Clinical Case Summary

Pancreas divisum is the most frequent pancreatic congenital malformation and results from the failure of fusion of the dorsal and ventral pancreatic ducts during embryogenesis. In these cases, most of the pancreatic exocrine secretion is drained into the duodenum predominantly by the Santorini duct through the minor papilla. It is estimated that 5% of patients with pancreas divisum may present with symptoms, due to raised intrapancreatic dorsal ductal pressure from ductal anomalies.
The authors report a case of a 73-year-old male patient with a history of 6 admissions for acute pancreatitis in the last 12 months. These episodes were of mild severity, without cholestasis or alterations in lipid panel or serum calcium. He had no history of alcohol consumption, neither medication, nor herbal products or drug use. He denied a family history of pancreatic diseases. Between episodes of acute pancreatitis, he was asymptomatic. Magnetic Resonance Cholangiopancreatography showed a tortuous pancreatic duct with prominent caliber, with preferential drainage through the minor papilla (confirming pancreas divisum). Endoscopic ultrasound showed a diffusely dilated and tortuouspancreatic duct. Endoscopic retrograde cholangiopancreatography was performed, with successful sphincterotomy of the minor papilla and placement a pancreatic plastic stent in the Santorini duct. No complications were recorded during the procedure or the subsequent 24-hour clinical monitoring period. Two weeks after the procedure, radiographic control was performed to rule out migration of the pancreatic stent, and its endoscopic removal was accomplished. At 6 months of follow-up, the patient remained asymptomatic, without new episodes of acute pancreatitis.
This case report aims to emphasize that endotherapy for pancreas divisum, including minor papilla sphincterotomy and stenting of dorsal pancreatic duct, allows for improvement of pancreatic ductal drainage and prevention of acute pancreatitis episodes

References

Image list:

1. A tortuous pancreatic duct with prominent caliber (6mm diameter in the cephalic region), with preferential drainage through the minor papilla (Magnetic Resonance Cholangiopancreatography).
2. A diffusely dilated and tortuous Wirsung duct (Endoscopic ultrasound).
3. Successful sphincterotomy of the minor papilla and placement of a 5 Fr x 5 cm pancreatic platic stent in the Santorini duct (Endoscopic retrograde cholangiopancreatography).

Clinical Case Summary

For decompensated advanced chronic liver disease (dACLD) individuals, the onset of refractory ascites (RA) represents a dramatic event (6-month survival rate < 50%). In this setting, a relevant proportion of RA patients develop Hepatorenal Syndrome-Acute Kidney Injury (HRS-AKI) with limited therapeutic and survival chances.
An 81-year-old female dACLD RA patient was admitted to our department to receive large-volume paracentesis (LVP). Eradicated HCV infection, type II diabetes, and chronic obstructive pulmonary disease were her comorbidities.
The AKI onset imposed the intravenous (i.v.) human albumin (HA) (1 g/kg/die) administration, followed by the proper dosage of terlipressin (for HRS-AKI) within the first 72 hours (h), subsequently discontinued due to the persistence of anuria and the worsening of respiratory failure.
To simultaneously address uremic symptoms and facilitate ascites drainage, a Tenckhoff catheter was placed, and peritoneal dialysis (PD) started with a single icodextrin dwell, resulting in the removal of 14 L of ascites and an improvement in AKI within the subsequent 72h. After one week, she was discharged, receiving a specific PD schedule. After the readmission due to the difficulties in administering i.v. HA, we proposed administering HA via the intraperitoneal route, creating an HA-enriched PD (PD+HA) home-performable schedule by adding two vials of 100 ml of HA 20% to 800 ml of icodextrin solution (40 g in 1000 ml/die; lasting: 12 hours; frequency: every other day) (Figure 1).
The patient has been performing this PD schedule for 12 months (~0.5 L of ascites is discharged every other day before performing PD+HA dwell). During the follow-up, no PD-related complications (e.g., peritonitis) and liver-related events requiring hospitalization have been observed.
We report the first successful use of PD+HA, highlighting the cruciality of a multidisciplinary (hepatologists-nephrologists) approach in the management of dACLD-RA HRS-AKI patients.

References

1. Moreau, R.; Delègue, P.; Pessione, F.; Hillaire, S.; Durand, F.; Lebrec, D.; Valla, D.-C. Clinical Characteristics and Outcome of Patients with Cirrhosis and Refractory Ascites. Liver Int 2004, 24, 457–464, doi:10.1111/j.1478-3231.2004.0991.x.
2. Moore, K.P.; Wong, F.; Gines, P.; Bernardi, M.; Ochs, A.; Salerno, F.; Angeli, P.; Porayko, M.; Moreau, R.; Garcia-Tsao, G.; et al. The Management of Ascites in Cirrhosis: Report on the Consensus Conference of the International Ascites Club. Hepatology 2003, 38, 258–266, doi:10.1053/jhep.2003.50315.
3. Nadim, M.K.; Kellum, J.A.; Forni, L.; Francoz, C.; Asrani, S.K.; Ostermann, M.; Allegretti, A.S.; Neyra, J.A.; Olson, J.C.; Piano, S.; et al. Acute Kidney Injury in Patients with Cirrhosis: Acute Disease Quality Initiative (ADQI) and International Club of Ascites (ICA) Joint Multidisciplinary Consensus Meeting. J Hepatol 2024, 81, 163–183, doi:10.1016/j.jhep.2024.03.031
4. Brown, E.A.; Blake, P.G.; Boudville, N.; Davies, S.; de Arteaga, J.; Dong, J.; Finkelstein, F.; Foo, M.; Hurst, H.; Johnson, D.W.; et al. International Society for Peritoneal Dialysis Practice Recommendations: Prescribing High-Quality Goal-Directed Peritoneal Dialysis. Perit Dial Int 2020, 40, 244–253, doi:10.1177/0896860819895364.

