Neutral-pH, low-glucose degradation product peritoneal dialysis (PD) solutions are widely used because of their favorable biocompatibility. These solutions are typically packaged in dual-chamber bags and must be mixed immediately before use. Although the mixing procedure is simple, improper preparation may occur, particularly in patients with cognitive impairment, potentially resulting in unintended electrolyte exposure. We report a case of severe hyponatremia with altered mental status associated with inadvertent infusion of an unmixed neutral-pH PD solution in an elderly patient undergoing automated peritoneal dialysis (APD). A man in his eighth decade with diabetic nephropathy and progressive cognitive decline presented with somnolence and severe hyponatremia after a dual-chamber PD bag with an unopened septum was connected. Based on the clinical course and the finding that a PD solution bag with an unopened inter-chamber septum had been connected, hyponatremia due to exposure to an unmixed dialysate compartment was diagnosed. Management consisted of immediate discontinuation of the improperly prepared dialysate and correction using appropriately mixed PD solutions, without administration of hypertonic saline. Serum sodium levels improved gradually without neurological complications, accompanied by recovery of mental status. This case highlights a rare but serious complication related to improper preparation of dual-chamber PD solutions. Increased awareness of this risk and careful monitoring of vulnerable patients, particularly those with cognitive impairment, are essential to ensure safe home PD therapy.

Hepatitis A virus (HAV) and hepatitis E virus (HEV) are common causes of acute viral hepatitis in developing countries where inadequate sanitation and contaminated water supplies facilitate fecal-oral transmission. Although both infections are usually self-limiting, co-infection may result in atypical presentations and pose diagnostic challenges. We report the case of a previously healthy 14-year-old girl who presented with a 5-day history of nausea, vomiting, and anorexia, followed by sudden-onset jaundice and dark urine. She denied fever, abdominal pain, pruritus, bleeding manifestations, or altered mental status. Physical examination revealed marked icterus without hepatosplenomegaly or stigmata of chronic liver disease. Laboratory investigations demonstrated significant hyperbilirubinemia and elevated liver transaminases. Serological testing confirmed acute HAV and HEV co-infection with positive anti-HAV IgM and anti-HEV IgM antibodies. Abdominal ultrasonography showed a normal-sized liver with altered echogenicity and a characteristic "starry sky" appearance, along with gallbladder wall thickening without calculi or sludge. The patient received supportive treatment, including intravenous fluids, antiemetics, and symptomatic care. Her clinical condition improved steadily, with resolution of symptoms and progressive normalization of liver function tests during hospitalization. She was discharged in stable condition and remained asymptomatic at 14-day follow-up, with complete biochemical and radiological recovery. This case highlights that HAV-HEV co-infection can present with isolated jaundice and minimal systemic symptoms despite significant hepatic involvement. Recognition of characteristic imaging findings and timely serological evaluation can facilitate early diagnosis. Favorable outcomes can be achieved with supportive management, while prevention through vaccination, safe drinking water, and improved hygiene remains essential in endemic regions.

While the clinical archetype of 3,4-methylenedioxymethamphetamine (MDMA) toxicity is traditionally associated with young individuals in nightlife environments, particularly in nightclubs and rave settings, its emerging role in therapeutic research may contribute to increasing unsupervised use. As MDMA gains mainstream attention for its potential mental health benefits, particularly for posttraumatic stress disorder, its use may involve a broader demographic, including older individuals in non-recreational contexts. This transition may create a diagnostic pitfall for emergency physicians, particularly through representativeness bias - the tendency to judge a clinical situation based on similarity to a stereotypical category without regard to underlying base rates. When severe hyponatremia occurs in an older patient during a mundane social setting, toxic etiologies may be overlooked, as the presentation does not match the expected profile of MDMA toxicity typically seen in younger individuals. We report a life-threatening case of MDMA-induced hyponatremic encephalopathy in a 55-year-old woman, occurring in a private domestic setting. The patient developed severe hyponatremia with neurological deterioration following self-directed "therapeutic" MDMA use. This case highlights the need to reconsider the demographic and contextual profile of synthetic drug toxicity in the era of emerging psychedelic-assisted therapy research and underscores the importance of maintaining a broad differential diagnosis for unexplained hyponatremia with altered mental status, regardless of patient age or social context.

