Assessing Pancreatic Enhancement Variability in ICU Patients with CT Hypoperfusion Complex: A Retrospective
Ana-Maria Ungureanu1,2, Bogdan-Florin Godje3,4,5, Anamaria Alec2
1Department XV, University Clinic of Radiology and Medical Imaging, "Victor Babeș" University of Medicine and Pharmacy, Eftimie Murgu Square, No. 2, 300041 Timișoara, Romania.
Abstract:
Background: The CT hypoperfusion complex describes a constellation of abdominal vascular, visceral, and parenchymal imaging signs occurring in severe systemic hypotension. Among these findings, pancreatic parenchymal enhancement remains controversial, with both hyperenhancement and hypoenhancement described in the literature. Methods: We performed a retrospective single-center analysis of contrast-enhanced abdominal CT examinations obtained between 1 October 2023 and 31 December 2024 in ICU patients with a clinically established diagnosis of shock. Of 266 patients identified using predefined shock-related ICD-10 codes, 94 underwent abdominal CT, and 44 unique patients fulfilled the imaging criteria for CT hypoperfusion complex, with one examination included per patient. Pancreatic attenuation was assessed across arterial, portal venous, and delayed phases and categorized relative to hepatic and splenic parenchyma as hyperenhancing, hypoenhancing, or isoenhancing. Enhancement categories were correlated with available clinical outcome and laboratory data. Results: The final cohort included 44 unique patients, each contributing one CT examination (mean age 59.5 ± 21.2 years; median 66 years; 28/44 women, 63.6%). Abnormal pancreatic enhancement was observed in 31/44 cases (70.5%): 20/44 (45.5%) showed hyperenhancement or mixed hyperenhancing patterns, 11/44 (25.0%) showed hypoenhancement without hyperenhancement, and 13/44 (29.5%) showed isoenhancement in all evaluable phases. In-hospital outcome data were available for 30/44 patients (68.2%). Among patients with known outcomes, mortality was 20/30 (66.7%). In an exploratory complete-case analysis, mortality was higher in patients with abnormal pancreatic enhancement than in those with isoenhancement (15/18, 83.3%, versus 5/12, 41.7%; Fisher's exact p = 0.045; OR 7.0, 95% CI 1.29-37.91). The highest observed mortality proportion was found in the hyperenhancement/mixed group (9/10, 90.0%); however, the global comparison across the three pancreatic enhancement categories did not reach statistical significance (Fisher-Freeman-Halton exact p = 0.064). Therefore, this observed high proportion should be interpreted descriptively and does not establish that the hyperenhancement/mixed group had the worst prognosis. In addition, outcome availability differed according to pancreatic enhancement category, and selection bias cannot be excluded. Conclusions: Pancreatic enhancement variability was common among ICU patients with CT hypoperfusion complex. The observed association between abnormal pancreatic enhancement and all-cause in-hospital mortality was derived from an exploratory, unadjusted complete-case analysis and may reflect the severity of the underlying shock. Because outcome data were missing for 31.8% of patients and outcome availability differed according to pancreatic enhancement category, selection bias cannot be excluded. These findings do not establish a causal or independent prognostic role for pancreatic enhancement.
