scholarly journals Continuous monitoring of carbon dioxide reactivity in traumatic brain injury

Critical Care ◽  
2009 ◽  
Vol 13 (Suppl 1) ◽  
pp. P87
Author(s):  
G De La Cerda ◽  
V Verma
Keyword(s):  
Carbon Dioxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Continuous Monitoring ◽  
Carbon Dioxide Reactivity

scholarly journals Age-related carbon dioxide reactivity in children after moderate and severe traumatic brain injury

2016 ◽  
Vol 18 (1) ◽  
pp. 73-78 ◽  
Author(s):  
Tensing Maa ◽  
Keith Owen Yeates ◽  
Melissa Moore-Clingenpeel ◽  
Nicole F. O'Brien
Keyword(s):  
Carbon Dioxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Minute Ventilation ◽  
Age Groups ◽  
Age Related ◽  
Negative Effect ◽  
Severe Tbi ◽  
Carbon Dioxide Reactivity ◽  
Artery Flow

OBJECTIVE The objective of this study is to assess carbon dioxide reactivity (CO2R) in children following traumatic brain injury (TBI). METHODS This prospective observational study enrolled children younger than 18 years old following moderate and severe TBI. Thirty-eight mechanically ventilated children had daily CO2R testing performed by measuring changes in their bilateral middle cerebral artery flow velocities using transcranial Doppler ultrasonography (TCD) after a transient increase in minute ventilation. The cohort was divided into 3 age groups: younger than 2 years (n = 12); 2 to 5 years old (n = 9); and older than 5 years (n = 17). RESULTS Children younger than 2 years old had a lower mean CO2R over time. The 2–5-year-old age group had higher mean CO2R than younger patients (p = 0.01), and the highest CO2R values compared with either of the other age groups (vs > 5 years old, p = 0.046; vs < 2 years old, p = 0.002). Having a lower minimum CO2R had a statistically significant negative effect on outcome at discharge (p = 0.0413). Impaired CO2R beyond Postinjury Day 4 trended toward having an effect on outcome at discharge (p = 0.0855). CONCLUSIONS Abnormal CO2R is prevalent in children following TBI, and the degree of impairment varies by age. No clinical or laboratory parameters were identified as risk factors for impaired CO2R. Lower minimum CO2R values are associated with worse outcome at discharge.

Association of Ventilation during Initial Trauma Resuscitation for Traumatic Brain Injury and Post-Traumatic Outcomes: A Systematic Review

2021 ◽  
pp. 1-6
Author(s):  
Mary Beth Howard ◽  
Nichole McCollum ◽  
Emily C. Alberto ◽  
Hannah Kotler ◽  
Mary E. Mottla ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Systematic Review ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Trauma Resuscitation ◽  
Cerebral Herniation ◽  
Full Text Review ◽  
Post Traumatic ◽  
Ventilation Strategies ◽  
End Tidal

Abstract Objectives: In the absence of evidence of acute cerebral herniation, normal ventilation is recommended for patients with traumatic brain injury (TBI). Despite this recommendation, ventilation strategies vary during the initial management of patients with TBI and may impact outcome. The goal of this systematic review was to define the best evidence-based practice of ventilation management during the initial resuscitation period. Methods: A literature search of PubMed, CINAHL, and SCOPUS identified studies from 2009 through 2019 addressing the effects of ventilation during the initial post-trauma resuscitation on patient outcomes. Results: The initial search yielded 899 articles, from which 13 were relevant and selected for full-text review. Six of the 13 articles met the inclusion criteria, all of which reported on patients with TBI. Either end-tidal carbon dioxide (ETCO2) or partial pressure carbon dioxide (PCO2) were the independent variables associated with mortality. Decreased rates of mortality were reported in patients with normal PCO2 or ETCO2. Conclusions: Normoventilation, as measured by ETCO2 or PCO2, is associated with decreased mortality in patients with TBI. Preventing hyperventilation or hypoventilation in patients with TBI during the early resuscitation phase could improve outcome after TBI.

