patients with cirrhosis causing ascites will need treatment for the underlying cause. If that cause is Hepatitis C or Hepatitis B, then starting antiviral therapy is crucial to reduce the liver’s inflammation. Diuresis is also very important to help with decreasing the ascites and in turn all the symptoms of ascites. Usually Furosemide and/or spironolactone can be used. In cases of mild ascites spironolactone is usually first line treatment. If the patient has recurrent ascites, they often are given a combination of spironolactone and loop diuretics like furosemide.
The recommended ratio of furosemide (Lasix) to spironolactone for the treatment of ascites is 40 mg of furosemide to 100 mg of spironolactone (a 1:2.5 ratio). Recommended max dose: 160 mg furosemide and 400 mg spironolactone daily. Dose adjustments can be made every 72 hours to minimize electrolyte disturbances.
Once the patient has ascites under control the diuretic dose is adjusted to the lowest effective dose to minimize side effects.
Medications to avoid, sodium and water restriction.
In conjunction with medical management, it is ideal that the patient stops alcohol if the patient has alcohol induced cirrhosis causing the ascites. The patient should also follow a low-sodium diet (less than 2 grams/day) to help prevent the fluid overload that worsens the ascites. Also, something very important is that the patient must avoid use of NSAIDs, b-blockers, and ACE/ARBs. Patients need to be educated on the importance of avoiding NSAIDS especially because these medications can be found over the counter and are readily accessible but very harmful to cirrhotic patients.
Fluid (water) restriction is generally not recommended for patients with liver cirrhosis and ascites unless they have moderate to severe hyponatremia (serum sodium ≤125–126 mEq/L). When indicated, fluid restriction is typically set at 1,000 mL per day for moderate hyponatremia. The fluid management in ascites is focused on sodium restriction.
Refractory ascites.
Sometimes there are people who have already received diuretics and have tried lifestyle changes, but the ascites continues to recur. In these cases, serial therapeutic paracentesis or trans jugular intra-hepatic portosystemic shunts (TIPS) can be done.
One special case is when the ascites is caused by a malignancy. In this case fluid will continue to accumulate even with repeat paracentesis. PleurX is another available treatment. PleurX is a thin, flexible silicone catheter and a one-way valve that is inserted into the peritoneal cavity to allow for drainage of the fluid. Usually, the patients are sent home with this catheter and have caregivers who help them drain fluid using vacuum bottles. This is useful in reducing hospitalization in patients. However, it is not recommended in patients with infection, chylous effusions, mediastinal shifts, or hemorrhage risks. If the patient is a good candidate, they can be put on a list for liver transplant.
Spontaneous bacterial peritonitis.
A patient with SBP usually presents with systemic inflammatory response syndrome (SIRS) and large volume ascites on abdominal US. SBP is confirmed via paracentesis with >250 PMNS/mL. Fluid should be sent to the lab for culture and then antibiotics should be started. IV 3rd generation cephalosporins are typically used. Fluoroquinolones are also used to prevent the recurrence of SBP.
If you desire to learn more about SBP, listen to our episode 123. By the way, propranolol is a frequently used medication to prevent GI bleeding from esophageal varices in cirrhosis and also to decrease the development of ascites. It should be used in patients who have compensated cirrhosis and must be avoided in patients with refractory ascites, hypotension, renal dysfunction or active infection.
So, to wrap things up we should remember that once we identify ascites with our physical exam of the patient, we should make sure to obtain a paracentesis as these results will be the main guide for our treatment. The treatment can then range from medical treatment such as spironolactone and/or loop diuretics to TIPS procedures, PleurX or even liver transplant. Always be on the lookout for SBP in patients with ascites and always remember to obtain a culture on the ascitic fluid prior to starting antibiotics.
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References:
- Ascites, Cleveland Clinic, https://my.clevelandclinic.org/health/diseases/14792-ascites.
- Huang LL, Xia HH, Zhu SL. Ascitic Fluid Analysis in the Differential Diagnosis of Ascites: Focus on Cirrhotic Ascites. J Clin Transl Hepatol. 2014 Mar;2(1):58-64. doi: 10.14218/JCTH.2013.00010. Epub 2014 Mar 15. PMID: 26357618; PMCID: PMC4521252. https://pmc.ncbi.nlm.nih.gov/articles/PMC4521252/.
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