2 articles
The clinical value of admission intra-abdominal pressure in patients with decompensated liver cirrhosis and refractory ascites remains insufficiently defined, particularly in relation to the different phenotypes of ascitic fluid infection.
An exploratory observational analysis was performed on a structured dataset that included 100 patients with decompensated liver cirrhosis, refractory ascites, and a Child-Pugh class C score. All patients had the results of the diagnostic paracentesis performed at admission and the transvesical measurement of intra-abdominal pressure available. Ascitic fluid phenotypes were defined on the basis of the polymorphonuclear cell count and the ascitic culture result: spontaneous bacterial peritonitis, bacterascites, and sterile ascites. Intra-abdominal hypertension was defined as an intra-abdominal pressure ≥12 mmHg. The primary objective was the comparison of admission intra-abdominal pressure among phenotypes. The secondary objectives consisted of examining the associations between admission intra-abdominal pressure and acute kidney injury, sepsis, acute-on-chronic liver failure, and the need for intensive care.
The cohort included 22 patients with spontaneous bacterial peritonitis, 10 with bacterascites, and 68 with sterile ascites. Median admission intra-abdominal pressure differed significantly among phenotypes, being highest in spontaneous bacterial peritonitis and lower in bacterascites and sterile ascites: 16.9 (15.2–17.9), 13.4 (11.7–15.4), and 13.4 (12.1–14.6) mmHg, respectively (p<0.001). Intra-abdominal hypertension was present in all patients with spontaneous bacterial peritonitis, in 60.0% of those with bacterascites, and in 75.0% of those with sterile ascites. In adjusted logistic models, each 1-mmHg increase in admission intra-abdominal pressure was independently associated with spontaneous bacterial peritonitis (odds ratio [OR] 3.06; 95% confidence interval [CI] 1.56–6.02), any infected ascites (OR 1.56; 95% CI 1.20–2.02), sepsis (OR 2.12; 95% CI 1.44–3.12), acute-on-chronic liver failure (OR 1.43; 95% CI 1.09–1.86), and the need for intensive care (OR 1.40; 95% CI 1.06–1.83), but not with acute kidney injury (OR 0.91; 95% CI 0.73–1.14).
Higher admission intra-abdominal pressure was associated with a higher probability of spontaneous bacterial peritonitis and with a more severe in-hospital course. Admission intra-abdominal pressure did not show an independent association with acute kidney injury and appears to reflect mainly infectious and general clinical severity.
Evidence on umbilical hernia repair in patients with decompensated cirrhosis, ascites, and Child–Pugh class C is limited. In this population, outcomes after emergency repair may reflect both the urgency of the presentation and the greater hepatic, renal, inflammatory, and metabolic derangement present at the time of surgery.
This retrospective single-center cohort study included all 40 eligible adults with decompensated cirrhosis, ascites, and Child–Pugh class C at admission who underwent open primary non-mesh umbilical hernia repair between January 2019 and December 2025. Twenty patients underwent elective repair, defined as definitive repair scheduled after a short period of inpatient optimization, and 20 underwent emergency repair after limited stabilization because an acute hernia-related indication made postponement unsafe. The primary outcome was all-cause 30-day mortality. Secondary outcomes were in-hospital mortality, acute kidney injury, sepsis, wound infection, persistent ascitic leakage, reoperation, length of hospital stay, and early postoperative clinical-biochemical status. Analyses were unadjusted and exploratory; no multivariable model was fitted.
At admission, the emergency group had higher total bilirubin, international normalized ratio, creatinine, leukocyte count, Child–Pugh score and MELD-Na score, and lower serum albumin and sodium (all p ≤ 0.006). During a median elective optimization interval of 4.5 (3.0–6.0) days, the MELD-Na score decreased by a median of 2 (1–3) points. On postoperative days 2–3, every reported clinical-biochemical indicator remained less favorable in the emergency group. Median hospital stay was 14.5 versus 11.0 days (p = 0.038). Thirty-day mortality was 35.0% versus 10.0% (risk difference 25.0%, 95% confidence interval −1.3 to 47.9; p = 0.127).
Patients undergoing emergency repair reached surgery with substantially greater clinical and biochemical derangement, had a less favorable early postoperative profile and stayed longer in the hospital, while the mortality difference did not reach statistical significance. Because operative timing was determined by the clinical course, the groups were not comparable at baseline and no causal effect of urgency or of preoperative optimization can be inferred. The findings support early multidisciplinary assessment while an elective operative pathway remains feasible.