Background and Objectives: Patients with traumatic injuries have often been excluded from studies that have attempted to pinpoint modifiable factors to predict the transient disturbance of the cognitive function in the postoperative settings. Anesthetists must be aware of the high risk of developing postoperative delirium and cognitive dysfunction (POCD) in patients undergoing emergency surgery. Monitoring the depth of anesthesia in order to tailor anesthetic delivery may reduce this risk. The primary aim of this study was to improve the prevention strategies for the immediate POCD by assessing anesthetic depth and nociception during emergency surgery. Material and Methods: Of 107 trauma ASA physical status II–IV patients aged over 18 years undergoing emergency noncardiac surgery, 95 patients were included in a prospective randomized study. Exclusion criteria were neurotrauma, chronic use of psychoactive substances or alcohol, impaired preoperative cognitive function, pre-existing psychopathological symptoms, or expected surgery time less than 2 h. Entropy and Surgical Pleth Index (SPI) values were constantly recorded for one group during anesthesia. POCD was assessed 24 h, 48 h, and 72 h after surgery using the Neelon and Champagne (NEECHAM) Confusion Scale. Results: Although in the intervention group, fewer patients experienced POCD episodes in comparison to the control group, the results were not statistically significant (p < 0.08). The study showed a statistically significant inverse correlation between fentanyl and the NEECHAM Confusion Scale at 24 h (r = −0.32, p = 0.0005) and 48 h (r = −0.46, p = 0.0002), sevoflurane and the NEECHAM Confusion Scale at 24 h (r = −0.38, p = 0.0014) and 48 h (r = −0.52, p = 0.0002), and noradrenaline and POCD events in the first 48 h (r = −0.46, p = 0.0013 for the first 24 h, respectively, and r = −0.46, p = 0.0002 for the next 24 h). Conclusions: Entropy and SPI monitoring during anesthesia may play an important role in diminishing the risk of developing immediate POCD after emergency surgery.

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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.