Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation. (Patel)

Donnelly J, et al. Individualizing Thresholds of Cerebral Perfusion Pressure Using Estimated Limits of Autoregulation. Crit Care Med. 2017 Sep;45(9):1464-1471.

OBJECTIVES: In severe traumatic brain injury, cerebral perfusion pressure management based on cerebrovascular pressure reactivity index has the potential to provide a personalized treatment target to improve patient outcomes. So far, the methods have focused on identifying “one” autoregulation-guided cerebral perfusion pressure target-called “cerebral perfusion pressure optimal”. We investigated whether a cerebral perfusion pressure autoregulation range-which uses a continuous estimation of the “lower” and “upper” cerebral perfusion pressure limits of cerebrovascular pressure autoregulation (assessed with pressure reactivity index)-has prognostic value.

DESIGN: Single-center retrospective analysis of prospectively collected data.

SETTING: The neurocritical care unit at a tertiary academic medical center.

PATIENTS: Data from 729 severe traumatic brain injury patients admitted between 1996 and 2016 were used. Treatment was guided by controlling intracranial pressure and cerebral perfusion pressure according to a local protocol.

INTERVENTIONS: None.

METHODS AND MAIN RESULTS: Cerebral perfusion pressure-pressure reactivity index curves were fitted automatically using a previously published curve-fitting heuristic from the relationship between pressure reactivity index and cerebral perfusion pressure. The cerebral perfusion pressure values at which this “U-shaped curve” crossed the fixed threshold from intact to impaired pressure reactivity (pressure reactivity index = 0.3) were denoted automatically the “lower” and “upper” cerebral perfusion pressure limits of reactivity, respectively. The percentage of time with cerebral perfusion pressure below (%cerebral perfusion pressure < lower limit of reactivity), above (%cerebral perfusion pressure > upper limit of reactivity), or within these reactivity limits (%cerebral perfusion pressure within limits of reactivity) was calculated for each patient and compared across dichotomized Glasgow Outcome Scores. After adjusting for age, initial Glasgow Coma Scale, and mean intracranial pressure, percentage of time with cerebral perfusion pressure less than lower limit of reactivity was associated with unfavorable outcome (odds ratio %cerebral perfusion pressure < lower limit of reactivity, 1.04; 95% CI, 1.02-1.06; p < 0.001) and mortality (odds ratio, 1.06; 95% CI, 1.04-1.08; p < 0.001).

CONCLUSIONS: Individualized autoregulation-guided cerebral perfusion pressure management may be a plausible alternative to fixed cerebral perfusion pressure threshold management in severe traumatic brain injury patients. Prospective randomized research will help define which autoregulation-guided method is beneficial, safe, and most practical.

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Intracranial Pressure Monitoring in Infants and Young Children With Traumatic Brain Injury. (Carroll)

Dixon RR, et al. Intracranial Pressure Monitoring in Infants and Young Children With Traumatic Brain Injury. Pediatr Crit Care Med. 2016 Nov; 17(11):1064-1072.

OBJECTIVE: To examine the use of intracranial pressure monitors and treatment for elevated intracranial pressure in children 24 months old or younger with traumatic brain injury in North Carolina between April 2009 and March 2012 and compare this with a similar cohort recruited 2000-2001.

DESIGN: Prospective, observational cohort study.

SETTING: Twelve PICUs in North Carolina.

PATIENTS: All children 24 months old or younger with traumatic brain injury, admitted to an included PICU.

INTERVENTIONS: None.

MEASUREMENT AND MAIN RESULTS: The use of intracranial pressure monitors and treatments for elevated intracranial pressure were evaluated in 238 children with traumatic brain injury. Intracranial pressure monitoring (risk ratio, 3.7; 95% CI, 1.5-9.3) and intracranial pressure therapies were more common in children with Glasgow Coma Scale less than or equal to 8 compared with Glasgow Coma Scale greater than 8. However, only 17% of children with Glasgow Coma Scale less than or equal to 8 received a monitoring device. Treatments for elevated intracranial pressure were more common in children with monitors; yet, some children without monitors received therapies traditionally used to lower intracranial pressure. Unadjusted predictors of monitoring were Glasgow Coma Scale less than or equal to 8, receipt of cardiopulmonary resuscitation, nonwhite race. Logistic regression showed no strong predictors of intracranial pressure monitor use. Compared with the 2000 cohort, children in the 2010 cohort with Glasgow Coma Scale less than or equal to 8 were less likely to receive monitoring (risk ratio, 0.5; 95% CI, 0.3-1.0), although the estimate was not precise, or intracranial pressure management therapies.

CONCLUSION: Children in the 2010 cohort with a Glasgow Coma Scale less than or equal to 8 were less likely to receive an intracranial pressure monitor or hyperosmolar therapy than children in the 2000 cohort; however, about 10% of children without monitors received therapies to decrease intracranial pressure. This suggests treatment heterogeneity in children 24 months old or younger with traumatic brain injury and a need for better evidence to support treatment recommendations for this group of children.

