Pressure autoregulation, intracranial pressure, and brain tissue oxygenation in children with severe traumatic brain injury

2009 ◽  
Vol 4 (5) ◽  
pp. 420-428 ◽  
Author(s):  
Anthony A. Figaji ◽  
Eugene Zwane ◽  
A. Graham Fieggen ◽  
Andrew C. Argent ◽  
Peter D. Le Roux ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Brain Injury ◽  
Mean Arterial Pressure ◽  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Arterial Pressure ◽  
Clinical Factors ◽  
Severe Tbi ◽  
Pressure Autoregulation

Object Cerebral pressure autoregulation is an important neuroprotective mechanism that stabilizes cerebral blood flow when blood pressure (BP) changes. In this study the authors examined the association between autoregulation and clinical factors, BP, intracranial pressure (ICP), brain tissue oxygen tension (PbtO2), and outcome after pediatric severe traumatic brain injury (TBI). In particular we examined how the status of autoregulation influenced the effect of BP changes on ICP and PbtO2. Methods In this prospective observational study, 52 autoregulation tests were performed in 24 patients with severe TBI. The patients had a mean age of 6.3 ± 3.2 years, and a postresuscitation Glasgow Coma Scale score of 6 (range 3–8). All patients underwent continuous ICP and PbtO2 monitoring, and transcranial Doppler ultrasonography was used to examine the autoregulatory index (ARI) based on blood flow velocity of the middle cerebral artery after increasing mean arterial pressure by 20% of the baseline value. Impaired autoregulation was defined as an ARI < 0.4 and intact autoregulation as an ARI ≥ 0.4. The relationships between autoregulation (measured as both a continuous and dichotomous variable), outcome, and clinical and physiological variables were examined using multiple logistic regression analysis. Results Autoregulation was impaired (ARI < 0.4) in 29% of patients (7 patients). The initial Glasgow Coma Scale score was significantly associated with the ARI (p = 0.02, r = 0.32) but no other clinical factors were associated with autoregulation status. Baseline values at the time of testing for ICP, PbtO2, the ratio of PbtO2/PaO2, mean arterial pressure, and middle cerebral artery blood flow velocity were similar in the patients with impaired or intact autoregulation. There was an inverse relationship between ARI (continuous and dichotomous) with a change in ICP (continuous ARI, p = 0.005; dichotomous ARI, p = 0.02); that is, ICP increased with the BP increase when ARI was low (weak autoregulation). The ARI (continuous and dichotomous) was also inversely associated with a change in PbtO2 (continuous ARI, p = 0.002; dichotomous ARI, p = 0.02). The PbtO2 increased when BP was increased in most patients, even when the ARI was relatively high (stronger autoregulation), but the magnitude of this response was still associated with the ARI. There was no relationship between the ARI and outcome. Conclusions These data demonstrate the influence of the strength of autoregulation on the response of ICP and PbtO2 to BP changes and the variability of this response between individuals. The findings suggest that autoregulation testing may assist clinical decision-making in pediatric severe TBI and help better define optimal BP or cerebral perfusion pressure targets for individual patients.

Decompressive craniectomy in a neurologically devastated pregnant woman to maintain fetal viability

2012 ◽  
Vol 116 (3) ◽  
pp. 487-490 ◽  
Author(s):  
Nathaniel Whitney ◽  
Ahmed M. Raslan ◽  
Brian T. Ragel
Keyword(s):  
Traumatic Brain Injury ◽  
Pregnant Woman ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Decompressive Craniectomy ◽  
Aggressive Management ◽  
Severe Tbi ◽  
Aggressive Medical Management ◽  
In Utero Development

Severe traumatic brain injury (TBI) in pregnant women can result in devastating outcomes for both the mother and the fetus. Historically, there has been concern regarding the issues involved when the fetus is not yet viable outside the womb. Currently, the ability to treat severe TBI with aggressive management of intracranial pressure (ICP) has led to the possibility of sustaining maternal life until the fetus is of a viable age and can be delivered. The authors present the case of a young woman 21 weeks pregnant with a severe TBI (Glasgow Coma Scale Score 3) in whom safe medical ICP management became ineffective. A decompressive craniectomy was performed to obviate the need for aggressive medical management of elevated ICP using fetal-toxic medications, and thus providing the fetus the best chance of continued in utero development until a viable gestational age was reached.

