RESUMO
Background: Spontaneous Bacterial Peritonitis (SBP) poses a significant risk to cirrhosis patients with ascites, emphasizing the critical need for early detection and intervention. This retrospective observational study spanning a decade aimed to devise predictive models for SBP using routine laboratory tests. Additionally, it aimed to propose a novel scoring system to aid SBP diagnosis. Methods: Data analysis encompassed 229 adult cirrhotic patients hospitalized for ascites between 2012 and 2021. Exclusions eliminated cases of secondary ascites unrelated to liver cirrhosis. Patients were categorized into SBP-positive (n=110) and SBP-negative (n=119) groups. Comparative analysis of demographic details and various laboratory indicators (Neutrophil-to-Lymphocyte Ratio (NLR), Mean Platelet Volume (MPV), C-Reactive Protein (CRP), Platelet (PLT), Alanine Transaminase (ALT), Aspartate Amino Transferase (AST), Potassium (K), Sodium (Na), Total Bilirubin (TB) and International Normalized Ratio (INR) was performed between the groups. The study presented effective SBP prediction models for prompt diagnosis and treatment: a multivariate logistic regression model and a simple scoring system. Findings: The study advocates early diagnosis and rapid treatment for all cirrhotic patients with ascites, regardless of cirrhosis stage. Furthermore, it recommends initiating SBP treatment for patients scoring 2-3 in the proposed scoring system while excluding SBP findings for those scoring zero. Conclusion: Combining age, sex, and specific laboratory tests (MPV, NLR, CRP, TB, and INR) within random forest models and a simple scoring system enables swift and accurate SBP diagnosis.
RESUMO
BACKGROUND & AIMS: The risk of exacerbating sub-clinical hepatic encephalopathy (HE) by propofol has not been established. The aim of this study is to determine whether the use of propofol, for upper endoscopy in patients with cirrhosis, precipitates sub-clinical HE. METHODS: Sixty-one patients with compensated HCV and HBV cirrhosis (CP score 5-6) were randomly selected and divided into two groups (intent-to-treat population) matched for age, gender, and BMI. The first group received a single propofol sedation (N = 31, age 57 ± 12, dose range 70-100 mg/procedure) and the second group (N = 30, age 56 ± 12, dose 3-6 mg/procedure) received a single midazolam sedation, all done by an anesthesiologist. All patients completed number connection test (NCT), cognitive function score, time to recovery, time to discharge sheets, and hemodynamic parameters before sedation, and at discharge from the endoscopy unit, 1h post-procedure. Thirty control subjects without cirrhosis were matched to the cirrhotic patients who received sedation with regard to age, gender, BMI, and education level. RESULTS: A total of 58/61 cirrhotic patients (95%) had sub-clinical encephalopathy before the endoscopy (mean NCT 84.7 ± 77 s, normal < 30 s). No patient developed overt HE after sedation. There were no differences between groups in the incidence of adverse effects, cognitive function, MELD score, CP score, oxygen saturation, or respiratory and heart rates before and after sedation. Propofol did not exacerbate minimal HE when compared to midazolam (NCT changed from 87.5 ± 62 s prior to sedation to 74.2 ± 58 s after sedation in the propofol group versus 72.8 ± 62 s before to 85.6 ± 72 s after sedation in the midazolam group; p < 0.01). Time to recovery (4.1 ± 1.9 min vs. 11.5 ± 5.0 min, p < 0.001), and time to discharge (38.0 ± 9 min vs. 110 ± 42 min, p < 0.001) were significantly shorter with propofol than midazolam. Pre- and post-procedure NCT (from 25 ± 20 s to 24 ± 20 s), cognitive function score (from 25 to 26), time to recovery (3.5 ± 1.0 min), and time to discharge (35 ± 10 min) did not change in the healthy controls. CONCLUSIONS: Sedation with propofol has a shorter time recovery and a shorter time to discharge than midazolam and does not exacerbate sub-clinical hepatic encephalopathy in patients with compensated liver cirrhosis.
