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Comment on "Levels of vancomycin in the cerebral interstitial fluid after severe head injury" by Caricato et al.
My paper 20 years later : cerebral venous oxygen saturation studied with bilateral samples in the internal jugular veins
Introduction: Jugular oxygen saturation monitoring was introduced in neurointensive care after severe traumatic brain injury (TBI) to explore the adequacy of brain perfusion and guide therapeutic interventions. The brain was considered homogeneous, and oxygen saturation was taken as representative of the whole organ. We investigated whether venous outflow from the brain was homogeneous by measuring oxygen saturation simultaneously from the two jugular veins.Methods: In 32 comatose TBI patients both internal jugular veins (IJs) were simultaneously explored using intermittent samples; hemoglobin saturation was also recorded continuously by fiber-optic catheters in five patients. In five cases long catheters were inserted bilaterally upstream, up to the sigmoid sinuses.Main findings: On average, measurements from the two sides were in agreement (mean and standard deviation of the differences between the saturation of the two IJs were respectively 5.32 and 5.15). However, 15 patients showed differences of more than 15 % in hemoglobin saturation at some point; three others showed differences larger than 10 %. No relationship was found between the computed tomographic scan data and the hemoglobin saturation pattern.Discussion/conclusion: Several groups have confirmed differences between oxygen saturation in the two jugular veins. After years of enthusiasm, interest for jugular saturation has decreased and more modern methods, such as tissue oxygenation monitoring, are now available. Jugular saturation monitoring has low sensitivity, with the risk of missing low saturation, but high specificity; moreover it is cheap, when used with intermittent sampling. Monitoring the adequacy of brain perfusion after severe TBI is essential. However the choice of a specific monitor depends on local resources and expertise
Cranial trauma and multiple trauma : from the street to the operating room
Brain injury occurs with a range of severity: even less severe cases should be carefully observed since they may deteriorate. By definition severe head injury has a Glasgow Coma Scale score of 8 or less; comatose patients are defined as cases who do not obey commands, do not open their eyes and do not speak. Very often (50% of case in our series) brain injury is associated with relevant extracranial injuries that may add to the severity of cases and may worsen outcome. The conceptual framework for treating head injury is based on the evidence that after the impact, the initial damage may be exacerbated by insults capable of further disturbing cerebral metabolism, leading to a final damage defined as secondary damage. Secondary damage represents the final end of many pathways that can be studied at the biochemical level and are centered in a calcium influx into the neuronal cell. Most probably there is a genetic susceptibility to secondary damage leading to a range of cellular dysfunctions for any given level of insult. The management of traumatic brain injury is aimed at interrupting the chain of events leading to secondary brain damage and from this perspective the fact that damage may develop over time can be seen as a window of opportunity for timely treatment. The milestone of treatment is the removal of surgical masses. This surgical treatment can be performed only in a brain that is properly perfused and once coagulation is preserved. Therefore the organization of treatment from rescue to neuro-traumatological centers should provide appropriate restoration of the volume and a normal oxygen delivery to the brain and to the overall organism
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