scholarly journals Modulated Neuroprotection in Unresponsive Wakefulness Syndrome after Severe Traumatic Brain Injury

2021 ◽  
Vol 11 (8) ◽  
pp. 1044
Author(s):  
Cristina Daia ◽  
Cristian Scheau ◽  
Aura Spinu ◽  
Ioana Andone ◽  
Cristina Popescu ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glasgow Coma Scale ◽  
Severe Traumatic Brain Injury ◽  
Functional Independence ◽  
Unresponsive Wakefulness Syndrome ◽  
Coma Scale ◽  
Severe Tbi ◽  
Neuroprotective Treatment ◽  
Gcs Score

Background: We aimed to assess the effects of modulated neuroprotection with intermittent administration in patients with unresponsive wakefulness syndrome (UWS) after severe traumatic brain injury (TBI). Methods: Retrospective analysis of 60 patients divided into two groups, with and without neuroprotective treatment with Actovegin, Cerebrolysin, pyritinol, L-phosphothreonine, L-glutamine, hydroxocobalamin, alpha-lipoic acid, carotene, DL-α-tocopherol, ascorbic acid, thiamine, pyridoxine, cyanocobalamin, Q 10 coenzyme, and L-carnitine alongside standard treatment. Main outcome measures: Glasgow Coma Scale (GCS) after TBI, Extended Glasgow Coma Scale (GOS E), Disability Rankin Scale (DRS), Functional Independence Measurement (FIM), and Montreal Cognitive Assessment (MOCA), all assessed at 1, 3, 6, 12, and 24 months after TBI. Results: Patients receiving neuroprotective treatment recovered more rapidly from UWS than controls (p = 0.007) passing through a state of minimal consciousness and gradually progressing until the final evaluation (p = 0.000), towards a high cognitive level MOCA = 22 ± 6 points, upper moderate disability GOS-E = 6 ± 1, DRS = 6 ± 4, and an assisted gait, FIM =101 ± 25. The improvement in cognitive and physical functioning was strongly correlated with lower UWS duration (−0.8532) and higher GCS score (0.9803). Conclusion: Modulated long-term neuroprotection may be the therapeutic key for patients to overcome UWS after severe TBI.

Cerebral Metabolism and Blood Flow Following Traumatic Brain Injury

2018 ◽  
Author(s):  
Ryan Martin ◽  
Lara Zimmermann ◽  
Marike Zwienenberg ◽  
Kee D Kim ◽  
Kiarash Shahlaie
Keyword(s):  
Traumatic Brain Injury ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Metabolism ◽  
Elevated Intracranial Pressure ◽  
Metabolic Demand ◽  
Cerebral Metabolic Rate

The management of traumatic brain injury focuses on the prevention of second insults, which most often occur because of a supply/demand mismatch of the cerebral metabolism. The healthy brain has mechanisms of autoregulation to match the cerebral blood flow to the cerebral metabolic demand. After trauma, these mechanisms are disrupted, leaving the patient susceptible to episodes of hypotension, hypoxemia, and elevated intracranial pressure. Understanding the normal and pathologic states of the cerebral blood flow is critical for understanding the treatment choices for a patient with traumatic brain injury. In this chapter, we discuss the underlying physiologic principles that govern our approach to the treatment of traumatic brain injury. This review contains 3 figures, 1 table and 12 references Key Words: cerebral autoregulation, cerebral blood flow, cerebral metabolic rate, intracranial pressure, ischemia, reactivity, vasoconstriction, vasodilation, viscosity

Trauma: Traumatic Brain Injury

2018 ◽  
pp. 95-100
Author(s):  
Ruchir Gupta
Keyword(s):  
Traumatic Brain Injury ◽  
Substance Abuse ◽  
Acute Respiratory Distress Syndrome ◽  
Cervical Spine ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Elevated Intracranial Pressure ◽  
Intraoperative Management ◽  
History Of

In this chapter the essential aspects of anesthesia for traumatic brain injury are discussed. Subtopics include manifestations and treatment of elevated intracranial pressure (ICP), Glasgow Coma Scale (GCS), drugs used to lower ICP, and patient monitoring. The case presented is an emergent craniotomy. The chapter is divided into preoperative, intraoperative, and postoperative sections with important subtopics related to the main topic in each section. Preoperative topics discussed are evaluation of trauma, use of the GCS in this case, assessing intracranial hypertension, history of substance abuse, and clearing the cervical spine. Issues related to intraoperative management in this case include induction and use of blood products. Postoperative concerns addressed include polyuria and acute respiratory distress syndrome.

