Intracranial Pressure Changes During Intrahospital Transports of Neurocritically Ill Patients

Background

Intrahospital transport is associated with a high rate of complications. Investigations of this problem using neuromonitoring remain scarce.

Methods

This is a monocentric, prospective observational study. Patients with severe brain diseases and intracranial pressure (ICP) monitoring were included. Continuous monitoring of ICP, cerebral perfusion pressure (CPP), oxygen saturation (SpO₂), heart rate, and mean arterial pressure was measured during seven different periods of intrahospital transport (baseline for 30 min, I = preparation, II = transport I, III = CT scan, IV = transport II, V = postprocessing, and follow-up for another 30 min). All complications were documented.

Results

Between July 2013 and December 2013, a total number of 56 intrahospital transports of 43 patients were performed from ICU to CT. Data recording was incomplete in six cases. Fifty transports have been taken into account for statistical analysis. Forty-two percent were emergency transports. Mean duration of the procedure was 17′ (preparation), 6′ (transport I), 9′ (CT scan), 6′ (transport II), and 15′ (postprocessing), respectively. Mean ICP at baseline was 8.53 mmHg. Comparing all periods of intrahospital transport and the follow-up period to the baseline showed a significant increase of ICP only during CT scan (15.83 mmHg, p < 0.01), not during the transport to and from the radiology department. An overall complication rate of 36 % (n = 18) was observed. In 26 % (n = 13), additional ICP therapy was necessary due to an elevation of ICP above 20 mmHg.

Conclusion

There is a considerable rate of complications during intrahospital transport of critically ill patients with severe brain diseases, with a significant increase of ICP during transport and CT scan. In one-fifth of all patients, additional therapy was necessary. From our point of view, transport of critically ill patients should only be performed by trained staff and under monitoring of ICP and CPP.

     

A Continuous Correlation Between Intracranial Pressure and Cerebral Blood Flow Velocity Reflects Cerebral Autoregulation Impairment During Intracranial Pressure Plateau Waves

Background

In the healthy brain, small oscillations in intracranial pressure (ICP) occur synchronously with those in cerebral blood volume (CBV), cerebrovascular resistance, and consequently cerebral blood flow velocity (CBFV). Previous work has shown that the usual synchrony between ICP and CBFV is lost during intracranial hypertension. Moreover, a continuously computed measure of the ICP/CBFV association (Fix index) was a more sensitive predictor of outcome after traumatic brain injury (TBI) than a measure of autoregulation (Mx index). In the current study we computed Fix during ICP plateau waves, to observe its behavior during a defined period of cerebrovascular vasodilatation.

Methods

Twenty-nine recordings of arterial blood pressure (ABP), ICP, and CBFV taken during ICP plateau waves were obtained from the Addenbrooke’s hospital TBI database. Raw data was filtered prior to computing Mx and Fix according to previously published methods. Analyzed data was segmented into three phases (pre, peak, and post), and a median value of each parameter was stored for analysis.

Results

ICP increased from a median of 22–44 mmHg before falling to 19 mmHg. Both Mx and Fix responded to the increase in ICP, with Mx trending toward +1, while Fix trended toward ?1. Mx and Fix correlated significantly (Spearman’s R = ?0.89, p < 0.000001), however, Fix spanned a greater range than Mx. A plot of Mx and Fix against CPP showed a plateau (Mx) or trough (Fix) consistent with a zone of “optimal CPP”.

Conclusions

The Fix index can identify complete loss of cerebral autoregulation as the point at which the normally positive CBF/CBV correlation is reversed. Both CBF and CBV can be monitored noninvasively using near-infrared spectroscopy (NIRS), suggesting that a noninvasive method of monitoring autoregulation using only NIRS may be possible.     

Relationship Between Brain Pulsatility and Cerebral Perfusion Pressure: Replicated Validation Using Different Drivers of CPP Change

Background

Determination of relationships between transcranial Doppler (TCD)-based spectral pulsatility index (sPI) and pulse amplitude (AMP) of intracranial pressure (ICP) in 2 groups of severe traumatic brain injury (TBI) patients (a) displaying plateau waves and (b) with unstable mean arterial pressure (MAP).

Methods

We retrospectively reviewed patients with severe TBI and continuous TCD monitoring displaying either plateau waves or unstable MAP from 1992 to 1998. We utilized linear and nonlinear regression techniques to describe both cohorts: cerebral perfusion pressure (CPP) versus AMP, CPP versus sPI, mean ICP versus ICP AMP, mean ICP versus sPI, and AMP versus sPI.

Results

Nonlinear regression techniques were employed to analyze the relationships with CPP. In plateau wave and unstable MAP patients, CPP versus sPI displayed an inverse nonlinear relationship (R ² = 0.820 vs. R ² = 0.610, respectively), with the CPP versus sPI relationship best modeled by the following function in both cases: PI = a + (b/CPP). Similarly, in both groups, CPP versus AMP displayed an inverse nonlinear relationship (R ² = 0.610 vs. R ² = 0.360, respectively). Positive linear correlations were displayed in both the plateau wave and unstable MAP cohorts between: ICP versus AMP, ICP versus sPI, AMP versus sPI.