scholarly journals 217 The end-tidal and arterial carbon dioxide gradient in serious traumatic brain injury after pre-hospital emergency anaesthesia: a retrospective observational study

2020 ◽  
Vol 37 (12) ◽  
pp. 847.1-847
Author(s):  
James Price ◽  
Daniel Sandbach ◽  
Ari Ercole ◽  
Alastair Wilson ◽  
Ed Barnard
Keyword(s):  
Carbon Dioxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Thoracic Injury ◽  
Secondary Brain Injury ◽  
Hospital Emergency ◽  
Hospital Arrival ◽  
Arterial Blood ◽  
End Tidal ◽  
Emergency Anaesthesia

Aims/Objectives/BackgroundIn the United Kingdom (UK), 20% of patients with severe traumatic brain injury (TBI) receive pre-hospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0–4.5kPa to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5kPa ETCO2-PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. Our primary aim was to report the ETCO2-PaCO2 gradient of TBI patients at hospital arrival.Methods/DesignA retrospective cohort study of adult patients with serious TBI, who received a PHEA by a pre-hospital critical care team in the East of England between 1st April 2015 to 31st December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% confidence intervals (95%CI). ETCO2-PaCO2 gradient data were compared with a two-tailed, unpaired, t-test.Results/Conclusions107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 minutes of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol.The mean ETCO2-PaCO2 gradient was 1.7 (±1.0) kPa, with only moderate correlation of ETCO2 and PaCO2 at hospital arrival (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95%CI 1.4–2.0) kPa with upper and lower limits of agreement of 3.6 (95%CI 3.0–4.1) kPa and -0.2 (95%CI -0.8–0.3) kPa respectively. There was no significant gradient correlation in patients with a co-existing serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2-PaCO2 gradient, 2.0 (±1.1) kPa, p=0.01. Patients who underwent pre-hospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa.Lower ETCO2 targets than previously recommended may be safe and appropriate. The use of pre-hospital PaCO2 measurement is advocated.

scholarly journals End-tidal and arterial carbon dioxide gradient in serious traumatic brain injury after prehospital emergency anaesthesia: a retrospective observational study

2020 ◽  
Vol 37 (11) ◽  
pp. 674-679
Author(s):  
James Price ◽  
Daniel D Sandbach ◽  
Ari Ercole ◽  
Alastair Wilson ◽  
Ed Benjamin Graham Barnard
Keyword(s):  
Carbon Dioxide ◽  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Secondary Brain Injury ◽  
Moderate Correlation ◽  
Hospital Arrival ◽  
Prehospital Emergency ◽  
The Mean ◽  
End Tidal ◽  
Emergency Anaesthesia

ObjectivesIn the UK, 20% of patients with severe traumatic brain injury (TBI) receive prehospital emergency anaesthesia (PHEA). Current guidance recommends an end-tidal carbon dioxide (ETCO2) of 4.0–4.5 kPa (30.0–33.8 mm Hg) to achieve a low-normal arterial partial pressure of CO2 (PaCO2), and reduce secondary brain injury. This recommendation assumes a 0.5 kPa (3.8 mm Hg) ETCO2–PaCO2 gradient. However, the gradient in the acute phase of TBI is unknown. The primary aim was to report the ETCO2–PaCO2 gradient of TBI patients at hospital arrival.MethodsA retrospective cohort study of adult patients with serious TBI, who received a PHEA by a prehospital critical care team in the East of England between 1 April 2015 and 31 December 2017. Linear regression was performed to test for correlation and reported as R-squared (R2). A Bland-Altman plot was used to test for paired ETCO2 and PaCO2 agreement and reported with 95% CI. ETCO2–PaCO2 gradient data were compared with a two-tailed, unpaired, t-test.Results107 patients were eligible for inclusion. Sixty-seven patients did not receive a PaCO2 sample within 30 min of hospital arrival and were therefore excluded. Forty patients had complete data and were included in the final analysis; per protocol. The mean ETCO2–PaCO2 gradient was 1.7 (±1.0) kPa (12.8 mm Hg), with moderate correlation (R2=0.23, p=0.002). The Bland-Altman bias was 1.7 (95% CI 1.4 to 2.0) kPa with upper and lower limits of agreement of 3.6 (95% CI 3.0 to 4.1) kPa and −0.2 (95% CI −0.8 to 0.3) kPa, respectively. There was no evidence of a larger gradient in more severe TBI (p=0.29). There was no significant gradient correlation in patients with a coexisting serious thoracic injury (R2=0.13, p=0.10), and this cohort had a larger ETCO2–PaCO2 gradient, 2.0 (±1.1) kPa (15.1 mm Hg), p=0.01. Patients who underwent prehospital arterial blood sampling had an arrival PaCO2 of 4.7 (±0.2) kPa (35.1 mm Hg).ConclusionThere is only moderate correlation of ETCO2 and PaCO2 at hospital arrival in patients with serious TBI. The mean ETCO2–PaCO2 gradient was 1.7 (±1.0) kPa (12.8 mm Hg). Lower ETCO2 targets than previously recommended may be safe and appropriate, and there may be a role for prehospital PaCO2 measurement.

