The treatment of quetiapine and/or citalopram poisoning is mainly supportive and involves gastric lavage, activated charcoal, intubation, and mechanical ventilation. Recently, however, there were reports of successful treatment with intravenous lipid emulsion. Here we report a case of a 19-year-old Caucasian girl who ingested approximately 6000 mg of quetiapine, 400 mg of citalopram, and 45 mg of bromazepam in a suicide attempt. The patient developed ventricular tachycardia and epileptic seizures 12 h after admission to the hospital. As the patient's condition deteriorated, we combined standard therapy (intubation, mechanical ventilation, and vasopressors) with low-dose intravenous lipid emulsion (ILE) (a total of 300 mL of 20 % lipid emulsion) and normalised her heart rhythm and stopped the seizures. She was discharged to the psychiatric ward after 48 h and home after a prolonged (2-month) psychiatric rehabilitation. Intravenous lipid emulsion turned out to be effective even in the lower dose range than previously reported for quetiapine poisoning in patients presenting with seizure and ventricular arrhythmia. To our knowledge, there are no case reports describing the use of ILE in treating citalopram poisoning.

Cytomegalovirus (CMV) is a common cause of infection in immunocompromised individuals, such as patients with hematological malignancies or AIDS, but can also occur in patients with other acquired immunodeficiencies. In tissue-invasive diseases, CMV diagnosis requires CMV DNA in the plasma and the histological confirmation of CMV in a tissue or organ. Evidence of CMV colitis requires a characteristic endoscopic picture with ulcers with a well-defined, convex appearance and CMV viral inclusions in the form of an “owl’s eye” on mucosal sections stained with hematoxylin and eosin. CMV-specific immunohistochemistry is the gold standard for identifying CMV in tissue biopsies. It is important to consider a CMV infection in the diagnostic process, as it may delay the diagnosis and the treatment. We present the case of a 78-year-old patient with amiodarone interstitial lung disease who was treated with methylprednisolone. Two weeks after the start of his treatment, he was admitted to the hospital for acute gastroenterocolitis and Addisonian crisis. An examination had confirmed a tissue-invasive CMV disease. He was treated with valganciclovir for a total of six weeks. After the completion of treatment, the patient showed no clinical signs of CMV infection, and both laboratory and histological examinations revealed no residual CMV disease. Tissue-invasive CMV disease can occur in patients with acquired immunodeficiency, which may result from various causes, including glucocorticoid treatment.

We present the case of a 58-year-old female with a history of a bleeding duodenal peptic ulcer. Endoscopic hemostasis was unsuccessful; therefore, a transcatheter arterial embolization of a culprit vessel was performed. She was admitted to the hospital two months later because of obstruction of the common bile duct with cholangitis. Attempts to endoscopically place a biliary stent failed. The treating medical team opted for a surgical choledocho-jejunostomy. After 20 months, she presented with a melena and a severe anemia. Diagnostic work-up revealed portal vein thrombosis with portal cavernoma and bleeding choledocho-jejunostomy varices. The case presents and discusses rare complications of duodenal ulcer disease, as well as possible causes and treatment options.

A 75 years old male presented to the Emergency Department (ED) with an unexplained hypotension. With a wide differential diagnosis we concluded it could be attributed to an unusually high antihypertensives dosage the patient was receiving, we started treating it as a calcium channel blocker (CCB) toxicity with success. The case report reviews the case with measured levels of medications and reviews treatment of CCB toxicity with current guidelines for treatment.

Background: Endoscopic retrograde cholangiopancreatography is an established therapeutic modality for pancreaticobiliary disease. Congenital anatomical anomalies, including situs inversus totalis and rare hepatobiliary malformations, substantially increase the technical complexity of endoscopic retrograde cholangiopancreatography and are seldom encountered in clinical practice. Published experience is limited predominantly to individual case reports and smaller case series. Methods: We present a report of three patients who underwent endoscopic retrograde cholangiopancreatography: two with situs inversus totalis and choledocholithiasis complicated by acute cholangitis, and one with a rare congenital anomaly consisting of a completely separated right hepatic lobe combined with choledocholithiasis. Results: Successful endoscopic retrograde cholangiopancreatography was achieved in all three patients. In both situs inversus totalis cases, biliary cannulation and stone clearance were accomplished using modified endoscopic techniques, including endoscope rotation and positional adjustments, without procedural complications. In the patient with the separated hepatic lobe, endoscopic retrograde cholangiopancreatography allowed common bile duct stone clearance; however, an attempted mechanical lithotripsy of a gallbladder calculus resulted in basket entrapment, necessitating surgical treatment. Conclusions: Endoscopic retrograde cholangiopancreatography is feasible and effective in patients with congenital hepatobiliary anomalies, but demands meticulous pre-procedural planning, thorough anatomical understanding, and technical versatility. A cautious step-by-step approach and readiness to adapt technique are essential to optimise outcomes and minimise risk.