TBI formed after head trauma is one of the main causes of morbidity and mortality in the pediatric age group [14]. Severe head injuries were found to be more common in boys than girls; but there was no statistically significant difference. There was no statistical difference between the genders in terms of age, admission GCS and surgical application. Mortality rate was similar for both boys and girls (p > 0.05) (Table 1).
Since brain development continues in children, complete axonal myelization has not occurred and brain tissue has a higher water content than adults. For this reason, brain damage is more common in children, while focal damage is more common in adults. Although children with TBI have a higher survival rate compared to adults, the picture in children is more devastating in terms of sequelaes and consequences [15].
The presence of acidosis may cause neural death by disrupting acid-base homeostasis in brain tissue [16]. Therefore, it has been accepted as an important indicator of morbidity and mortality in pediatric patients with TBI [17]. Kushi et al. [18] stated that jugular venous blood pH levels are useful as an early prognostic indicator in the evaluation of neurological function in patients with TBI. pH averagevalues in our study were measured as 7.15 in non-survivors and 7.35 in survivors. The presence of acidosis and mean PH values in the cases that resulted in mortality as a result of TBI were statistically significant compared to the surviving cases.
In patients with TBI, during head injury as the cause of the damage, besides primary brain injury the efficacy of the presence of hypotension and hypoxia was mentioned [19]. Whether surgery is performed or not, adequate oxygenation is important to reduce damage. In children with severe head trauma with oxygen saturation < 90% or PaO2 < 60 mmHg, firstly, the importance of correcting hypoxia and increasing cerebral perfusion pressure was mentioned [20]. Rapid intubation and mechanical ventilation implementation are recommended to achieve this [21]. The presence of hypoxia has been associated with poor prognosis in pediatric TBI [22]. In a similar study, it has been shown that post-traumatic hypoxia significantly increases the likelihood of mortality in patients with brain damage [23]. Chiaretti et al. [24] reported that post traumatic hypoxia and hypotension are associated with poor outcome. However, there are also studies in which hypoxia is not seen as a factor that statistically affects poor prognosis [25, 26]. In a study involving severe head trauma, no significant statistical result was found in patients with normal PO2 levels in ABG measured in the emergency department, even if they showed a better prognosis [27].
In our study, the presence of hypoxia did not differ between survivors and those who died. We think that the PO2 values of our patients were not associated with mortality, since hypoxia was corrected at the time of the first intervention.
Hypercapnia is known to increase cerebral blood flow and volume through cerebral vasodilation; However, its effect on recovery has not been demonstrated directly in humans [6]. It has been stated that it is important to bring PCO2 to normal as soon as possible in patients with severe head trauma [28]. Dumont et al. [29] studied 65 patients with TBI to determine the effect of prehospital hyperventilation on in-hospital mortality; found that the survival rate in patients with normocapnia was better than in patients with hypercapnia. He stated that ABG PCO2 levels can be used as a predictor of outcome in patients with TBI. However, in the study of Rahimi et al. [25] it was shown that hypocapnia or hypercapnia does not have a statistically significant relationship with mortality in children with severe head trauma.
In our study, PCO2 mean value was 49.29 ± 5.59 mmHg in the deceased and 36.29 ± 4.75 mmHg in the survivors, and the difference between them was statistically significant. The presence of hypercapnia in the patients who died was statistically significant. In the ROC analysis performed to evaluate the relationship of PCO2 values with mortality, the specificity of 49 mmHg ≥ values of PCO2 for mortality was 58.8% and its sensitivity was 96.8%. Our study shows that the presence of hypercapnia and high PCO2 values adversely affect the prognosis.
Lactate is a byproduct of anaerobic metabolism and serum lactate level reflects the degree of tissue hypoperfusion and hypoxia [8]. As the lactate level increases, its use as a cerebral energy fuel increases and this preserves cerebral glucose in patients with TBI [30]. High arterial lactate causes an increase in cerebral blood flow by vasodilation in cerebral vessels [31]. Hypertonic lactate solutions given exogenously may show cerebral edema and intracranial pressure reducing effects. In addition, it has been reported that it may have a neuroprotective effect on high lactate, intracranial pressure, cerebral blood flow and cerebral cellular metabolism [32]. However, some studies have stated that high lactate measured in ABG is associated with increased mortality in critically ill patients and after severe trauma [33, 34]. The role of lactate in TBI is not very clear, a study conducted with adults showed that high arterial lactate may impair cerebral blood flow regulation and thus negatively affect the outcome in TBI [35].
Measuring lactate level in ABG is a fast and practical method compared to serum. When we conducted a literature review, we found that studies investigating the relationship between lactate level in blood gas and determining prognosis in pediatric TBI were insufficient. Ramanathan et al. [36] found that lactate levels were high in pediatric trauma patients hospitalized in the intensive care unit. Similarly, Shah et al. [37] found that the lactate level measured after trauma was high in pediatric patients who needed intensive care. In our study, the presence of hyperlactatemia in non-alive and average lactate values in ABG were statistically significant compared to those who were alive. In ROC analysis, ABG lactate values were found to be a strong indicator for mortality. The specificity of 4.5 mmol / L values of lactate for mortality in pediatric patients with severe head trauma was 82.4% and its centivity was 93.6%. Our study shows that high levels of lactate in TBI are associated with mortality.
BE is known as an important indicator of tissue perfusion and hypoxia in trauma patients [38]. It has been stated that BE measurement values are important as a prognostic marker in patients with multiple trauma [39]. However, there are not many studies on BE in TBI. A study mentions the prevalence of surgery in patients with TBI with BE > 4 mmol / L [40]. In our study, we accepted BE values of 4 mmol / L ≥ as significant in terms of the presence of BE. The mean BE values of the non-survivors were higher than those who were alive, but the effect of the presence or absence of BE on the outcome could not be determined.
For patients with TBI, it is necessary to determine some biomarkers for good prognosis, to measure them quickly and to correct pathological values, if any. Therefore, starting the treatment process as soon as possible is important to prevent secondary damage. This study shows that some parameters in early period ABG in pediatric TBI can be a biomarker for prognosis.