Methemoglobinemia is a rare, life-threatening condition that occurs when the body is exposed to oxidative stress. We present the case of a 72-year-old female with a past medical history of hypertension, obesity, dyslipidemia, and heart failure who was admitted to the emergency department with altered mental status and respiratory failure. After admission, we also identified an atrioventricular block 2:1, anemia, and skin discoloration. We performed endotracheal intubation and started mechanical ventilation due to respiratory failure; however, the patient retained an oxygen "saturation gap" despite adequate ventilation. In the initial laboratory evaluation, methemoglobinemia was found to be 13%, reaching a maximum level of 16%. An electroencephalogram revealed status epilepticus after her admission to the intensive care unit. Despite all efforts and supportive care, methylene blue therapy was never attempted, and the patient died. Our case emphasizes the importance of a high index of suspicion for methemoglobinemia, especially in the presence of an oxygen "saturation gap," and that despite relatively low levels of methemoglobinemia, it can have a more severe clinical presentation in patients with comorbidities. In these patients, a reduced threshold for administering methylene blue should be taken into account.

Idiopathic hypereosinophilic syndrome is a rare condition characterized by persistent severe eosinophilia and organ damage without any apparent cause. A 20-year-old male patient with no significant medical history was admitted to the Emergency Department with retrosternal chest pain, fatigue and asthenia. EKG showed ST elevation I, II, III, aVF, V4-V6 and blood tests showed elevated troponin levels. An echocardiogram was performed revealing severe global left ventricular systolic dysfunction. Further evaluations included cardiac magnetic resonance imaging and endomyocardial biopsy, confirming the diagnosis of eosinophilic myocarditis. The patient was started on systemic corticosteroid therapy, resulting in clinical improvement. The patient was discharged after 12 days of hospitalization, following a recovery of biventricular function and he was told to continue oral corticosteroid therapy at home. Further investigation ruled out other causes of hypereosinophilic syndromes, therefore the diagnosis of idiopathic hypereosinophilic syndrome was assumed. Despite the attempt to reduce corticosteroid therapy, the eosinophil count became elevated again, so the dosage was increased and associated with azathioprine with subsequent favorable analytical evolution. This case highlights the challenges in diagnosing and managing idiopathic hypereosinophilic syndrome and emphasizes the importance of prompt treatment initiation to prevent complications.

The coronavirus disease 2019 pandemic has brought about significant changes in the medical field. While primarily characterized as a respiratory syndrome, COVID-19 is also associated with vascular events, particularly thrombotic complications. These events can manifest as initial presentations or develop as complications during the course of the disease, predominantly driven by immune-mediated mechanisms. MethodsPatients with thrombotic complications followed in the post-COVID-19 thrombosis consult of 2021 were retrospectively analyzed and assessed for predisposing factors for pulmonary embolism (PE), including thrombophilias. Patients underwent reassessments over a minimum six-month period following diagnosis to evaluate vascular reperfusion and the potential discontinuation of anticoagulant therapy. ResultsAll patients with PE exhibited segmental or subsegmental PE. Pulmonary CT angiography revealed that only one patient did not show complete reperfusion after six months of anticoagulant therapy alone. There were no instances of recurrent thrombotic events observed during this observation period. Among the studied patients, hypertension, diabetes, and obesity were identified as the most prevalent predisposing factors. No patients were diagnosed with thrombophilias or other relevant factors. Despite extensive research on the predisposing mechanisms of this complication in recent years, limited data exist regarding patients with this specific complication. Discussion and conclusionContinued research into COVID-19 patients and their complications is crucial for understanding the pathophysiological mechanisms and risk factors associated with these complications. The findings of this study support the existence of a multifactorial mechanism, with a significant pro-inflammatory component exacerbated by pre-existing risk factors, rather than a purely prothrombotic mechanism.