Metformin is widely prescribed for type 2 diabetes mellitus and is generally considered safe. However, metformin-associated lactic acidosis (MALA) is a rare but potentially fatal complication. Although typically associated with renal or hepatic dysfunction, intentional overdose can also lead to severe acidosis and high mortality. A 42-year-old woman with no medical history ingested 12 g of metformin in a suicide attempt. She presented with stable vital signs and normal renal and hepatic function. Initial arterial blood gas showed metabolic acidosis (pH 7.21, HCO3− 12 mmol/L, lactate 8 mmol/L). Intermittent hemodialysis was initiated, but her acidosis worsened. She developed hypotension requiring norepinephrine and subsequently deteriorated neurologically. Despite 2 hemodialysis sessions, she progressed to cardiac arrest and died. This case demonstrates that massive metformin overdose can overwhelm normal metabolic and clearance mechanisms, resulting in refractory lactic acidosis. Even with early hemodialysis, tissue sequestration of metformin and ongoing mitochondrial dysfunction may sustain lactate overproduction. Massive metformin overdose can be fatal even in healthy individuals. Close monitoring is essential, and prolonged or continuous renal replacement therapies may be warranted when initial dialysis fails to correct severe acidosis.

Background: Patients with heart failure (HF) admitted to the intensive care unit (ICU) often require respiratory support, yet comparative data on different respiratory modalities in this population remain limited. The aim of our study was to analyze clinical characteristics and outcomes of HF patients in the ICU receiving various respiratory therapies, while also identifying factors associated with mortality. Methods: This retrospective observational study categorized patients (n = 692) based on their respiratory treatments into four groups: no treatment (T-NR; n = 280); oxygen therapy (T-O₂; n = 220); non-invasive mechanical ventilation (T-NIMV; n = 99); and invasive mechanical ventilation (T-IMV; n = 93). The groups were compared in terms of clinical characteristics, laboratory values at ICU admission and discharge, length of stay, and outcomes. Results: The T-IMV group had significantly higher Acute Physiology and Chronic Health Evaluation II (APACHE II) and updated Charlson Comorbidity Index scores, alongside lower ejection fractions and higher rates of vasopressor/inotrope use (p < 0.05). This group also exhibited higher mortality, longer ICU stays, and more adverse laboratory profiles (elevated lactate, creatinine, N-terminal pro-B-type natriuretic peptide-NT-proBNP, bilirubin; lower albumin). Multivariable analysis confirmed that the APACHE II score, vasopressor/inotrope requirement, and lactate and NT-proBNP levels (at admission) were independently associated with mortality (p < 0.05). Conclusions: Patients requiring IMV demonstrated greater severity of illness, as reflected by higher APACHE II scores, elevated NT-proBNP and lactate levels at admission, as well s increased requirement for vasopressor/inotrope therapy. These variables were associated with mortality, suggesting that the poorer prognosis observed in the IMV group was due to their underlying disease burden.

We aim to present an 80-year old male who has a history of Ozaki’s procedure and presented with 2 weeks of diarrhea and fever. The patient was screened for gastrointestinal diseases and in conclusion he was diagnosed with infective endocarditis according to modified Duke criteria. The patient was started on appropriate intravenous antibiotics. Prolonged diarrhea could be a presenting symptom and should be further evaluated. Reconstructive cardiac valve surgery techniques which are used in the management of IE may be the cause of IE.

A 30-year-old previously healthy male presented to the emergency department with malaise, nausea, and abdominal pain. He was alert and oriented but in significant discomfort. Examination revealed abdominal guarding without peritoneal signs, and other systemic examinations were unremarkable. Initial laboratory evaluation was severely limited by extreme lipemia, preventing biochemical analysis and resulting in diagnostic uncertainty. Complete blood count showed leukocytosis, thrombocytosis, and hemoconcentration (hemoglobin 24.6 g/dL [SI: 246 g/L]; reference range 12.0-17.0 g/dL [SI: 120-170 g/L]). Acute pancreatitis was suspected, but abdominal computed tomography showed no definitive pancreatic abnormalities. The patient was admitted to the intensive care unit due to diagnostic uncertainty and concern for severe metabolic derangement. In the absence of confirmatory laboratory data, empiric insulin infusion with dextrose supplementation and hourly glucose monitoring was initiated to treat presumed hypertriglyceridemia via lipoprotein lipase activation. On day 3, biochemical testing confirmed hypertriglyceridemia with triglycerides of 6300 mg/dL (SI: 71.2 mmol/L) (reference range <150 mg/dL, [SI: <1.7 mmol/L]). Triglycerides decreased to 243 mg/dL (SI: 2.74 mmol/L) by day 8. Follow-up imaging demonstrated a 5 cm pancreatic pseudocyst managed conservatively. The patient was discharged on lipid-lowering therapy and dietary modification. At 6-week follow-up, the pseudocyst had regressed and he remained asymptomatic.