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A 58-Year-Old Man With Worsening Symptoms of Cirrhosis and Renal Function

Ronald N. Rubin, MD1,2Adam M. Rubin MD3

  • Introduction. A 58-year-old man is brought to the office by his family for worsening signs and symptoms of his known, pre-existing cirrhosis of the liver.

    Patient history. The patient has a long medical history, punctuated with multiple complications and admissions for alcoholic hepatitis, alcohol withdrawal with delirium tremens, acute pancreatitis, and in recent years, the onset of cirrhosis of the liver with ascites, which occurred 2 years ago.

    The ascites have become permanent and progressive. Unfortunately, he has not abstained from alcohol despite vigorous attempts by his family to get him to stop. They have noted increased abdominal girth, some edema of the ankles and feet, and episodes of confusion and diminished mentation in recent weeks. His only medications are multivits, spironolactone 100 mg/day, and lactulose twice daily. However, the family noted that his compliance is erratic.

    Physical examination. The patient’s physical exam reveals an icteric man with obvious ascites. The vital signs are as follows: pulse is 88/min; respirations are 14/min; blood pressure is 95/70, and temperature is 37° C. The physical exam revealed scleral icterus and numerous spider angiomas on the skin. The patient's chest is clear and his heart is regular without murmurs or gallops. The patient has a distended abdomen with tense ascites, which makes palpation for liver/spleen difficult. A caput medusa is present around the umbilicus. There is (+)1 to (+)2 edema of the ankles, but no gross anasarca. The patient shows diminished mental acuity and occasional bursts of asterixis with wrist extension. His stool was hematest negative.

    Diagnostic testing. A set of labs drawn in the office showed: Hemoglobin of 10.1 gms/dL with mean corpuscular volume (MCV) 100 u3 (10.9 gms/dL, MCV 99 u3), white blood cell count of 4.0 K, and his platelets are 92 K (4.4K, 95K). Basal chemistries show normal glucose, serum Na 128 meq/L, serum K 3.7 meq/L (unchanged), while blood urea nitrogen test is 4 mg/dL. His last creatinine test showed 1.9 mg/L compared to 0.7 mg/dL 1 month prior. Comprehensive biochemical testing reveals essentially unchanged and normal alanine transaminase and aspartate transaminase, albumin 1.9 gm/dL and bilirubin 6.7 mg/dL (increased from 5.2 mg/dL).

    Considering the deterioration clinically (mentation change, worsening ascites) and the very worrisome change in renal function, he was admitted for hospital care and treatment. Immediate testing on admission included blood cultures and small needle paracentesis, which had less than 250 polymorphonuclear/cc3 and was sent for culture. Echocardiography was negative for structural heart disease with ejection fraction 45% and chest radiograph was negative for pulmonary congestion.

References
  1. Nadim MK and Garcia-Tao G. Acute kidney injury in patients with cirrhosis. N Eng J Med. 2023; 388:733-745.

  2. Pitre T, Kiglen M, Helmesz W et al. The comparative effectiveness os vasoactive treatments for the management of hepatorenal syndrome systemic review and network meta analysis. Crit Care Med. 2022:50:1429-1439.

  3. Wong F, Pappas SC, Curry MP et al. Terlipressin plus albumin for the treatment of type 1 hepatorenal syndrome. N Eng J Med. 2021:384:818-828.

  4. Zarbock A, Kellum JA, Schmidt C et al. Effect of early versus delayed initiation of renal replacement therapy on mortality in critically ill patients with acute kidney injury: the ELAIN randomized clinical trial. JAMA. 2016;315:2190-2199.

  5. Wald R, Bagshw SM. Timing of initiation of renal replacement therapy in acute kidney injury. N Eng J Med. 2020;383:1797-1798.


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