Clinical Case Summary

A 24-year-old male presented with jaundice and mild vertigo after a 10-day prodrome (asthenia, nausea, headache, fever). Ibuprofen (1200 mg/d) was taken for these symptoms only during the first 5 days. Labs revealed acute hepatocellular injury and elevated cholestasis (AST 215, ALT 862, FA 134, GGT 126 IU/L), marked mixed hyperbilirubinemia (Total 13.5 mg/dL, Direct 7.58 mg/dL) and coagulopathy (INR 1.59). Ultrasound showed hepatosplenomegaly. Viral hepatitis (HAV/HBV/HCV/CMV) and autoimmune/metabolic causes were excluded. Epstein-Barr Virus (EBV) serology showed low-titer positive VCA IgM but negative VCA IgG, EBNA IgG, and serum EBV DNA PCR, indicating recent non-active infection. Given ibuprofen timing and high RUCAM score, drug-induced liver injury (DILI) with a hepatocellular pattern was suspected. Liver biopsy confirmed acute hepatitis with lymphomonocytic infiltrate, necrosis and canalicular cholestasis. Despite improving liver function tests post-ibuprofen cessation, he developed worsening vertigo, severe ataxia, nausea, vomiting, hypophonia, necessitating nasogastric feeding/bed confinement. Cerebrospinal fluid (CSF) showed mild mononuclear pleocytosis (16 cells/mm³); a multiplex PCR pathogen panel (including EBV) was negative. Brain MRI/EEG were normal. Post-infectious EBV acute cerebellar ataxia was diagnosed concurrently with DILI, based on timing post-recent EBV, exclusion of active neurological infection (negative CSF PCR, normal imaging), mild pleocytosis, and supported by later IgG seroconversion. IV methylprednisolone treatment, chosen for clinical severity, led to significant neurological improvement within days and eventual recovery after physiotherapy. This case highlights the significant challenges of diagnosis and management of concomitant DILI and recent EBV infection with neurological sequelae, requiring careful differentiation of liver damage patterns (hepatocellular DILI vs cholestatic EBV) and optimal management of neurological symptoms.

References

Illustrative Material References:
- Liver biopsy histology slides (highlighting lymphomonocytic infiltrate, necrosis, and canalicular cholestasis characteristic of DILI).
- Table/Graph showing serial Liver Function Tests (AST, ALT, Bilirubin) over time, depicting injury peak and recovery trend.
- Table summarizing sequential Epstein-Barr Virus (EBV) serology results (VCA IgM, VCA IgG, EBNA IgG) demonstrating seroconversion.
- Table summarizing Cerebrospinal fluid (CSF) analysis results (cell count, protein, glucose, negative multiplex PCR).
- Representative Brain MRI images (axial/sagittal views) confirming absence of structural lesions or encephalitis signs.

Introduction

Artificial intelligence (AI) characterization (CADx) systems for colonic polyps exhibit high diagnostic accuracy. However, they may only support, not replace, clinical decision-making and little is known of this human-AI interaction – even less so with trainee endoscopists. This issue is difficult to explore, but data from a study investigating CADx-supported trainee endoscopists compared to AI-blinded experts could give insight.

Aims & Methods

This analysis draws on data from a prospective observational study comparing the diagnostic performance of CADx-supported trainee endoscopists (using GI Genius®, Medtronic) to expert endoscopists blinded to AI support. Two key scenarios were explored: (a) instances in which the CADx system produced a ‘no prediction’ output, and (b) cases where trainees actively overruled AI-generated diagnoses. These were assessed to examine the impact of AI absence and human-AI discordance on diagnostic accuracy.

Results

The baseline cohort included 11 trainees performing 225 colonoscopies, mean age 63.8 years (SD 12.7), 48.9% male patients. Baseline ADR was 57.8%. Of 630 resected lesions (median size 3 mm, IQR 2;4), 40.0% were in the rectosigmoid, and 53.6% were non-adenomatous. CADx failed to provide a prediction in 19.2% (n=121) of cases. These ‘no prediction’ polyps were smaller (median 3 mm, p=0.048) and more often located in the right colon (72% vs. 58%, p=0.005. In the absence of AI support, trainee diagnostic accuracy declined significantly by 12.8% (63.6% vs. 76.4%, p=0.007). Interestingly, expert endoscopists—despite being blinded to AI—also performed worse on these polyps (64.7% vs. 73.9%, p=0.045), suggesting an inherent difficulty in classifying these lesions.
Trainees overruled AI suggestion leading to discordant diagnoses in 9.0% (57/630) of polyps, comprised of 20 (35.1%) non-adenomatous, and 37 (64.9%) adenomatous lesions. Trainees incorrectly overruled AI in 59.6% (34/57), which mostly consisted of downgrading lesions to NICE 1. Discordant polyps did not differ in size (3 mm vs. 3 mm, p=0.413), but were more often located proximally (77.2% vs. 58.1%, p=0.005). The difference in false negative rate (FNR) between trainees and AI was 62.16% (81.07% vs. 18.92%, p<0.0001), demonstrating a risk of missed adenomas when trainees override AI. Blinded expert endoscopists achieved identical overall diagnostic accuracy in those polyps as the AI system (59.6%). However, their error profiles differed – In this subset, blinded experts and AI performed equally in overall accuracy (59.6%), although with differing error profiles: AI showed a numerically lower FNR (18.9% vs. 35.1%, Δ16.2%, p=0.17), offset by a higher false positive rate (80.0% vs. 50.0%).

