Severe cases of traumatic brain injury (TBI) require neurocritical care, the goal being to stabilize hemodynamics and systemic oxygenation to prevent secondary brain injury. It is reported that approximately 45 % of dysoxygenation episodes during critical care have both extracranial and intracranial causes, such as intracranial hypertension and brain edema. For this reason, neurocritical care is incomplete if it only focuses on prevention of increased intracranial pressure (ICP) or decreased cerebral perfusion pressure (CPP). Arterial hypotension is a major risk factor for secondary brain injury, but hypertension with a loss of autoregulation response or excess hyperventilation to reduce ICP can also result in a critical condition in the brain and is associated with a poor outcome after TBI. Moreover, brain injury itself stimulates systemic inflammation, leading to increased permeability of the blood–brain barrier, exacerbated by secondary brain injury and resulting in increased ICP. Indeed, systemic inflammatory response syndrome after TBI reflects the extent of tissue damage at onset and predicts further tissue disruption, producing a worsening clinical condition and ultimately a poor outcome.Elevation of blood catecholamine levels after severe brain damage has been reported to contribute to the regulation of the cytokine network, but this phenomenon is a systemic protective response against systemic insults. Catecholamines are directly involved in the regulation of cytokines, and elevated levels appear to influence the immune system during stress. Medical complications are the leading cause of late morbidity and mortality in many types of brain damage. Neurocritical care after severe TBI has therefore been refined to focus not only on secondary brain injury but also on systemic organ damage after excitation of sympathetic nerves following a stress reaction.

IntroductionWe developed a protocol to initiate surgical source control immediately after admission (early source control) and perform initial resuscitation using early goal-directed therapy (EGDT) for gastrointestinal (GI) perforation with associated septic shock. This study evaluated the relationship between the time from admission to initiation of surgery and the outcome of the protocol.MethodsThis examination is a prospective observational study and involved 154 patients of GI perforation with associated septic shock. We statistically analyzed the relationship between time to initiation of surgery and 60-day outcome, examined the change in 60-day outcome associated with each 2 hour delay in surgery initiation and determined a target time for 60-day survival.ResultsLogistic regression analysis demonstrated that time to initiation of surgery (hours) was significantly associated with 60-day outcome (Odds ratio (OR), 0.31; 95% Confidence intervals (CI)), 0.19-0.45; P <0.0001). Time to initiation of surgery (hours) was selected as an independent factor for 60-day outcome in multiple logistic regression analysis (OR), 0.29; 95% CI, 0.16-0.47; P <0.0001). The survival rate fell as surgery initiation was delayed and was 0% for times greater than 6 hours.ConclusionsFor patients of GI perforation with associated septic shock, time from admission to initiation of surgery for source control is a critical determinant, under the condition of being supported by hemodynamic stabilization. The target time for a favorable outcome may be within 6 hours from admission. We should not delay in initiating EGDT-assisted surgery if patients are complicated with septic shock.

Injury severity determines the degree of IL-1beta protein level elevation after TBI. The effects of posttraumatic hypothermia on IL-1beta protein levels (an important mediator of neurodegeneration after TBI) may partly explain the established effects of posttraumatic temperature manipulations on inflammatory processes after TBI.

Rapid and marked increase in TNFalpha mRNA expression and protein levels follows moderate and severe TBI. Injury severity and posttraumatic temperature play a modest but significant role on TNFalpha expression and protein levels. These findings suggest that the effects of posttraumatic temperature on histopathological and behavioral outcome primarily may involve secondary mediators that do not operate directly through their effect on TNFalpha.