Clinical Case Summary

A 23-year-old female presented with epigastric pain, jaundice, and elevated liver enzymes. Imaging confirmed a mildly dilated common bile duct (CBD) with multiple filling defects. ERCP revealed a normal ampulla and a half-sphincterotomy was performed with three stones retrieved via balloon trawl. The procedure was uneventful, and she was discharged the same day.
Three days later, she re-presented with dizziness, melaena, and a haemoglobin drop from 127 g/L to 85 g/L. Gastroscopy demonstrated active oozing from the sphincterotomy site, managed successfully with placement of a fully covered metal stent (FCMS). She remained stable and was discharged with outpatient follow-up.
Three weeks later, she re-presented with partial stent blockage and underwent repeat ERCP for stent removal and duct clearance. Within 24 hours, she developed acute left shoulder tip and chest pain. Cardiac investigations were negative. CT imaging demonstrated a large haemoperitoneum and a bulging splenic haematoma without active bleeding, confirmed on a diagnostic laparoscopy .
She was managed conservatively in intensive care and follow up imaging confirmed complete resolution of the haematoma.
This case illustrates splenic haematoma as a rare yet significant complication of ERCP, with only a handful of cases described in the literature. Proposed mechanisms involve shear forces transmitted via the splenogastric ligament, typically in patients with known risk factors such as intra-abdominal adhesions, previous surgery, chronic pancreatitis, or cirrhosis. However, this case highlights its occurrence in a young, healthy patient with no risk factors, suggesting procedural technique or anatomical variation to be a potential trigger for injury. Symptoms such as shoulder or upper quadrant pain following ERCP should prompt consideration of splenic injury. Early recognition is key, as many cases resolve with conservative management but may carry a risk of life-threatening bleeding if unrecognised.

References

MRCP Image Demonstrating CBD Filling Defects
Coronal MRCP showing a mildly dilated common bile duct with multiple signal voids consistent with choledocholithiasis.
ERCP Image Showing Duct Clearance
Fluoroscopic image during ERCP showing balloon trawl and retrieval of multiple CBD stones following half-sphincterotomy.
Blood Results Demonstrating Haemoglobin Drop
Laboratory panel showing haemoglobin decline from 127 g/L to 85 g/L following gastrointestinal bleeding.
Gastroscopy Image Demonstrating Oozing and FCMS Placement
Endoscopic image showing active oozing at the sphincterotomy site and successful placement of a fully covered metal stent.
CT Image of Splenic Haematoma
Axial CT abdomen showing extensive haemoperitoneum and a bulging splenic haematoma in the left upper quadrant.
Follow-up CT Confirming Resolution
Interval CT imaging showing complete resolution of the previously identified splenic haematoma.

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

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

We report a rare and fatal case of diffuse hepatic hemangiomatosis (DHH) in a 50-year-old male presented with acute painless jaundice of 10 days’ duration, dark urine, and hepatosplenomegaly. Laboratory workup revealed normocytic anemia, indirect hyperbilirubinemia, and elevated LDH levels, suggesting hemolysis, though the direct Coombs test was negative. Liver function tests showed cholestatic and hepatocellular injury patterns, while creatinine and coagulation profiles were initially normal. Abdominal ultrasound and triphasic computed tomography demonstrated hepatosplenomegaly and multiple hepatic focal lesions with peripheral nodular enhancement and centripetal fill-in. Liver biopsy revealed markedly dilated sinusoids without malignant infiltration. Unlikely, the patient developed acute kidney injury, hematemesis, and hepatic encephalopathy, culminating in death from liver failure within one month from the onset of his illness.

