In this clinical-pearl-packed session, Dr. Suchita Shah Sata from Duke University Hospital in Durham, N.C., recaps the breadth of knowledge needed by hospitalists to manage this complex patient population. Outlining the objectives of the talk, Dr. Sata describes the pathophysiology of cirrhosis and how this leads to the complications that are seen in the decompensated state, suggests a framework for evaluating the etiologies of decompensated cirrhosis, and applies current evidence to delineate best practices in inpatient management of common complications of cirrhosis.
Reviewing the pathophysiology of decompensated cirrhosis, increased intrahepatic resistance results in increased portal pressures and congestion, with splanchnic vasodilation and the development of venous varices. Vasodilator release and low oncotic pressure due to the decline in hepatic albumin production decreases peripheral vascular resistance and results in low systemic blood pressure with decreased effective arterial blood volume experienced by the kidneys. A sodium avid state develops with retention of both sodium and fluid, resulting in ascites and edema.
The complications of decompensated cirrhosis are deeply intertwined, with one complication often resulting in a cascade of others. When admitting a patient with new-onset ascites or a worsening decompensated state, Dr. Shah Sata asks the question, “Why is this patient sick today? Why now?” to understand why a patient might be developing ascites, encephalopathy, spontaneous bacterial peritonitis (SBP), or hepatorenal syndrome (HRS) at this junction in their illness. One cause of worsening decompensation, portal vein thrombosis, should be ruled out in any patient with new or worsening ascites by obtaining a right-upper-quadrant ultrasound with Doppler.
These patients should also undergo diagnostic paracentesis, as SBP can present without any typical infectious signs or symptoms such as fever, abdominal pain, or leukocytosis. Ascitic fluid should be sent for cell count and differential, culture, gram stain, fluid protein, and fluid albumin; a serum albumin level should be drawn. These laboratory studies can help support the cause of ascites as consistent with liver etiology by calculating a serum-albumin-ascites gradient. A polymorphonuclear leukocyte count >250/mm3 is consistent with SBP, even without the presence of bacteria on the gram stain or culture, and warrants treatment with a third-generation cephalosporin. SBP prophylaxis should be considered in any patient with a history of SBP, advanced cirrhosis meeting specific laboratory parameters, and/or active gastrointestinal bleeding.
A key high-value care opportunity includes the appropriate use of blood products prior to paracentesis. The American Association for the Study of Liver Diseases does not recommend routine administration of fresh frozen plasma or platelets prior to diagnostic paracentesis, as patients with cirrhosis have both pro-thrombotic and anticoagulant physiology, and studies show that neither international normalized ratio (INR) nor platelet count accurately predict bleeding risk.
Managing ascites in cirrhosis can be challenging. While hospitalists often first reach for furosemide to manage hypervolemia, the most effective diuretic to manage ascites in cirrhosis is spironolactone, starting at a dose of 100 mg daily. While furosemide is helpful to augment diuresis and maintain potassium balance, spironolactone targets the underlying renin-angiotensin system and results in sufficient diuresis to control ascites in many patients. If diuretics are not sufficient, large volume paracentesis, as defined by removal of greater than four to five L of ascites, can be employed to manage fluid buildup.
However, hospitalists should be aware of the risk of paracentesis-induced circulatory dysfunction, as rapid fluid shifts can drive a patient into renal failure. To prevent this, albumin administration of six to eight g of albumin per liter of ascites should be provided. For patients who do develop renal impairment such as HRS, diuresis should be stopped. Patients should receive volume expansion with albumin and be provided octreotide and midodrine to improve renal perfusion.
One of the most feared complications of cirrhosis, variceal bleeding, should be treated with octreotide, conservative transfusion threshold of seven to nine g/dL, pre-emptive SBP treatment, and gastrointestinal consultation for esophagogastroduodenoscopy with band ligation or injection. Non-selective beta-blockers such as propranolol or nadolol should be started for prevention of rebleeding after the patient is stabilized and any hypotension has resolved. For patients with hepatic encephalopathy, an aggressive lactulose regimen should be started with 30 mL every two to three hours until mentation is clearing. Do not check plasma ammonia levels; Dr. Shah Sata calls this out specifically as a low-value practice. Rifaximin can be used in addition to lactulose.
Other key tips include avoiding nonsteroidal anti-inflammatory agents in patients with cirrhosis due to the propensity for renal dysfunction, and never placing a drain in a hepatic hydrothorax due to rapid volume depletion. Transplant evaluation and palliative care are additional key pillars in the care of advanced liver disease and should be discussed early in the patient’s disease course.
- Complications of cirrhosis are often intertwined, and it is important to understand the physiology of decompensated cirrhosis to evaluate and treat its complications.
- Patients with new-onset ascites, known ascites admitted to the hospital for any emergent reason, or with new signs or symptoms of infection should undergo diagnostic paracentesis.
- Polymorphonuclear leukocyte count >250/mm3 is consistent with SBP, even without the presence of bacteria on the gram stain or culture, and warrants treatment with a third-generation cephalosporin.
- Do not routinely administer fresh frozen plasma or platelets prior to diagnostic paracentesis, as patients with cirrhosis have both pro-thrombotic and anticoagulant physiology, and studies show that neither INR nor platelet count accurately predict bleeding risk.
- The most effective diuretic to manage ascites in cirrhosis is spironolactone, starting at a dose of 100 mg daily. Furosemide may be added to maintain potassium balance.
- Do not check ammonia levels in suspected hepatic encephalopathy, as this is a low-value practice that should not dictate treatment plans.
- Evidence-based indications for the use of albumin include prevention of post-paracentesis circulatory dysfunction, volume expansion in HRS, and prevention of HRS in cirrhotic patients with SBP.
- Consider initiating discussions early regarding referral for transplantation and palliative care in patients with advanced liver disease.
Dr. Burdick (@GoBlueBurd) is an adult internal medicine hospitalist, clinical assistant professor of internal medicine at Michigan State University College of Human Medicine, and medical director of the Clinical Standardization Program at Corewell Health, both in Grand Rapids, Michigan.