Continuous monitoring of cerebral metabolism in traumatic brain injury: a focus on cerebral microdialysis

2006 ◽  
Vol 12 (2) ◽  
pp. 112-118 ◽  
Author(s):  
Lars Hillered ◽  
Lennart Persson ◽  
Pelle Nilsson ◽  
Elisabeth Ronne-Engstrom ◽  
Per Enblad
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Continuous Monitoring ◽  
Cerebral Metabolism ◽  
Cerebral Microdialysis

Patient-specific thresholds of intracranial pressure in severe traumatic brain injury

2014 ◽  
Vol 120 (4) ◽  
pp. 893-900 ◽  
Author(s):  
Christos Lazaridis ◽  
Stacia M. DeSantis ◽  
Peter Smielewski ◽  
David K. Menon ◽  
Peter Hutchinson ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Severe Traumatic Brain Injury ◽  
Continuous Monitoring ◽  
Cross Validation ◽  
Area Under The Curve ◽  
Reactivity Index ◽  
Patient Specific ◽  
Pressure Reactivity

Object Based on continuous monitoring of the pressure reactivity index (PRx), the authors defined individualized intracranial pressure (ICP) thresholds by graphing the relationship between ICP and PRx. These investigators hypothesized that an “ICP dose” based on individually assessed ICP thresholds would correlate more closely with the 6-month outcome when compared with ICP doses derived by the recommended universal thresholds of 20 and 25 mm Hg. Methods This study was a retrospective analysis of prospectively collected data from 327 patients with severe traumatic brain injury. Results Individualized thresholds were visually identified from graphs of PRx versus ICP; PRx > 0.2 was the cutoff. Intracranial pressure doses were then computed as the cumulative area under the curve above the defined thresholds in graphing ICP versus time. The term “Dose 20” (D20) was used to refer to an ICP threshold of 20 mm Hg; the markers D25 and DPRx were calculated similarly. Separate logistic regression models were fit with death as the outcome and each dose as the predictor, both alone and adjusted for covariates. The discriminative ability of each dose for mortality was assessed by receiver operating characteristic AUC analysis in which 5-fold cross-validation was used. A clearly identifiable PRx-based threshold was possible in 224 patients (68%). The DPRx (AUC 0.81, 95% CI 0.74–0.87) was found to have the highest area under the curve (AUC) over both D20 (0.75, 95% CI 0.68–0.81) and D25 (0.77, 95% CI 0.70–0.83); in the cross-validation model, DPRx remained the best discriminator of mortality (DPRx: AUC 0.77 [95% CI 0.68–0.89]; D20: 0.72 [95% CI 0.66–0.81]; and D25: 0.65 [95% CI 0.56–0.73]). Conclusions The authors explored the importance of different ICP thresholds for outcome by calculating patient-specific ICP doses based on the continuous monitoring of cerebrovascular pressure reactivity. They found that these individualized doses of intracranial hypertension were stronger predictors of death than doses derived from the universal thresholds of 20 and 25 mm Hg. The PRx could offer a method that can be directed toward individualizing the ICP threshold.

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