Hypothermia as an Outcome Predictor Tool in Pediatric Trauma: A Propensity-Matched Analysis.

OBJECTIVE: Hypothermia is an independent risk factor for mortality in adult trauma patients. Two small studies have shown similar results in pediatric trauma patients. Temperature is not included in any pediatric trauma assessment scores. This study sought to compare mortality and various descriptive outcomes between pediatric hypothermic and normothermic trauma patients. METHODS: Data were obtained from the National Trauma Database from 2009 to 2012. Patients meeting inclusion criteria were stratified by presence of isolated head injury, head injury with multiple trauma, and absence of head injury. These groups were then subdivided into hypothermic (temperature ≤36°C) and normothermic groups. We used propensity score matching to 1:1 match hypothermic and normothermic patients. Mortality, neurosurgical interventions, endotracheal intubation, blood transfusion, length of stay, laparotomy, thoracotomy, conversion of cardiac rhythm, and time receiving mechanical ventilation were evaluated. RESULTS: Data from 3,011,482 patients were obtained. There were 414,562 patients who met the inclusion criteria. In all patients meeting inclusion criteria, hypothermia was a significant risk factor in all outcomes measured. Following stratification and 1:1 matching, in all groups, hypothermia was associated with increased mortality (P < 0.0001), increased rate of endotracheal intubation (P < 0.0002), increased need for blood transfusion (P < 0.0025), and conversion of cardiac rhythm (P < 0.0027). CONCLUSION: Hypothermia has been shown to be a significant prognostic indicator in the pediatric trauma patient with further potential application. Future studies are indicated to evaluate the incorporation of hypothermia into the Pediatric Trauma Score not only to help predict injury severity and mortality but also to improve appropriate and expeditious patient transfer to pediatric trauma centers and potentially facilitate earlier intervention.

Cerebral oximetry with blood volume index and capnography in intubated and hyperventilated patients.

OBJECTIVE: Hyperventilation-induced hypocapnia leads to cerebral vasoconstriction and hypoperfusion. Intubated patients are often inadvertently hyperventilated during resuscitations, causing theoretical risk for ischemic brain injury. Current emergency department monitoring systems do not detect these changes. The purpose of this study was to determine if cerebral oximetry (rcSo2) with blood volume index (CBVI) would detect hypocapnia-induced cerebral tissue hypoxia and hypoperfusion. METHODS: Patients requiring mechanical ventilation underwent end-tidal CO2 (ETco2), rcSo2, and CBVI monitoring. Baseline data was analyzed and then the effect of varying ETco2 on rcSo2 and CBVI readings was analyzed. Median rcSo2 and CBVI values were compared when above and below the ETco2 30 mmHg threshold. Subgroup analysis and descriptive statistics were also calculated. RESULTS: Thirty-two patients with neurologic emergencies and potential increased intracranial pressure were included. Age ranged from 6 days to 15 years (mean age, 3.1 years; SD, 3.9 years; median age, 1.5 years: 0.46-4.94 years). Diagnoses included bacterial meningitis, viral meningitis, and seizures. ETco2 crossed 30 mm Hg 80 times. Median left and right rcSO2 when ETCO2 was below 30 mmhg was 40.98 (35.3, 45.04) and 39.84 (34.64, 41) respectively. Median left and right CBVI when ETCO2 was below 30 mmhg was -24.86 (-29.92, -19.71) and -22.74 (-27.23, - 13.55) respectively. Median left and right CBVI when ETCO2 was below 30 mmHg was -24.86 (-29.92, -19.71) and -22.74 (-27.23, -13.55) respectively. Median left and right rcSO2 when ETCO2 was above 30 mmHg was 63.53 (61.41, 66.92) and 63.95 (60.23, 67.58) respectively. Median left and right CBVI when ETCO2 was above 30 mmHg was 12.26 (0.97, 20.16) and 8.11 (-0.2, 21.09) respectively. Median duration ETco2 was below 30 mmHg was 17.9 minutes (11.4, 26.59). Each time ETco2 fell below the threshold, there was a significant decrease in rcSo2 and CBVI consistent with decreased cerebral blood flow. While left and right rcSO2 and CBVI decreased quickly once ETCO2​ was below 30 mmHg, increase once ETCO2​ was above 30 mmHg was much slower. CONCLUSION: This preliminary study has demonstrated the ability of rcSo2 with CBVI to noninvasively detect the real-time effects of excessive hyperventilation producing ETco2 < 30 mmHg on cerebral physiology in an emergency department. We have demonstrated in patients with suspected increased intracranial pressure that ETco2 < 30 mmHg causes a significant decrease in cerebral blood flow and regional tissue oxygenation.