Effectiveness of Pharmacological Therapies for Intracranial Hypertension in Children With Severe Traumatic Brain Injury-Results From an Automated Data Collection System Time-Synched to Drug Administration.

Shein SL, et al. Effectiveness of Pharmacological Therapies for Intracranial Hypertension in Children With Severe Traumatic Brain Injury-Results From an Automated Data Collection System Time-Synched to Drug Administration. Pediatr Crit Care Med. 2016 Mar; 17(3):236-45.

OBJECTIVES: To describe acute cerebral hemodynamic effects of medications commonly used to treat intracranial hypertension in children with traumatic brain injury. Currently, data supporting the efficacy of these medications are insufficient.

DESIGN: In this prospective observational study, intracranial hypertension (intracranial pressure ≥ 20 mm Hg for > 5 min) was treated by clinical protocol. Administration times of medications for intracranial hypertension (fentanyl, 3% hypertonic saline, mannitol, and pentobarbital) were prospectively recorded and synchronized with an automated database that collected intracranial pressure and cerebral perfusion pressure every 5 seconds. Intracranial pressure crises confounded by external stimulation or mechanical ventilator adjustments were excluded. Mean intracranial pressure and cerebral perfusion pressure from epochs following drug administration were compared with baseline values using Kruskal-Wallis analysis of variance and Dunn test. Frailty modeling was used to analyze the time to intracranial pressure crisis resolution. Mixed-effect models compared intracranial pressure and cerebral perfusion pressure 5 minutes after the medication versus baseline and rates of treatment failure.

SETTING: A tertiary care children’s hospital.

PATIENTS: Children with severe traumatic brain injury (Glasgow Coma Scale score ≤ 8).

INTERVENTIONS: None.

MEASUREMENTS AND MAIN RESULTS: We analyzed 196 doses of fentanyl, hypertonic saline, mannitol, and pentobarbital administered to 16 children (median: 12 doses per patient). Overall, intracranial pressure significantly decreased following the administration of fentanyl, hypertonic saline, and pentobarbital. After controlling for administration of multiple medications, intracranial pressure was decreased following hypertonic saline and pentobarbital administration; cerebral perfusion pressure was decreased following fentanyl and was increased following hypertonic saline administration. After adjusting for significant covariates (including age, Glasgow Coma Scale score, and intracranial pressure), hypertonic saline was associated with a two-fold faster resolution of intracranial hypertension than either fentanyl or pentobarbital. Fentanyl was significantly associated with the most frequent treatment failure.

CONCLUSIONS: Intracranial pressure decreased after multiple drug administrations, but hypertonic saline may warrant consideration as the first-line drug for treating intracranial hypertension, as it was associated with the most favorable cerebral hemodynamics and fastest resolution of intracranial hypertension.

Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials. (Petrillo)

Wang X, Ding X, Tong Y, Zong J, Zhao X, Ren H, Li Q. Ketamine does not increase intracranial pressure compared with opioids: meta-analysis of randomized controlled trials. J Anesth. 2014 May 24. [Epub ahead of print]

BACKGROUND: Ketamine is traditionally avoided in sedation management of patients with risk of intracranial hypertension. However, results from many clinical trials contradict this concern. We critically analyzed the published data of the effects of ketamine on intracranial pressure (ICP) and other cerebral hemodynamics to determine whether ketamine was safe for patients with hemodynamic instability and brain injuries.

METHODS: We systematically searched the online databases of PubMed, Medline, Embase, Current Controlled Trials, and Cochrane Central (last search performed on January 15, 2014). Trial characteristics and outcomes were independently extracted by two assessors (Xin Wang, Xibing Ding). For continuous data, mean differences (MD) were formulated. If the P value of the chi-square test was >0.10 or I 2 <50 %, a fixed-effects model was used; otherwise, the random effects model was adopted.

RESULTS: Five trials (n = 198) met the inclusion criteria. Using ICP levels within the first 24 h of ketamine administration as the main outcome, the use of ketamine leads to the same ICP levels as opioids [MD = 1.94; 95 % confidence interval (95 % CI), -2.35, 6.23; P = 0.38]. There were no significant differences in mean arterial pressure values between the two groups (MD = 0.99; 95 % CI, -2.24, 4.22; P = 0.55). Ketamine administration was also comparable with opioids in the maintenance of cerebral perfusion pressure (MD = -1.07; 95 % CI, -7.95, 5.8; P = 0.76).

CONCLUSIONS: The results of this study suggest that ketamine does not increase ICP compared with opioids. Ketamine provides good maintenance of hemodynamic status. Clinical application of ketamine should not be discouraged on the basis of ICP-related concerns.

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