Pain management in multiple trauma patients presents a complex clinical challenge due to competing priorities such as hemodynamic instability, polypharmacy, coagulopathy, and the urgency of life-saving interventions. In this context, peripheral nerve blocks (PNBs) are increasingly recognized as a valuable asset for their role in managing pain in patients with multiple traumatic injuries. By reducing reliance on systemic opioids, PNBs support effective pain control and facilitate early mobilization, aligning with enhanced recovery principles. This narrative review summarizes current evidence on the use of PNBs in the context of polytrauma, focusing on their analgesic efficacy, integration within multimodal analgesia protocols, and contribution to improved functional outcomes. Despite these advantages, clinical application is limited by specific concerns, including the potential to mask compartment syndrome, the risk of nerve injury or local anesthetic systemic toxicity (LAST), and logistical barriers in acute trauma settings. Emerging directions in the field include the refinement of ultrasound-guided PNB techniques, the expanded use of continuous catheter systems, and the incorporation of fascial plane blocks for anatomically complex or multisite trauma. Parallel efforts are focusing on the development of decision-making algorithms, improved risk stratification tools, and integration into multimodal analgesic pathways. There is also growing emphasis on standardized clinical protocols, simulation-based training, and patient education to enhance safety and consistency in practice. As evidence continues to evolve, the long-term impact of PNBs on functional recovery, quality of life, and healthcare utilization must be further explored. With thoughtful implementation, structured training, and institutional support, PNBs may evolve into a cornerstone of modern trauma analgesia.

Nutritional support in critically ill patients has been acknowledged as a pillar of ICU care, playing a pivotal role in preserving muscle mass, supporting immune function, and promoting recovery during and after critical illness. Providing effective nutritional support requires adapting it to the patient’s diagnosis, unique characteristics, and metabolic state to minimize the risks of overfeeding or underfeeding while mitigating muscle loss. This level of care requires a comprehensive nutritional assessment and the establishment of a nutrition-focused protocol. Regular, consistent and detailed nutritional evaluation can influence both therapeutic decisions and clinical interventions, thus ensuring that the specific needs of critically ill patients are met from the acute phase through their entire recovery process. Bioelectrical impedance analysis (BIA) is increasingly recognized as a valuable tool for enhancing nutritional care in critically ill patients. By delivering precise, real-time insights into key aspects of body composition, BIA is thought to provide clinicians with a more comprehensive understanding of the complex physiological changes that occur during critical illness. This narrative review highlights the potential of BIA in offering these precise assessments, facilitating the development of more accurate and personalized nutritional strategies for critically ill patients. If BIA can reliably assess dynamic shifts in hydration and tissue integrity, it holds the promise of further advancing individualized care and optimizing clinical outcomes in this vulnerable population.

The administration of intravenous lipid emulsion (ILE) is a proven antidote used to reverse local anesthetic-related systemic toxicity. Although the capacity of ILE to generate blood tissue partitioning of lipophilic drugs has been previously demonstrated, a clear recommendation for its use as an antidote for other lipophilic drugs is still under debate. Venlafaxine (an antidepressant acting as a serotonin–norepinephrine reuptake inhibitor (SNRI)) and quetiapine (a second-generation atypical antipsychotic) are widely used in the treatment of psychotic disorders. Both are lipophilic drugs known to induce cardiotoxicity and central nervous depression. We report the case of a 33-year-old man with a medical history of schizoaffective disorder who was admitted to the emergency department (ED) after having been found unconscious due to a voluntary ingestion of 12 g of quetiapine and 4.5 g of venlafaxine. Initial assessment revealed a cardiorespiratory stable patient but unresponsive with a GCS of 4 (M2 E1 V1). In the ED, he was intubated, and gastric lavage was performed. Immediately after the admission to the intensive care unit (ICU), his condition quickly deteriorated, developing cardiovascular collapse refractory to crystalloids and vasopressor infusion. Junctional bradycardia occurred, followed by spontaneous conversion to sinus rhythm. Subsequently, frequent ventricular extrasystoles, as well as patterns of bigeminy, trigeminy, and even episodes of non-sustained ventricular tachycardia, occurred. Additionally, generalized tonic–clonic seizures were observed. Alongside supportive therapy, antiarrhythmic and anticonvulsant therapy, intravenous lipid emulsion bolus, and continuous infusion were administered. His condition progressively improved over the following hours, and 24 h later, he was tapered off the vasopressor. On day 2, the patient repeated the cardiovascular collapse and a second dose of ILE was administered. Over the next few days, the patient’s clinical condition improved, and he was successfully weaned off ventilator and vasopressor support. ILE has the potential to become a form of rescue therapy in cases of severe lipophilic drug poisoning and should be considered a viable treatment for severe cardiovascular instability that is refractory to supportive therapy.