Conclusion

CADx systems generate ‘no prediction’ outputs in a substantial proportion of polyps, significantly impairing trainee diagnostic performance. These cases may represent inherently more challenging lesions. Despite CADx’s high accuracy, trainees overrule AI in almost every tenth polyp, most often incorrectly downstaging polyps. Structured training on appropriate use of CADx, emphasizing both its capabilities and limitations, may enhance clinical effectiveness. Further research on human-AI interaction and trust is warranted, as these factors will be critical for successful integration of CADx into routine endoscopic practice.

Disclosure

The original study (AC-CADx) received technical support by Medtronic. Medtronic was not involved in the design of the study or analysis of the data, neither in the original study nor this exploratory analysis.

Introduction

Massive gastrointestinal bleeding is a clinical condition that is poorly studied due to its abrupt presentation, involvement of various clinical services, and the high and rapid mortality of patients. We present the preliminary results of a multicenter registry that includes 21 hospitals from Spain and Hispanic America, analyzing factors related to mortality and need for intervention.

Aims & Methods

Since January 2023, 403 patients over 18 years old who presented to the emergency departments of participating hospitals with massive gastrointestinal bleeding, defined as bleeding accompanied by signs of shock and requiring transfusion of at least 2 units of blood within the first 24 hours of admission, were included. Demographic variables, comorbidities, treatments including NSAIDs, antiplatelets, and anticoagulants, clinical presentation variables, medical, endoscopic, and surgical variables, and a 6-month follow-up were collected.
The aim of this study was to analyze factors related to mortality and the need for intervention in patients with massive gastrointestinal bleeding.

Results

A total of 403 patients with a mean age of 64.5 ± 15.7 years were included (male 68.7%). Main comorbidities were cirrhosis (31%), diabetes (28%) and a previous UGIB (25%). 8.4% of patients had already been admitted to the hospital, and 29% were on antithrombotic (16.6% antiplatelets and 16.4% anticoagulants). On admission we observed SPB: 91±22 mmHg, heart rate 101 ± 21; and an altered mental status in 31%. Mean hemoglobin levels 7.6±2.5 g/dl, urea: 98±67, albumin 2.16±1.3, INR: 3.9±7. The most common causes were esophageal varices (29%), gastric ulcer (25%) and duodenal ulcer (25%). Endoscopic intervention was needed in 60%, with mortality rate of15.4%. Mean admission was 8.6±10 days, and patients needed 4±3 red blood cells units. When analyzing in-hospital mortality, we observed that the age of patients who died was higher than that of survivors (68.2±15 vs. 63.6±16; p=0.033), with the former requiring more packed red blood cells (5±5.5 vs. 3.5±2; p=0.043). Patients who died had a lower frequency of gastric ulcer (14% vs. 27%; p=0.034), a higher frequency of altered mental status (42.6% vs. 29%; p=0.036), and a lower rate of endoscopic therapy applied (43.3% vs. 63.6%; p<0.0001). In logistic regression, gastric ulcer etiology and endoscopic therapy were protective factors against mortality (Table 2).
Regarding the need for intervention, more patients with liver cirrhosis required it (73% vs. 60%, p=0.018), patients with hematemesis (73% vs. 52%; p<0.0001), patients without melena (60% vs. 76%; p=0.002), with syncope (76.3% vs. 61%; p=0.06), etiologies other than gastric ulcer (78% vs. 56%; p=0.028), and the presence of esophageal varices (83% vs. 57%; p<0.0001). In binary logistic regression, liver cirrhosis, hematemesis, and syncope were risk factors for the need for intervention.

Conclusion

Age, altered mental status, and lower frequency of endoscopic therapy are risk factors for mortality due to massive gastrointestinal bleeding. Gastric ulcer as an etiology and receiving endoscopic therapy acted as protective factors against mortality. Indeed, in both situations, it might be related to an opportunity window to receive appropriate treatment, especially when compared with more cataclysmic types of bleeding, such as variceal or posterior duodenal bulb wall, which sometimes can be challenging and utterly abrupt. Regarding the need for intervention, liver cirrhosis, hematemesis, and syncope were independent risk factors for the need for endoscopy, surgery, or interventional radiology.