Sepsis is a life-threatening condition resulting from an inflammatory overreaction that is induced by an infectious factor, which leads to multi-organ failure. Sepsis-associated encephalopathy (SAE) is a common complication of sepsis that can lead to acute cognitive and consciousness disorders, and no strict diagnostic criteria have been created for the complication thus far. The etiopathology of SAE is not fully understood, but plausible mechanisms include neuroinflammation, blood–brain barrier disruption, altered cerebral microcirculation, alterations in neurotransmission, changes in calcium homeostasis, and oxidative stress. SAE may also lead to long-term consequences such as dementia and post-traumatic stress disorder. This review aims to provide a comprehensive summary of substances with neuroprotective properties that have the potential to offer neuroprotection in the treatment of SAE. An extensive literature search was conducted, extracting 71 articles that cover a range of substances, including plant-derived drugs, peptides, monoclonal antibodies, and other commonly used drugs. This review may provide valuable insights for clinicians and researchers working in the field of sepsis and SAE and contribute to the development of new treatment options for this challenging condition.

Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection. The brain is one of the organs involved in sepsis, and sepsis-induced brain injury manifests as sepsis-associated encephalopathy (SAE). SAE may be present in up to 70% of septic patients. SAE has a very wide spectrum of clinical symptoms, ranging from mild behavioral changes through cognitive disorders to disorders of consciousness and coma. The presence of SAE increases mortality in the population of septic patients and may lead to chronic cognitive dysfunction in sepsis survivors. Therefore, therapeutic interventions with neuroprotective effects in sepsis are needed. Melatonin, a neurohormone responsible for the control of circadian rhythms, exerts many beneficial physiological effects. Its anti-inflammatory and antioxidant properties are well described. It is considered a potential therapeutic factor in sepsis, with positive results from studies on animal models and with encouraging results from the first human clinical trials. With its antioxidant and anti-inflammatory potential, it may also exert a neuroprotective effect in sepsis-associated encephalopathy. The review presents data on melatonin as a potential drug in SAE in the wider context of the pathophysiology of SAE and the specific actions of the pineal neurohormone.

There is growing evidence that periodic limb movements in sleep (PLMS) may lead to increased blood pressure (BP) values during the night. The aim of this study was to assess if patients with disordered sleep and an increased number of PLMS have higher BP values at night. We analyzed 100 polysomnographic (PSG) recordings of patients with disordered sleep, with the exclusion of sleep-related breathing disorders. Patients also registered beat-to-beat blood pressure during PSG. We compared the BP of patients with an increased number of PLMS (more than 5 PLMS per hour of sleep) during the night (examined group, n = 50) to the BP of patients with a PLMS number within the normal range (up to 5 PLMS per hour of sleep) (control group, n = 50). Patients from the examined group had significantly higher values of systolic BP during the night (119.7 mmHg vs. 113.3 mmHg, p = 0.04), sleep (119.0 mmHg vs. 113.3 mmHg, p = 0.04), and wake (122.5 mmHg vs. 117.2 mmHg, p = 0.04) periods and of diastolic BP during the night (75.5 mmHg vs. 70.6 mmHg, p = 0.04) and wake (77.6 mmHg vs. 71.5 mmHg, p = 0.01) periods. Our results suggest a relationship between the number of PLMS during the night and the values of nocturnal blood pressure. It is possible that their treatment could lower nocturnal BP in patients with sleep disorders, therefore improving their vascular risk profile.

Global sepsis statistics exhibit a morbidity of 48.9 million with 11.0 million sepsis-related deaths. Despite ongoing research and guideline updates it remains a serious epidemiological concern. Sepsis-associated encephalopathy (SAE) is one of the more dangerous sepsis complications, due to its potential to cause permanent central nervous system damage. This study aimed to examine the prevalence, symptoms, risk factors, and impact of SAE on disease course in emergency department patients. This retrospective study was performed in an emergency department of a university hospital. We analyzed medical records of patients from January 2021 till the end of December 2022. All admitted patients diagnosed with sepsis according to the sepsis-3 consensus were included. Patients with disseminated neoplastic disease, chronic neurological conditions with impact on cognitive and communicative functions, and pediatric patients were excluded. Based on laboratory tests and clinical symptoms of encephalopathy, the patients were divided into SAE and non-SAE groups. Chi-square test was used to assess results’ significance. A total of 443 patients with sepsis were included in the study, of whom 240 presented with SAE. The most common SAE symptoms include general consciousness deterioration, disorientation, and somnolence. Patients with SAE were older and had heart failure more frequently. Mortality rate in the SAE group was significantly higher and equaled 45.42% vs 7.88% in the non-SAE group (p-value < 0.001). The most commonly identified pathogens in the blood cultures were Escherichia coli and Staphylococcus aureus. The study showed that SAE is a common sepsis complication (54% prevalence) that significantly increases in-hospital mortality. Older patients with chronic neurological disorders and heart failure are particularly vulnerable. The SOFA, NEWS, and Glasgow Coma Scale scores have proven to be reliable predictors of SAE occurrence. This study is not a clinical trial.