VCOM Research Day Program Book 2023

Medical Resident Research Case Reports

14 Barriers to Early Recognition of Hepatorenal Syndrome

Alexa J. Krebs, MD; Ryan O’Connell, DO Corresponding author: alexa.krebs@lpnt.net

SOVAH Health Internal Medicine Residency Program

three days. Labs were remarkable for a positive urinalysis and elevated creatinine of 2.12. She was subsequently admitted for severe sepsis secondary to acute uncomplicated cystitis and acute kidney injury, which resolved with fluids and antibiotics. Her liver enzymes slowly trended up and reached 10x the upper limit of normal on hospital day 6. A right upper quadrant ultrasound revealed no acute process but did show a mildly nodular contour concerning for early changes of cirrhosis. Her hepatitis panel was non reactive. Shortly thereafter, creatinine trended up, and she developed metabolic acidosis. A bicarbonate drip was initiated. The patient’s condition declined quickly, requiring invasive mechanical ventilation and ICU care. She developed fulminant liver failure with DIC and bleeding from all orifices. Despite rapid intervention, the patient succumbed to her condition on hospital day 10. Discussion: Timely diagnosis of hepatorenal syndrome, particularly HRS-AKI type, is crucial

for patient outcome and survival. Identification and diagnosis of liver disease in the hospital setting can be delayed; meanwhile, hepatorenal syndrome has already begun. In addition, hepatorenal syndrome is a diagnosis of exclusion, which can make early recognition challenging. Pre-renal azotemia and acute tubular necrosis are similar to hepatorenal syndrome, which can obscure the diagnosis. The absence of shock and nephrotoxic agents and lack of obstruction or parenchymal disease on imaging can further help to differentiate. Urinary biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), which is seen in ATN only, may also provide benefit. Other criteria to exclude hepatorenal syndrome include protein excretion < 500 mg/day and lack of improvement in kidney function after two days of IV albumin.

Introduction: Hepatorenal syndrome is a cause of acute kidney injury that occurs because of arterial vasodilation of the splanchnic vessels initiated by acute or chronic liver disease. HRS-AKI, or hepatorenal syndrome type 1, is the more severe type of hepatorenal syndrome defined as at least a 2.5 mg/ dL increase in serum creatinine over less than two weeks. If not recognized in time, the prognosis is very poor and leads to death within days to weeks. Thus, early recognition is crucial; however, timely diagnosis can be difficult due to the rapid progression of the disease, as well as hepatorenal syndrome being a diagnosis of exclusion with no specific test available. Case: The patient is a 59-year-old white female with a past medical history of hypertension, hyperlipidemia, non-insulin-dependent diabetes mellitus type II, morbid obesity, and rheumatoid arthritis (RA) who presented to the emergency department (ED) due to nausea, vomiting, fever, generalized weakness, and fatigue for the past

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