Management and outcomes of hepatorenal syndrome at an urban academic medical center: a retrospective study.

OBJECTIVES: This study is aimed to evaluate the management of acute kidney injury (AKI) in our inner city, American hospital. We intended to ascertain whether or not there is prompt recognition of AKI in cirrhosis according to International Club of Ascites and acute kidney injury network criteria as well how effective we are at distinguishing among different causes of AKI. We aimed to calculated the mortality of hepatorenal syndrome (HRS) in our hospital, and to evaluate the adequacy of the established treatment of AKI at each stage of its algorithm. PATIENTS AND METHODS: ICD diagnostic codes were used to identify patients with liver cirrhosis and acute renal failure. A total of 725 patients met the search criteria. We excluded the patients without clinical or imaging evidence of ascites, heart failure, on hemodialysis, baseline creatinine more than 1.5 mg/dl and patients who died within 48 h of developing acute renal failure. 291 patients met the inclusion criteria. All statistical analyses were performed using SPSS version 23.0 software with a two-sided significance level set at P value less than 0.05. RESULTS: Mean age was 55.7 ± 0.61 and baseline serum creatinine was 0.94 ± 0.14. 66.5% of patients were African American, 27.3%, Hispanic, and 4.3% White. The average rise in creatinine from baseline was 1.36 ± 0.08 mg/dl. 27.2% of patients met the diagnostic criteria of HRS. 92.3% of patients with HRS received intravenous fluids and 75.4% received intravenous albumin within 48 h of acute creatinine rise. The in-hospital mortality rate was 14.1, 23.3, and 41.5% for patients with pre-renal azotemia, ARF, and HRS, respectively (P < 0.01). CONCLUSION: This study demonstrates that with present tools, there is significantly higher mortality in HRS despite guideline-based treatment. Biomarkers for early diagnosis of HRS are necessary to avoid delays in initiation of HRS treatment while establishing the diagnosis. As well, worldwide standardization of the treatment of HRS will be important if the outcome is to be improved.

Spice/K2 synthetic marijuana-induced toxic hepatitis treated with N-acetylcysteine.

BACKGROUND: Spice/K2 is one of several street names for synthetic marijuana. These hallucinogens are increasingly sold over the internet and in "head" shops. They are usually household herbs that are sprayed with chemicals that become centrally active compounds when burned together and inhaled by smoking. CASE REPORT: We present a case of a 45-year-old male substance abuser who was admitted with evidence of hepatocellular necrosis and worsening liver failure. Tests for acetaminophen were negative, as were tests for alcohol. The patient was empirically treated with N-acetylcysteine. Hepatocellular damage was abated and the patient made a full recovery. Upon regaining consciousness, the patient admitted to smoking Spice/K2. Other toxicities have been reported with synthetic marijuana use, but not liver toxicity. CONCLUSIONS: Physicians need to have a high index of suspicion for unknown hepatotoxins in substance abusers. N-acetylcysteine can be given if there is no contraindication.

Case report of acute-on-chronic liver failure secondary to diffuse large B-cell lymphoma.

Acute liver failure is a rare presentation of hematologic malignancy. Acute on chronic liver failure (ACLF) is a newly recognized clinical entity that describes acute hepatic decompensation in persons with preexisting liver disease. Diffuse large B-cell lymphoma (DLBCL) is an aggressive non-Hodgkin's lymphoma (NHL) with increasing incidence in older males, females and blacks. However, it has not yet been reported, to present with acute liver failure in patients with preexisting chronic liver disease due to human immunodeficiency virus (HIV)/hepatitis C virus (HCV) co-infection. We describe a case of ACLF as the presenting manifestation of DLBCL in an elderly black man with HIV/HCV co-infection and prior Hodgkin's disease in remission for three years. The rapidly fatal outcome of this disease is highlighted as is the distinction of ACLF from decompensated cirrhosis. Due to the increased prevalence of HIV/HCV co-infection in the African American 1945 to 1965 birth cohort and the fact that both are risk factors for chronic liver disease and NHL we postulate that the incidence of NHL presenting as ACLF may increase.