Leucine-rich glioma-inactivated 1 limbic encephalitis (LGI1-Ab LE) is a rare cause of altered mental status (AMS). Here we present a case of a 59-year-old male who arrived at the hospital with AMS and several months of abnormal movements. He possessed several risk factors for AMS, including intoxication, possible withdrawal, and electrolyte abnormalities. However, due to his atypical symptoms, a thorough evaluation was performed, and a video-electroencephalogram was positive for faciobrachial dystonic seizures (FBDS), which are pathognomonic for LGI1-Ab LE. FBDS are a specific type of seizure characterized by brief ipsilateral contractions of the arm and face. Results from a lumbar puncture later confirmed the diagnosis, which was positive for LGI-1 antibodies. The patient's symptoms improved with systemic steroids and lacosamide. LGI1-Ab LE is the second most common type of autoimmune encephalitis and can be challenging to diagnose. This case highlights important clinical features that can aid in early recognition, leading to improved patient outcomes.

Traumatic brain injury (TBI) can lead to lasting neurological and emotional effects. Latent Toxoplasma gondii (T. gondii) infection, prevalent worldwide, may exacerbate these outcomes by altering immune and neurochemical pathways. This cross-sectional observational study investigated whether chronic T. gondii infection is associated with structural brain differences and long-term outcomes in survivors of moderate-to-severe TBI ≥ 10 years post-injury. 89 TBI survivors (≥10 years post-injury) were recruited from a tertiary-centre database; 35 (39%) tested positive for latent T. gondii via plasma IgG. Thirty-two age- and sex-matched controls without TBI were included (25% T. gondii-seropositive). Nonparametric regression analyses adjusted for age, sex, and intracranial volume, with false discovery rate corrections applied. Primary outcomes were MRI-based measures of white matter microstructure, cortical thickness, and subcortical volumes. Secondary outcomes included neuropsychological assessments of anxiety, depression, cognition, and TBI blood biomarkers. Within the TBI group, T. gondii-positive individuals had reduced fibre density and increased diffusivity in the posterior corpus callosum, increased cortical thickness (insula, cuneus), and reduced brainstem volume. They also reported higher anxiety and mediation analysis showed brainstem volume partially mediated the link between infection and anxiety. Within controls, T. gondii infection was not significantly associated with anxiety, cognition, white matter microstructure, or blood biomarkers. However, controls with T. gondii infection did have increased cortical thickness in the left inferior temporal gyrus and reduced volume in the left caudate compared to their uninfected counterparts. Taken together, latent T. gondii infection may alter brain structure and exacerbate anxiety in chronic TBI. These findings support considering infection status in TBI prognostics and call for further research into its mechanistic and clinical implications.

Perforated duodenal ulcers represent a surgical emergency requiring prompt operative intervention. The Graham omental patch is the most commonly performed procedure for emergent repair; however, postoperative findings suggestive of leakage remain a serious concern and are associated with significant morbidity and mortality. Traditionally, suspected postoperative leaks have prompted early surgical re-exploration due to the risk of peritonitis and sepsis. However, select patients with concerning postoperative findings may be managed successfully with appropriate drainage, decompression, and nutritional support. We present the case of a 79-year-old male patient who was brought to the emergency department with progressive altered mental status and generalized abdominal pain. Imaging revealed findings consistent with a perforated duodenal ulcer, and the patient underwent emergent exploratory laparotomy with Graham patch repair and placement of a Jackson-Pratt drain. During the postoperative period, bilious output from the drain raised concern for a possible duodenal leak. A contrast-enhanced CT scan with enteric (oral) contrast demonstrated contrast entering the drain, prompting surgical re-exploration. Intraoperatively, the previous repair was found to be intact without evidence of active leakage; instead, a retroperitoneal abscess extending along the duodenal sweep was identified and drained. With continued supportive management, including nasogastric decompression, antibiotics, proton-pump inhibitor therapy, and nutritional support via gastrostomy tube, the patient demonstrated progressive clinical improvement. Drain output gradually diminished and ceased, consistent with resolution of the postoperative process. This case highlights that postoperative findings suggestive of duodenal leak may not represent true failure of the primary repair and underscores the importance of correlating radiologic, intraoperative, and clinical findings. Careful assessment and appropriate supportive management may allow for favorable outcomes in selected hemodynamically stable patients following Graham patch repair.

