Intubation, which requires sedation and myorelaxants, may lead to inaccurate neurological evaluation of severely head-injured patients. Aims of this study were to describe the early clinical evolution of traumatic brain injured (TBI) patients admitted to intensive care unit (ICU), to identify cases of over-estimated neurological severity, and to quantify the risk factors for this over-estimation. A total of 753 TBI patients consecutively admitted to ICU of three academic neurosurgical hospitals (NSH) were assessed. Cases whose severity was potentially over-estimated were identified by four criteria and indicated as "mistakenly severe" (MS): (1) no surgical intracranial masses; (2) could not follow commands at neurological assessment; (3) were dismissed from the ICU in Յ3 days to a regular ward; and (4) had regained the ability to obey commands. A total of 675 patients were intubated and/or sedated-paralyzed at the post-stabilization evaluation. In all, 304 patients had surgically treated intracranial masses. Among the 449 non-surgical cases, 58 patients fulfilling the criteria for MS were identified. The main features distinguishing MS from truly severe cases were younger age, higher Glasgow Coma Scale (GCS) score at all time points, Marshall classification of Computerized Tomographic (CT) scan mostly Diffuse Injury I and II, fewer pupillary abnormalities, and a lower frequency of hypoxia, hypotension, and extra-cranial injuries. In a certain proportion of non-surgical TBI patients, mostly intubated and sedated, neurological examination is difficult and severity can be over-estimated. Risk factors for this inaccurate evaluation can be identified, and clinical decisions should be based on further examination.

Multiple episodes of brain hypoxia occurred over the first 5 days following severe TBI. PtiO2 was lower in peri-contusional tissue than in normal-appearing tissue. In peri-contusional tissue, a progressive increase of PtiO2 from pathologic to normal values was observed over time, suggestive of an improvement at microcirculatory level.

Intubation, which requires sedation and myorelaxants, may lead to inaccurate neurological evaluation of severely head-injured patients. Aims of this study were to describe the early clinical evolution of traumatic brain injured (TBI) patients admitted to intensive care unit (ICU), to identify cases of over-estimated neurological severity, and to quantify the risk factors for this over-estimation. A total of 753 TBI patients consecutively admitted to ICU of three academic neurosurgical hospitals (NSH) were assessed. Cases whose severity was potentially over-estimated were identified by four criteria and indicated as "mistakenly severe" (MS): (1) no surgical intracranial masses; (2) could not follow commands at neurological assessment; (3) were dismissed from the ICU in Յ3 days to a regular ward; and (4) had regained the ability to obey commands. A total of 675 patients were intubated and/or sedated-paralyzed at the post-stabilization evaluation. In all, 304 patients had surgically treated intracranial masses. Among the 449 non-surgical cases, 58 patients fulfilling the criteria for MS were identified. The main features distinguishing MS from truly severe cases were younger age, higher Glasgow Coma Scale (GCS) score at all time points, Marshall classification of Computerized Tomographic (CT) scan mostly Diffuse Injury I and II, fewer pupillary abnormalities, and a lower frequency of hypoxia, hypotension, and extra-cranial injuries. In a certain proportion of non-surgical TBI patients, mostly intubated and sedated, neurological examination is difficult and severity can be over-estimated. Risk factors for this inaccurate evaluation can be identified, and clinical decisions should be based on further examination.

Background Pro‐protein convertase subtilisin/kexin 9 (PCSK9) is a proenzyme primarily known to regulate low‐density lipoprotein receptor re‐uptake on hepatocytes. Whether PCSK9 can concurrently trigger inflammation or not remains unclear. Here, we investigated the potential association between circulating levels of PCSK9 and mortality in patients with severe sepsis or septic shock. Methods Plasma PCSK9 levels at days 1, 2 and 7 were measured in 958 patients with severe sepsis or septic shock previously enrolled in the Albumin Italian Outcome Sepsis (ALBIOS) trial. Correlations between levels of PCSK9 and pentraxin 3 (PTX3), a biomarker of disease severity, were evaluated with ranked Spearman’s coefficients. Cox proportional hazards models were used to assess the association of PCSK9 levels at day 1 with 28‐ and 90‐day mortality. Results Median plasma PCSK9 levels were 278 [182–452] ng mL−1 on day 1. PCSK9 correlated positively with PTX3 at the three time‐points, and patients with septic shock within the first quartile of PCSK9 showed higher levels of PTX3. Similar mortality rates were observed in patients with severe sepsis across PCSK9 quartiles. Patients with septic shock with lower PCSK9 levels on day 1 (within the first quartile) showed the highest 28‐ and 90‐day mortality rate as compared to other quartiles. Conclusion In our sub‐analysis of the ALBIOS trial, we found that patients with septic shock presenting with lower plasma PCSK9 levels experienced higher mortality rate. Further studies are warranted to better evaluate the pathophysiological role of PCSK9 in sepsis.