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Sepsis is defined as life-threatening organ dysfunction caused by a dysregulated host response to infection, and remains a global issue due to its high incidence and mortality. Many randomized controlled trials have investigated sepsis, but no specific treatments have been established. This is due to "heterogeneity," which indicates that a diagnosis of sepsis includes various pathophysiological states. To resolve this issue, efforts are being made to identify subclasses of sepsis. Past studies have selected different variables, such as expressed genes, cytokines, and vital signs, and identified subclasses based on clinical or biomarker-expression features. We also identified subclasses of sepsis with different coagulation features, and found that a specific anticoagulant agent (recombinant human thrombomodulin) was associated with improved survival rates in only one subclass. We also developed a model that could predict the subclass. However, none of the reported subclasses had shared characteristics, and they are not in clinical use. Further research is required to identify subclasses that are strongly associated with the pathophysiological mechanism and reproducible in any cohort.

The main objectives of critical care of severe traumatic brain injury(TBI)are the prevention and treatment of intracranial hypertension and secondary brain insults, preservation of cerebral perfusion pressure, and optimization of cerebral oxygenation. The critical care management of severe TBI will be discussed with a focus on the monitoring and avoidance or minimization of secondary brain insults, with emphasis on understanding the underlying physiology and pathophysiology. The evolution of critical care of severe traumatic brain injury will also be discussed along with the accumulating knowledge and experience.

A 46-year-old male patient was found unconscious in his room. There were remnants of burned-out charcoal briquettes. On arrival to our ER, the concentration of carbon monoxide (CO) hemoglobin was detected in 16.2%, and he was diagnosed with CO poisoning based on both his circumstantial evidence and laboratory results. Brain CT obtained on Day 1 revealed low density area in the basal part of the left temporal lobe, and T2-weighted MR images of the brain on Day 8 showed hyperintensity in the same region. MR images on Day 15 showed findings caused by white matter encephalopathy, and signal intensity in the left temporal lobe was decreased. To our best knowledge, it is very rare to see abnormal signal changes in the temporal lobe on radiological imaging of the patients who is suspected CO poisoning in acute phase because it has been reported that white matter encephalopathy after CO poisoning is commonly seen in delayed timing.