Malignant catatonia is a rare but life-threatening neuropsychiatric emergency characterized by catatonic features, autonomic instability, and fever. Prompt recognition is essential to avoid serious complications. We report a case of a 49-year-old Filipino male with schizoaffective disorder who presented with altered mental status and persistent fever. Initial investigations revealed severe hyponatremia, which was corrected, yet the patient remained encephalopathic. Despite an extensive workup, no infectious or structural cause was identified. He exhibited classic catatonic signs, including mutism, stupor, and echophenomena. A Bush-Francis Catatonia Rating Scale helps to support the diagnosis of malignant catatonia. Treatment with lorazepam led to rapid clinical improvement and resolution of fever. This case underscores the diagnostic complexity of malignant catatonia, particularly when presenting with fever and altered consciousness. Differentiation from neuroleptic malignant syndrome and encephalitis is critical due to differing management strategies.

Hyperammonemia is an idiosyncratic adverse effect associated with valproic acid (VPA). We report 2 patients with neurocognitive disorder who were prescribed low doses of VPA for neuropsychiatric symptoms associated with neurocognitive disorder, and they presented with changes in behavior. On workup, both patients had elevated ammonia concentrations. The aims of the case report are to highlight the importance of laboratory testing for ammonia concentrations in patients with altered mental status especially in the setting of VPA therapy irrespective of the dosage and to discuss possible mechanisms associated with VPA-induced hyperammonemia.

Human granulocytic anaplasmosis (HGA) is a tick-borne disease endemic to the northeastern United States but remains extremely rare in Japan. We report an imported case of HGA in a 77-year-old man who had recently traveled from the United States. He presented with a 5-day history of fever, lethargy, and loss of appetite, followed by altered consciousness. Laboratory findings revealed thrombocytopenia, elevated transaminases, and increased creatine kinase levels. Computed tomography was unremarkable except for mild splenomegaly. Considering his recent stay in Bemidji, Minnesota-a region with a high risk of tick exposure-empirical doxycycline therapy was promptly initiated for suspected tick-borne illness. Although indirect immunofluorescence antibody (IFA) assays for IgM and IgG against Anaplasma phagocytophilum were negative at admission, polymerase chain reaction (PCR) testing of whole blood targeting the groEL gene yielded a positive result. Sequence analysis revealed complete (100%) identity of the amplified 16S rRNA, groEL, and p44 fragments with reference A. phagocytophilum sequences (CP000235). These findings confirmed the diagnosis of HGA. The patient responded rapidly to doxycycline therapy and was discharged on hospital day 5. This case highlights the diagnostic value of molecular methods during the early phase of infection, when serology may remain negative, and underscores the importance of considering travel and tick exposure history when evaluating febrile patients.

Small bowel neuroendocrine tumours (NETs) are uncommon neoplasia that often occur with non-specific gastrointestinal symptoms, leading to considerable delays in diagnosis and treatment, and overlapping findings that often distract the clinical focus from the underlying pathology. We present the case of a 49-year-old woman who reported to us with a one-month history of epigastric pain, nausea, vomiting, and unintentional weight loss of about two stones. Initial imaging showed deranged liver markers and cholelithiasis on ultrasound without biliary enlargement, which resulted in a tentative diagnosis of cholecystitis. On the third day of admission, the patient acutely worsened with intense pain in the abdomen, distension, refractory vomiting, and hyperlactatemia. Acute small bowel obstruction was shown on urgent computed tomography, and an emergency laparotomy was undertaken, which revealed a circumferential stricturing ileal tumour with mesenteric lymphadenopathy, and surgical resection was done. Acute confusion and altered mental status complicated the postoperative course, necessitating further workup, which included metabolic screening, cerebral spinal fluid analysis, and neuroimaging, but they all came back clear, and the episode was considered postoperative delirium. While tumour markers were normal, histopathology revealed a well-differentiated Grade 1 NET with muscularis propria invasion and focal subserosa involvement. One-month follow-up CT showed no residual or recurrent disease, and a surveillance plan was laid out at a special NET multidisciplinary team meeting. The case underscores the difficulties in diagnosing small bowel NETs in cases where the incidental findings mask the initial pathology. This case highlights the significance of considering a wider range of differential diagnoses in patients presenting with unclear gastrointestinal symptoms to avoid potential delays in investigations and further treatment.