Clinical Case Summary

Drug-induced liver injury is an adverse effect of many pharmaceutical agents. Alverine citrate, an antispasmodic agent found in the fixed-dose combination Meteospasmyl (alverine citrate and simethicone), is widely used in functional gastrointestinal disorders. To date, only three cases are published in the literature. We report a case, with strong evidence, including a rechallenge confirming the causality.
Patient Observation: A 43-year-old woman presented with biliary-type abdominal pain. Her medical history was limited to hypertension treated with bisoprolol with no alcohol use or recent medication. Abdominal ultrasound revealed uncomplicated cholelithiasis; liver tests were normal. Alverine citrate was prescribed for symptomatic relief. Within two weeks, she developed jaundice and fatigue with a normal clinical examination. Blood tests showed severe hepatocellular injury: ALT and AST were 22× and 39× ULN, bilirubin was 274 µmol/L, and GGT/ALP were mildly elevated. Viral and autoimmune panels were negative. Imaging excluded biliary obstruction. Liver biopsy revealed portal inflammation with eosinophilic infiltrates, suggestive of immunoallergic hepatitis. The discontinuation of the drug led to normalization of liver enzymes. 3 years later, the patient was inadvertently re-exposed to alverine citrate, triggering a reproducible episode of acute hepatitis, thereby confirming causality. Diagnostic probability was assessed with the RUCAM score (12, "highly probable") and Naranjo scale (8, "probable"). Only three prior cases of alverine citrate-induced hepatitis, none of which reported a confirmed rechallenge. Although liver biopsy is not routinely required in DILI, it was essential here for diagnostic clarification.
Alverine citrate should be recognized as a rare cause of acute hepatitis. This case confirms its hepatotoxic potential and underscores the importance of early recognition and drug withdrawal to prevent recurrence.

References

1. RUCAM Scale: https://clincasequest.hospital/rucam-scale/
2. Naranjo Scale: https://proeurodilinet.eu/wp-content/uploads/2019/03/Causality-assessment-training-course-15-MARCH-.pdf
3. Couzigou P et al. Hepatitis and Alverine Citrate. J Hepatol. 1997. https://www.sciencedirect.com/science/article/abs/pii/S0168827897801870
4. Turkish case report. Turk J Gastroenterol. 2004. https://pubmed.ncbi.nlm.nih.gov/15259090/
5. Korean case report. Korean J Hepatol. 2010. https://pubmed.ncbi.nlm.nih.gov/20375645/
6. Simethicone safety review. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4033443/
7. Zhang X et al. Histopathologic Manifestations of Drug-induced Hepatotoxicity. Clin Liver Dis. 2013.

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.

Clinical Case Summary

Although liver involvement is common in leukemia, acute hepatitis as its initial presentation is rare. This case highlights the diagnostic challenge of distinguishing reactive hematological changes from underlying malignancies in patients with unexplained hepatitis.
A 35-year-old woman presented in February 2024 with myalgias, fever with chills (38°C), jaundice, and right upper quadrant discomfort. Relevant history included recent intake of herbal supplements (vitamin C, zinc, echinacea, elderberry).
Initial laboratory findings showed leukocytosis, lymphocytosis (25%), monocytosis (12%), blasts (3%), thrombocytopenia (136×10⁹/L), and abnormal liver tests (AST 448 U/L, ALT 686 U/L, ALP 242 U/L, GGT 147 U/L, total bilirubin 4.14 mg/dL, direct bilirubin 2.9 mg/dL), with normal INR. Peripheral blood smear revealed mononuclear pleomorphism and lymphocytes with prominent nucleoli. Abdominal computed tomography showed moderate hepatomegaly without biliary or vascular abnormalities. Comprehensive testing for infeccious, autoimmune and metabolic causes was negative.
Liver tests improved and leukocytosis turned into leukopenia. Repeat blood smear was deemed reactive by Hematology. She was discharged and in early March re-evaluation, liver parameters normalized and leukopenia improved.
Later that month, she returned with fever, night sweats, and abdominal pain. Laboratory findings showed recurrent cytopenias and cytocholestasis. Blood smear revealed increasing blast count, and immunophenotyping suggested monoclonality. Bone marrow and liver biopsy confirmed B-cell acute lymphoblastic leukemia (ALL) with hepatic infiltration.
This case illustrates an unusual presentation of ALL as relapsing acute hepatitis. It reinforces the need to consider hematological malignancy in cryptogenic hepatitis, particularly when associated with evolving hematological changes. Serial blood smears, immunophenotyping, and timely bone marrow evaluation are essential to avoid diagnostic delay.

References

1. Hepatic biopsy: clusters of intermediate to large cells expressing TdT, CD20, PAX5, CD10, BCL6, CD43.
2. Bone marrow aspirate: 64% blasts, CD10+, CD20+ (strong homogeneous expression).
3. Bone marrow biopsy: increased cellularity due to diffuse interstitial infiltration by intermediate cells with blast-like morphology and lymphoid immunophenotype (TdT+, CD34+, MPO-, CD20+).