scholarly journals High Serum Caspase-Cleaved Cytokeratin-18 Levels and Mortality of Traumatic Brain Injury Patients

2019 ◽  
Vol 9 (10) ◽  
pp. 269 ◽  
Author(s):  
Leonardo Lorente ◽  
María M. Martín ◽  
Agustín F. González-Rivero ◽  
Antonia Pérez-Cejas ◽  
Mónica Argueso ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Glasgow Coma Scale ◽  
Area Under The Curve ◽  
High Serum ◽  
Early Mortality ◽  
Cytokeratin 18 ◽  
New Findings ◽  
Severe Tbi ◽  
Time Of Admission

Objective: Apoptosis increases in traumatic brain injury (TBI). Caspase-cleaved cytokeratin (CCCK)-18 in blood during apoptosis could appear. At the time of admission due to TBI, higher blood CCCK-18 levels were found in non-surviving than in surviving patients. Therefore, the objective of our study was to analyze whether serum CCCK-18 levels determined during the first week after TBI could predict early mortality (at 30 days). Methods: Severe TBI patients were included (considering severe when Glasgow Coma Scale < 9) in this observational and multicentre study. Serum CCCK-18 levels were determined at day 1 of TBI, and at days 4 and 8 after TBI. Results: Serum CCCK-18 levels at day 1 of TBI, and in the days 4 and 8 after TBI were higher (p < 0.001) in non-surviving than in surviving patients (34 and 90 patients, respectively) and could predict early mortality (p < 0.001 in the area under the curve). Conclusions: The new findings from our study were that serum CCCK-18 levels at any moment of the first week of TBI were higher in non-surviving patients and were able to predict early mortality.

Transcranial Doppler to Screen on Admission Patients With Mild to Moderate Traumatic Brain Injury

Neurosurgery ◽  
2011 ◽  
Vol 68 (6) ◽  
pp. 1603-1610 ◽  
Author(s):  
Pierre Bouzat ◽  
Gilles Francony ◽  
Philippe Declety ◽  
Céline Genty ◽  
Affif Kaddour ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
At Risk ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Brain Injury ◽  
Glasgow Coma Scale ◽  
Pulsatility Index ◽  
Area Under Curve ◽  
Moderate Traumatic Brain Injury ◽  
Patients At Risk

Abstract BACKGROUND: Detecting patients at risk for secondary neurological deterioration (SND) after mild to moderate traumatic brain injury is challenging. OBJECTIVE: To assess the diagnostic accuracy of transcranial Doppler (TCD) on admission in screening these patients. METHODS: This prospective, observational cohort study enrolled 98 traumatic brain injury patients with an initial Glasgow Coma Scale score of 9 to 15 whose initial computed tomography (CT) scan showed either absent or mild lesions according to the Trauma Coma Data Bank (TCDB) classification, ie, TCDB I and TCDB II, respectively. TCD measurements of the 2 middle cerebral arteries were obtained on admission under stable conditions in all patients. Neurological outcome was reassessed on day 7. RESULTS: Of the 98 patients, 21 showed SND, ie, a decrease of ≥ 2 points from the initial Glasgow Coma Scale or requiring any treatment for neurological deterioration. Diastolic cerebral blood flow velocities and pulsatility index measurements were different between patients with SND and patients with no SND. Using receiver-operating characteristic analysis, we found the best threshold limits to be 25 cm/s (sensitivity, 92%; specificity, 76%; area under curve, 0.93) for diastolic cerebral blood flow velocity and 1.25 (sensitivity, 90%; specificity, 91%; area under curve, 0.95) for pulsatility index. According to a recursive-partitioning analysis, TCDB classification and TCD measurements were the most discriminative among variables to detect patients at risk for SND. CONCLUSION: In patients with no severe brain lesions on CT after mild to moderate traumatic brain injury, TCD on admission, in complement with brain CT scan, could accurately screen patients at risk for SND.

scholarly journals Increased mortality in patients with severe traumatic brain injury treated without intracranial pressure monitoring

