Calcium channel blockers and beta-blockers toxicity/poisoning are one of the most common causes of poisoning. More importantly, they are among the deadliest types of poisoning caused by cardiac drugs that emergency physicians can encounter. Common toxidrome caused by these medications includes the following symptoms: hypotension, bradycardia, hypoglycemia/hyperglycemia, hypothermia, arrhythmia, and seizures. Treatment is usually complex, It consists of administration of various medications, such as crystalloids, intravenous calcium, glucagon, vasopressors/inotropes, and especially high-dose insulin euglycemic therapy. In this paper, we will review the mechanism for this type of treatment, propose a potential protocol for its application and address possible adverse effects. High-dose insulin euglycemic therapy should be an integral part of the treatment protocol for calcium channel blockers and beta-blockers toxicity.
Background: Pulmonary embolism (PE) is a common diagnosis in an emergency department. It also represents a large share of patients admitted to hospital wards. Patients with PE can be risk-stratified and discharged early from the emergency department. This results in better availability of hospital beds for other patients and a significant reduction of treatment costs for the healthcare system. This paper aims to describe the protocols used in our emergency department, with special emphasis on risk stratification, for adverse events and bleeding risk, treatment strategies, and outcomes for this type of protocol.Materials and methods: This paper is a retrospective analysis of patients discharged from the emergency department in a of two-year period (2020-2021) with a low-risk pulmonary embolism.Results: We have included in this study 42 patients discharged after a short-term observation from the emergency department (<24h) or short-term hospitalization; <24h). Ninety-one percent of patients were discharged with direct oral anticoagulant as a treatment for PE. We did not notice any adverse events (hemorrhage, progression of PE, or major cardiovascular issues).Conclusion: In the cohort of patients with PE, early discharge and outpatient treatment was safe and effective, with lower healthcare costs and almost no adverse events for patients
The objective of this case report is to present a patient with acquired methemoglobinemia due to poisoning of an unknown cause. A 55-year-old man was brought to the emergency department, university hospital Center Zagreb, with an unwell appearance, cyanotic, restless, and presented with a quantitative consciousness disorder. An initial assessment showed decreased oxygen saturation (Spo2 85 [%]), while point-of-care arterial blood gas (Abg) analysis assessed normal partial pressure of oxygen (po2). Severe lactic acidosis with a compensatory drop in partial pressure of carbon dioxide (pCo2) and high rates of methemoglobin were found. Supportive oxygen therapy and crystalloid solutions were administered, which resulted in rapid clinical recovery within 40 minutes of the initial assessment. Clinical recovery was accompanied by normalized Abg test results taken serially. typical antidotes, methylene blue and vitamin C, were not administered due to rapid clinical improvement. Methemoglobinemia can be congenital (hereditary) or acquired (toxic). both conditions are rarely seen in emergency departments, nevertheless, they should be approached properly since methemoglobinemia can be a severe, and fatal, condition. Methemoglobinemia symptoms are the results of inadequate oxygen transport. The diagnosis was confirmed by co-oximetry, while three clinical entities suspected methemoglobinemia: refractory hypoxia, "cyanosis-saturation gap" and dark brown blood. This paper reports our patient's clinical presentation, discusses the causes and mechanisms of possible poisoning, and reviews recent guidelines for methemoglobinemia management.
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