Low central venous saturation predicts poor outcome in patients with brain injury after major trauma: a prospective observational study

Organ and tissue damages caused by a trauma impact lead to the development of systemic inflammatory response syndrome (SIRS) [1]. The local and systemic release of inflammation mediators produces oxidative stress, capillary leakage, microcirculatory disturbances, metabolic alteration, imbalance of pro- and anti-inflammatory mechanisms, ischaemia/reperfusion injury, coagulation disturbances [1]. In major trauma, occult tissue hypoperfusion within the first 24 hours after event precedes multiple organ dysfunction syndrome (MODS) [2]. Despite the unquestionable usefulness of routinely monitoring of hemodynamic parameters, such as arterial lactate, central venous pressure, blood pressure, heart rate, urinary volume, hypoxia may exist despite normal clinical values [3]. Continuous monitoring of central venous oxygen saturation (ScvO₂) has been proposed as an indicator of tissue hypoperfusion. Although the reliability of ScvO₂, compared with mixed venous oxygen saturation (SvO₂), is still under discussion, particularly under shock conditions [3], the prognostic importance of low level (≤ 65%) of ScvO₂ has been highlighted in severe sepsis [4, 5], myocardial infarction [6], cardiac failure [7], and trauma [8]. Moreover, ScvO₂ can be easily monitored with a central venous line, whereas SvO₂ requires a pulmonary artery catheterization.

In a recent investigation about the cause of death in trauma Soreige K et al.[9] found a high percentage of head trauma (67%) and concluded that focus on brain injuries prevention is imperative.

To our knowledge, no studies have evaluated ScvO₂ in patients affected by brain injury after major trauma so far. Thus, the aim of the present investigations was to assess the useful of an early monitoring (first 24 hours) of ScvO₂ in patients with major trauma and head injury.

The aim of the present investigation was to assess the role of early ScvO₂ monitoring in trauma patients with associated head injury. We assumed that a persistent low ScvO₂ could be the expression of the dangerous effects of generalized and, concomitant, brain hypoperfusion in patients with brain injury and major trauma and, therefore, that it could predict a worst evolution.

The prognostic importance of low level (≤ 65%) of ScvO₂ has been emphasized in severe sepsis [4, 5], myocardial infarction [6], and cardiac failure [7]. The significance of ScvO₂ in patients with major trauma has been previously reported in 26 injured patients [8]. In their investigation, Scalea and co-workers found that ScvO₂ measurement was a trustworthy parameter to estimate blood loss, especially in patients who showed an ScvO₂ below 65% despite stable clinical signs [8]. In opposition with this observation, a subsequent study did not confirm the reliability of ScvO₂ as indicator of blood loss in 40 trauma patients [14]. According with Scalea et al., the lack of linear correlation between low ScvO₂ and stable clinical signs has been also corroborated by Rady and colleagues in a nonrandomized study on sixteen patients presenting to the emergency department in shock conditions, who presented ScvO₂ below 65% in almost 50% of cases, despite the hemodynamic stabilization [5].

The ScvO₂ cut-off value of ≤ 65% has been chosen in the present investigation based on existing literature [5, 8, 14] and on the average we found in our patients deceased at 28 days (66.7%, Table 2). The main finding of this study was the relationship between an ScvO₂ values ≤ 65%, for at least 15 minutes during the first 24 hours from trauma, and mortality rates (Table 4). It must be noted that in the group with lower ScvO₂ also injury scores and lactate levels were worst. In regard, the absolute significance of ScvO₂ in predicting mortality in the multivariate analysis was lower than Marshall score and lactate levels in our investigation. However, the inclusion of ScvO₂ in a multiple regression model showed that mortality prediction can be improved from 86.6% to 87.6%: this improvement, whereas not ample, could be relevant in the day to day clinical practice. In consideration of our results, ScvO₂should be never considered as a substitute of lactate monitoring or injury scores in predicting outcome. In addition to these observations, patients with ScvO₂ values > 65% discharged alive from ICU, showed significantly reduction in both ICU and total hospital LOS (Table 4). Our findings are partially in accordance with a recent study performed on 96 critically ill patients admitted in a multidisciplinary ICU, in which an ScvO₂ value below 60% at admission was related with high mortality rate but not with a prolonged ICU LOS [15]. On regard, it must be considered that the study of Bracht and co-workers was performed on unselected critically ill patients, with a not specified number of central nervous system injured patients (less than 30% of total patients enrolled), whereas our population included polytraumatized patients with head injury. In our study, the association between low level of ScvO₂ and ICU/hospital LOS appeared strong; however, this finding could be also related with the differences in age and injuries observed in the two subgroups (Table 4).

The most numerous and extensive studies on ScvO₂ optimization have been performed on septic patients. To our knowledge, no study has investigated the usefulness of ScvO₂ monitoring to guide hemodynamic stabilization and to improve outcome in patients with major trauma [3]. The pathogenic changes following major trauma include SIRS, oxidative stress, capillary leakage, metabolic alterations, and diffuse tissue hypoxia as a result of circulatory abnormalities [1]. This pathophysiological process is somehow very similar with what observed in septic patients, although sepsis presents a different aetiology, evolution and possibility to be treated with antibiosis. In our investigation, ScvO₂ was not included as a target parameter for hemodynamic optimization, so none can be gathered from our data on application of early-goal directed therapy protocol in major trauma. Nevertheless, considering the good evidence in patients with severe sepsis/septic shock, the use of ScvO₂ to guide hemodynamic optimization in polytraumatized patients would merit to be adequately investigated.

Limits of present findings merit considerations. 1) We did not included data on fluids administration in the first 24 hours, brain damages evolutions, intracranial pressure, and their relationship with ScvO₂ levels. Second, the exclusion of patients who died in the first 24 hours from the study protocol might be a potential bias. The reason of this choice depended from our goal to investigate the role of ScvO₂ in the first 24 hours, which are considered critical in the evolution of MODS in polytrauma [2]. Third, we were not blinded for the primary end points (but in an emergency setting is not so easy), but the collection of data was made by an external investigator that was blind for the end points. Finally, the lack of a control group with a pulmonary artery catheter with SvO₂ monitoring did not allow a comparison between ScvO₂ and SvO₂, although previous studies showed that changes of both values proceed in a parallel manner, even under shock conditions [3, 16].

In conclusion, an early monitoring of ScvO₂ could aid to predict the outcome in patients with major trauma and head injury. In particular, we found that a value less than 65%, measured during the first 24 hours after admission, was associated with higher mortality rate and prolonged ICU and hospital LOS. So, our results seem to suggest the use of ScvO₂ as a target of resuscitation in patients with brain injury after major trauma. The validation of ScvO₂ in monitoring of cerebral metabolism and as a target for hemodynamic resuscitation in polytraumatized patients remains to be investigated.