Trace elements are essential for several physiological processes. To date, various data have suggested that inadequate levels of trace elements may be involved in the pathogenesis of different chronic diseases, including immune-mediated ones, or may develop during their course. Systemic sclerosis (SSc) is a complex autoimmune multisystemic disease, primarily characterized by microvascular dysregulation, the widespread activation of the immune system and tissue fibrosis. According to the latest reports regarding the pathogenesis of SSc, the main pathophysiological processes—inflammation, vasculopathy and fibrosis—may include various trace element derangements. The present literature review aims to update the available data regarding iron, zinc, copper and selenium status in SSc as well as to underline the possible implications of these trace elements in the complexity of the pathogenic process of the disease. We observe that the status of trace elements in SSc plays a crucial role in numerous pathogenic processes, emphasizing the necessity for proper monitoring and supplementation. The reported data are heterogenous and scarce, and future studies are needed in order to draw clearer conclusions about their complete spectrum.

Background and Objectives: Conditions such as trauma, burns, sepsis, or acute intoxications have considerable consequences on the endocrine status, causing “sick euthyroid syndrome”. Organophosphate exposure may induce an increase in acetylcholine levels, thus altering the thyroid’s hormonal status. The present study aims to identify the effects of acetylcholinesterase inhibition on thyroid hormones. Material and methods: A prospective experimental study was conducted on twenty Wistar rats. Blood samples were drawn to set baseline values for thyroid-stimulating hormone (TSH), triiodothyronine (T3), and thyroxine (T4). Chlorpyrifos 0.1 mg/kg was administered by oral gavage to induce acetyl-cholinesterase inhibition. After exhibiting cholinergic symptoms, blood samples were collected to assess levels of cholinesterase and thyroid hormones using ELISA. Results: Butyrylcholinesterase levels confirmed major inhibition immediately after intoxication compared to the baseline, certifying the intoxication. A significant increase in T4 levels was noted (p = 0.01) both at 2 h and 48 h after administration of organophosphate in sample rats. Similarly, T3 almost doubled its value 2 h after poisoning (4.2 ng/mL versus 2.5 ng/mL at baseline). Surprisingly, TSH displayed acute elevation with an afterward slow descending trend at 48 h (p = 0.1), reaching baseline value. Conclusions: This study demonstrated that cholinesterase inhibition caused major alterations in thyroid hormone levels, which may be characterized by a transient hypothyroidism status with an impact on survival prognosis.

Cardiac tamponade is a rare presentation in patients with COVID-19, which may be induced by the associated exacerbated inflammatory response. The onset of cardiac tamponade may be concomitant with the acute phase of the disease or may develop subsequently as a new health condition secondary to the disease. We report four cases of cardiac tamponade that occurred late after the acute phase of the disease. One of them may be considered a post-acute complication of the disease, and three of them may be classified as a new health condition induced by COVID-19. Only two cases had a history of severe respiratory distress due to COVID-19. In all four cases, pericardiocentesis was imposed, and surprisingly, in every case, hemorrhagic fluid was evacuated. In this case, series, immune-mediated etiology is supported by histopathological results, where the main identified feature was fibrous pericarditis with inflammatory infiltrate. Only one patient included in this report died, and three of them were discharged after anti-inflammatory treatment was initiated.