Clinical Case Summary

In advanced chronic liver disease (ACLD) patients, the endoscopic evidence of esophageal and/or gastric varices denotes the presence of clinically significant portal hypertension (CPSH), representing the main clinical consequence of portal hypertension (PH).
In this setting, although infrequently, besides typical sites (i.e., esophagus and stomach), PH-related varices can manifest even in other atypical portosystemic-shunt districts, including the vagina. CSPH-related vaginal varices bleeding can occur as a rare complication documented by limited case reports.
A 62-year-old female patient with viral (eradicated Hepatitis C Virus infection)-related- decompensated (grade 2 ascites)-ACLD, complicated by CSPH (grade F2 esophageal varices), was admitted to our Department in February 2025 for microcitic anemia. Anamnesis revealed a previous gastric cancer managed with total gastrectomy resection in 2021.
On admission, abdominal imaging showed radiological signs of ACLD/PH (coarse pattern, splenomegaly, dilated splenic-portal axis). Esophagogastroduodenoscopy ruled out active sources of bleeding, whereas colonoscopy revealed anal congestive not-bleeding varices. During the hospitalization, an episode of metrorrhagia imposed gynecologic evaluation with vaginal speculum examination. This assessment documented vaginal varices with the relative rupture as the current cause of the bleeding, suggesting this site is the further district for (CS)PH manifestation consequently to potentially occurred total gastrectomy-determined changes in abdominal vascular anatomy.
In ACLD patients receiving surgery altering abdominal vascularization, variceal bleeding represents a possible CSPH-related complication occurring even in atypical sites, such as the vagina. This scenario imposes an adequate tailored management, monitoring unusual bleeding signs, and adopting appropriate preventive strategies by including gynecologic evaluation in follow-up.

References

1. McHugh PP, Jeon H, Gedaly R, Johnston TD, Depriest PD, Ranjan D. Vaginal varices with massive hemorrhage in a patient with nonalcoholic steatohepatitis and portal hypertension: Successful treatment with liver transplantation. Liver Transpl. 2008 Oct;14(10):1538-40. doi: 10.1002/lt.21506. PMID: 18825698.
2. Kreek MJ, Raziano JV, Hardy RE, Jeffries GH. Portal hypertension with bleeding vaginal varices. Ann Intern Med. 1967 Apr;66(4):756-9. doi: 10.7326/0003-4819-66-4-756. PMID: 6067181.
3. Chan G, Taqi A, Drage M, Quan D. A case report of massive vaginal variceal hemorrhage in a patient with cirrhosis secondary to nonalcoholic steatohepatitis unresolved even after successful liver transplantation. Transplant Proc. 2013 Mar;45(2):835-7. doi: 10.1016/j.transproceed.2012.04.033. Epub 2012 Sep 19. PMID: 23267803.
4. Lebrec D, Benhamou JP. Ectopic varices in portal hypertension. Clin Gastroenterol. 1985 Jan;14(1):105-21. PMID: 3872747.
5. Nagata J, et al. Vaginal bleeding in a patient with type C liver cirrhosis without a past history of laparotomy: successful treatment with partial splenic artery embolization. Clin J Gastroenterol. 2012 Aug;5(4):275-81. doi: 10.1007/s12328-012-0316-3. Epub 2012 Jun 30. PMID: 26182393.

Clinical Case Summary

Introduction: Cirrhosis complicated by portal hypertension often leads to gastrointestinal bleeding, predominantly from esophageal varices. However, the occurrence of lower GI bleeding from rectal varices and angiodysplasias represents a rarer and more complex clinical scenario. We report the case of a 62-year-old man with cirrhosis and multiple vascular anomalies requiring multidisciplinary management.
Patient observation: The patient, with a history of Type 2 diabetes, coronary artery disease, and prior cholecystectomy, was diagnosed with cirrhosis of presumed autoimmune origin, despite non-confirmatory liver biopsy. He experienced recurrent upper GI bleeding from esophageal varices, managed with beta-blocker therapy. More recently, a massive lower GI bleed led to endoscopic assessment revealing gigantic rectal varices and diffuse colonic angiodysplasias. Stabilisation was achieved by treating the angioddysplasias endoscopically with APC.
Figure 1&2: endoscopic images
Discussion: This case illustrates the difficulty of managing complex portal hypertension complications. While beta-blockers reduce bleeding risk from esophageal varices, rectal varices and angiodysplasias pose additional therapeutic challenges. Endoscopic sclerotherapy, band ligation, or embolization may be required, but their efficacy in diffuse vascular anomalies remains limited. The presence of multiple bleeding sources demands vigilant surveillance and individualized management strategies. Moreover, coexisting comorbidities like diabetes and cardiovascular disease complicate procedural risks and therapeutic decisions.
Conclusion: Managing cirrhosis complicated by giant rectal varices and angiodysplasias requires a multidisciplinary and tailored approach. This case highlights the importance of ongoing surveillance, optimized medical therapy, and readiness for endoscopic or interventional radiology techniques to prevent further decompensations and preserve quality of life.