Abdominal ascites with furosemide resistance, Quiz question

Quiz: Ascites With Cirrhosis, Furosemide Resistant

Background: 49-year-old is admitted to the hospital for ascites with cirrhosis. Escalation of outpatient diuretics and a low-salt diet have not improved her ascites. The ascites has worsened. She has trace edema. The patient is confused. 

Patient with trace lower extremity edema and ascites with cirrhosis
The patient has trace lower extremity edema and ascites with cirrhosis. After admission to hospital, intravenous furosemide has not markedly improved the patient’s condition. What is the next step for this patient with cirrhosis?

Intravenous furosemide (Lasix) is commenced in the hospital without effect. The ascites remains. Spironolactone is on board. The blood pressure is 98/68. The serum creatinine level has increased from 1.1 to 1.4, indicating acute kidney injury (AKI). Nephrology is consulted.

An abdominal ultrasound confirms 4 quadrant ascites. A urinalysis shows a bland urine sediment with low urine sodium excretion.

Please answer the following questions:

What is the best next step to approach the patient’s ascites?
* Start a furosemide (lasix) drip
* Add albumin
* Add the diuretic metolazone
* Stop spironolactone
* Ask interventional radiology to perform paracentesis

Diuretic approach:
Explain why switching from furosemide to bumetanide (one loop diuretic to another loop diuretic) or adding a thiazide diuretic is not recommended to treat the ascites, but coadministration of a mineralocorticoid receptor antagonist such as spironolactone is standard of care in the above case study.

What risk is associated with more aggressive diuresis in the setting of cirrhosis with ascites with only trace amounts of peripheral edema for this patient?

Define the potential role of albumin-assisted diuresis in managing the patient’s ascites. Is this approach going to help the patient’s symptoms?

Discussion:

Management of Refractory Ascites With Cirrhosis

Overview

A patient with cirrhosis and refractory ascites should be managed with large volume paracentesis when diuretic therapy fails.

Pathophysiology and Complications

Ascites that does not respond to diuretic therapy in cirrhosis is linked to higher mortality and acute kidney injury, AKI. The multifactorial pathophysiology involves portal hypertension, splanchnic vasodilation, porto-systemic shunts, and a decrease in effective arterial blood volume.

Treatment Approach

  • First steps include dietary sodium restriction and diuretics to induce negative sodium balance.
  • Patients unresponsive to medical therapy should undergo large volume paracentesis with albumin coadministration to prevent complications like worsening acute kidney injury. Note: the reason albumin, given with diuretics, was the wrong choice, and the better option is to perform large volume paracentesis is we are removing the ascites from the problematic compartment. So although albumin is indeed given, if large volume paracentesis were not performed, the patient would still be symptomatic, and her condition would not likely improve quickly.

Transjugular Intrahepatic Portosystemic Shunt (TIPS)

TIPS is an invasive procedure that bypasses the cirrhotic liver to reduce intravascular pressure within the portal vein. While effective, it carries high morbidity and mortality risks and is not a first-line therapy, especially in the presence of hepatic encephalopathy.

Diuretic Therapy Considerations

  • Switching from furosemide to bumetanide or adding a thiazide diuretic is not likely to improve ascites.
  • Mineralocorticoid receptor antagonist coadministration is recommended in this setting and is part of guideline directed therapy. See inspiration below for more information.
  • Aggressive diuresis in the setting of trace peripheral edema could worsen acute kidney injury. In fact, we may want to decrease the patient’s loop diuretics at this time.

Inspiration: Guidelines on the management of ascites in cirrhosis, National Library of Medicine

American Society of Nephrology, Education

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