Razvan M. Chirila

BACKGROUND: Publicly reported 30-day acute myocardial infarction (AMI) mortality rates are widely used to benchmark hospital performance. However, these measures may lack validity when they include deaths among patients with do-not-resuscitate (DNR) orders or those receiving palliative care—groups for whom mortality may be expected and goal-concordant. METHODS: We analyzed the national 100% Medicare Inpatient Standard Analytic File and Medicare Beneficiary Summary file to assess 30-day AMI mortality rates stratified by DNR status (absent, present-on-admission, and postadmission) and palliative care involvement. We then conducted a retrospective chart review of all 30-day AMI mortalities at a single academic medical center (2019–2025), applying Global Registry of Acute Coronary Events and a Palliative Performance Scale scores to identify unpreventable deaths, which we defined as a Global Registry of Acute Coronary Events >190.5 or Palliative Performance Scale ≤40%. Global Registry of Acute Coronary Events is a risk-stratification tool using clinical and laboratory variables whereas the Palliative Performance Scale is a bedside functional status and palliative care assessment quantifying patient’s self-care ability. RESULTS: Across n=467 259 total AMI encounters, mean (SD) age was 75.1 (10.5), and the population was 44% women. Thirty-day mortality was 10.4% (39 112/376 062) among patients without DNRs, 43.1% (26 181/60 719) in those with present-on-admission DNR, and 72.1% (21 984/30 478) in those with postadmission DNR. Among 9.2% (43 090/467 259) of encounters with palliative care, there was a 76.9% mortality rate (33 151/43 090). Hazard ratios for mortality were 5.25 (95% CI, 5.17–5.33) for present-on-admission DNR and 10.73 (95% CI, 10.55–10.91) for postadmission DNR as compared with encounters without DNRs. Among n=24 AMI mortalities at our institution, 71% (17/24) had DNRs, and 33% (8/24) met the unpreventable death criteria. CONCLUSIONS: The validity of 30-day AMI mortality metrics may be undermined by their inclusion of high-acuity, end-of-life patients, which may disincentivize hospitals from delivering appropriate, patient-centered care. Removal of DNR or palliative cases from performance measures should be explored to better identify opportunities for reducing preventable deaths.

Renal dysfunction is highly prevalent among patients with cirrhosis and has major implications for management, prognostication, and liver transplant decision-making. Both acute kidney injury (AKI) and chronic kidney disease (CKD) occur frequently in this population and are driven by a complex interplay of hemodynamic derangements, systemic inflammation, and intrinsic or functional renal injury. Accurate assessment of kidney function is essential, as serum creatinine and estimated glomerular filtration rate (eGFR) calculations directly influence MELD-based transplant allocation, eligibility for simultaneous liver–kidney transplantation (SLKT), and clinical decisions such as drug dosing and peri-transplant immunosuppression strategies. However, creatinine-based assessments are fundamentally limited in cirrhosis due to reduced creatinine production, sarcopenia, expanded volume of distribution, increased tubular secretion, and assay interference from hyperbilirubinemia, resulting in frequent overestimation of true GFR. Alternative methods, including cystatin C-based equations, combined creatinine–cystatin C equations, timed urine clearances, and direct GFR measurement using exogenous filtration markers (iohexol, iothalamate), offer potential advantages but also carry important limitations, particularly in decompensated disease with ascites or inflammation. Newer cirrhosis-specific eGFR equations such as the GRAIL and Royal Free Hospital formulas attempt to address these shortcomings, yet validation studies demonstrate inconsistent accuracy across patient cohorts. This review summarizes the pathophysiologic contributors to renal dysfunction in cirrhosis, evaluates the performance and pitfalls of existing kidney function assessment tools, and highlights the ongoing need for reliable, validated methods tailored to this unique population. Until improved approaches are widely accessible, serum creatinine remains the most practical—albeit imperfect—marker guiding clinical decision-making in cirrhotic patients.

Background/Objectives: Autoimmune inner ear disease (AIED) causes sensorineural hearing loss that classically presents as fluctuating, asymmetric loss of hearing. Associated vestibular and other ear symptoms can be present in many patients. First-line treatment of AIED is high-dose corticosteroids. AIED can present either as a primary condition limited to ear involvement or secondary, as part of an underlying systemic autoimmune rheumatic disease, the most common of which include vasculitis and relapsing polychondritis. We described our cohort of primary AIED, including demographics, treatment, and outcomes. We excluded from this review sensorineural hearing loss in the context of vasculitis and relapsing polychondritis. Methods: We performed a chart review of patients with the diagnosis of AIED at Mayo Clinic and compared the cohort by sex. Results: Thirty-one patients met the inclusion criteria. The mean age was 48.5 years, and 17 were men. Patients were initially evaluated at the Department of Otorhinolaryngology or Internal Medicine, and 29 patients were subsequently referred to the Department of Rheumatology, with a mean of 12.2 weeks after the first evaluation. Treatment with corticosteroids showed improvement in hearing and vestibular symptoms during the first month but no further improvement by the end of the third month. Other immunosuppressive medications were used with various degrees of response. Methotrexate was the second most used therapy, with 11 of 17 patients reporting an improvement in symptoms. Conclusions: Corticosteroid therapy is an effective initial treatment for AIED and should be followed with corticosteroid-sparing agents to prevent further damage to the cochlea.

Autoimmune hepatitis is an immune-mediated inflammatory condition of the liver of undetermined cause that affects both sexes, all ages, races, and ethnicities. Its clinical presentation can be very broad, from having an asymptomatic and silent course to presenting as acute hepatitis, cirrhosis, and acute liver failure potentially requiring liver transplantation. The diagnosis is based on histological abnormalities (interface hepatitis), characteristic clinical and laboratory findings (increased aspartate aminotransferase, alanine aminotransferase, and serum IgG concentration), and the presence of one or more characteristic autoantibodies. The large heterogeneity of these clinical, biochemical, and histological findings can sometimes make a timely and proper diagnosis a difficult task. Treatment seeks to achieve remission of the disease and prevent further progression of liver disease. First-line therapy includes high-dose corticosteroids, which are later tapered to decrease side effects, and azathioprine. In the presence of azathioprine intolerance or a poor response to the standard of care, second-line therapy needs to be considered, including mycophenolate mofetil. AIH remains a diagnostic and therapeutic challenge, and a further understanding of the pathophysiological pathways of the disease and the implementation of randomized controlled trials are needed.