2012 ◽  
Vol 117 (4) ◽  
pp. 729-734 ◽  
Author(s):  
Arash Farahvar ◽  
Linda M. Gerber ◽  
Ya-Lin Chiu ◽  
Nancy Carney ◽  
Roger Härtl ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Severe Traumatic Brain Injury ◽  
Lower Mortality ◽  
Icp Monitoring ◽  
Improvement Program ◽  
Severe Tbi ◽  
Gcs Score

Object Evidence-based guidelines recommend intracranial pressure (ICP) monitoring for patients with severe traumatic brain injury (TBI), but there is limited evidence that monitoring and treating intracranial hypertension reduces mortality. This study uses a large, prospectively collected database to examine the effect on 2-week mortality of ICP reduction therapies administered to patients with severe TBI treated either with or without an ICP monitor. Methods From a population of 2134 patients with severe TBI (Glasgow Coma Scale [GCS] Score <9), 1446 patients were treated with ICP-lowering therapies. Of those, 1202 had an ICP monitor inserted and 244 were treated without monitoring. Patients were admitted to one of 20 Level I and two Level II trauma centers, part of a New York State quality improvement program administered by the Brain Trauma Foundation between 2000 and 2009. This database also contains information on known independent early prognostic indicators of mortality, including age, admission GCS score, pupillary status, CT scanning findings, and hypotension. Results Age, initial GCS score, hypotension, and CT scan findings were associated with 2-week mortality. In addition, patients of all ages treated with an ICP monitor in place had lower mortality at 2 weeks (p = 0.02) than those treated without an ICP monitor, after adjusting for parameters that independently affect mortality. Conclusions In patients with severe TBI treated for intracranial hypertension, the use of an ICP monitor is associated with significantly lower mortality when compared with patients treated without an ICP monitor. Based on these findings, the authors conclude that ICP-directed therapy in patients with severe TBI should be guided by ICP monitoring.

scholarly journals Increased S-Nitrosothiols and S-Nitrosoalbumin in Cerebrospinal Fluid after Severe Traumatic Brain Injury in Infants and Children: Indirect Association with Intracranial Pressure

2003 ◽  
Vol 23 (1) ◽  
pp. 51-61 ◽  
Author(s):  
Hülya Bayir ◽  
Patrick M. Kochanek ◽  
Shang-Xi Liu ◽  
Antonio Arroyo ◽  
Anatoly Osipov ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cerebrospinal Fluid ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
Fold Increase ◽  
Infants And Children ◽  
No Production ◽  
Secondary Damage ◽  
Severe Tbi ◽  
Pediatric Tbi

Nitric oxide (NO) is implicated in both secondary damage and recovery after traumatic brain injury (TBI). Transfer of NO groups to cysteine sulfhydryls on proteins produces S-nitrosothiols (RSNO). S-nitrosothiols may be neuroprotective after TBI by nitrosylation of N-methyl-D-aspartate receptor and caspases. S-nitrosothiols release NO on decomposition for which endogenous reductants (i.e., ascorbate) are essential, and ascorbate is depleted in cerebrospinal fluid (CSF) after pediatric TBI. This study examined the presence and decomposition of RSNO in CSF and the association between CSF RSNO level and physiologic parameters after severe TBI. Cerebrospinal fluid samples (n = 72) were obtained from 18 infants and children on days 1 to 3 after severe TBI (Glasgow Coma Scale score < 8) and 18 controls. Cerebrospinal fluid RSNO levels assessed by fluorometric assay peaked on day 3 versus control (1.42 ± 0.11 μmol/L vs. 0.86 ± 0.04, P < 0.05). S-nitrosoalbumin levels were also higher after TBI (n = 8, 0.99 ± 0.09 μmol/L on day 3 vs. n = 6, 0.42 ± 0.02 in controls, P < 0.05). S-nitrosoalbumin decomposition was decreased after TBI. Multivariate analysis showed an inverse relation between CSF RSNO and intracranial pressure and a direct relation with barbiturate treatment. Using a novel assay, the presence of RSNO and S-nitrosoalbumin in human CSF, an ∼1.7-fold increase after TBI, and an association with low intracranial pressure are reported, supporting a possible neuroprotective role for RSNO. The increase in RSNO may result from increased NO production and/or decreased RSNO decomposition.

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