Conclusions

There is an inverse relationship through nonlinear regression between CPP versus AMP and CPP versus sPI display. This provides evidence to support a previously-proposed model of TCD pulsatility index. ICP shows a positive linear correlation with AMP and sPI, which is also established between AMP and sPI.

     

The Effect of Positive End-Expiratory Pressure on Intracranial Pressure and Cerebral Hemodynamics

Background

Lung protective ventilation has not been evaluated in patients with brain injury. It is unclear whether applying positive end-expiratory pressure (PEEP) adversely affects intracranial pressure (ICP) and cerebral perfusion pressure (CPP). We aimed to evaluate the effect of PEEP on ICP and CPP in a large population of patients with acute brain injury and varying categories of acute lung injury, defined by PaO₂/FiO₂.

Method

Retrospective data were collected from 341 patients with severe acute brain injury admitted to the ICU between 2008 and 2015. These patients experienced a total of 28,644 paired PEEP and ICP observations. Demographic, hemodynamic, physiologic, and ventilator data at the time of the paired PEEP and ICP observations were recorded.

Results

In the adjusted analysis, a statistically significant relationship between PEEP and ICP and PEEP and CPP was found only among observations occurring during periods of severe lung injury. For every centimeter H₂O increase in PEEP, there was a 0.31 mmHg increase in ICP (p = 0.04; 95 % CI [0.07, 0.54]) and a 0.85 mmHg decrease in CPP (p = 0.02; 95 % CI [?1.48, ?0.22]).

Conclusion

Our results suggest that PEEP can be applied safely in patients with acute brain injury as it does not have a clinically significant effect on ICP or CPP. Further prospective studies are required to assess the safety of applying a lung protective ventilation strategy in brain-injured patients with lung injury.

     

Does Prone Positioning Increase Intracranial Pressure? A Retrospective Analysis of Patients with Acute Brain Injury and Acute Respiratory Failure

Purpose

The objective of our trial was to obtain more comprehensive data on the risks and benefits of kinetic therapy in intensive care patients with intracerebral pathology.

Methods

Standardized data of prone positioning in our NeuroIntensive Care Unit were collected from 2007 onward. A post hoc analysis of all available data was undertaken, with special consideration given to values of intracranial pressure (ICP), cerebral perfusion pressure (CPP) and oxygenation in correlation to prone (PP), or supine positioning (SP) of patients. Cases were considered eligible if kinetic therapy and ICP were documented. Prone positioning was performed in a 135° position for 8 h per treatment unit.

Results

A total of 115 patients treated with prone positioning from 2007 to 2013 were identified in our medical records. Of these, 29 patients received ICP monitoring. Overall, 119 treatment units of prone positioning with a mean duration of 2.5 days per patient were performed. The mean baseline ICP in SP was 9.5 ± 5.9 mmHg and was increased significantly during PP (p < 0.0001). There was no significant difference between CPP in SP (82 ± 14.5 mmHg) compared to PP (p > 0.05). ICP values >20 mmHg occurred more often during PP than SP (p < 0.0001) and were associated with significantly more episodes of decreased CPP <70 mmHg (p < 0.0022). The mean paO₂/FiO₂ ratio (P/F ratio) was increased significantly in prone positioning of patients (p < 0.0001).

Conclusions

The analyzed data allow a more precise understanding of changes in ICP and oxygenation during prone positioning in patients with acute brain injury and almost normal baseline ICP. Our study shows a moderate, yet significant elevation of ICP during prone positioning. However, the achieved increase of oxygenation by far exceeded the changes in ICP. It is evident that continuous monitoring of cerebral pressure is required in this patient group.     

Cessation of Diastolic Cerebral Blood Flow Velocity: The Role of Critical Closing Pressure

Background

Reducing cerebral perfusion pressure (CPP) below the lower limit of autoregulation (LLA) causes cerebral blood flow (CBF) to become pressure passive. Further reductions in CPP can cause cessation of CBF during diastole. We hypothesized that zero diastolic flow velocity (FV) occurs when diastolic blood pressure becomes less than the critical closing pressure (CrCP).

Methods

We retrospectively analyzed studies of 34 rabbits with CPP below the LLA, induced with pharmacologic sympathectomy (N = 23) or cerebrospinal fluid infusion (N = 11). Basilar artery blood FV and cortical Laser Doppler Flow (LDF) were monitored. CrCP was trended using a model of cerebrovascular impedance. The diastolic closing margin (DCM) was monitored as the difference between diastolic blood pressure and CrCP. LDF was recorded for DCM values greater than and less than zero.

Results

Arterial hypotension caused a reduction of CrCP (p < 0.001), consistent with decreased wall tension (p < 0.001) and a drop in intracranial pressure (ICP; p = 0.004). Cerebrospinal infusion caused an increase of CrCP (p = 0.002) accounted for by increasing ICP (p < 0.001). The DCM was compromised by either arterial hypotension or intracranial hypertension (p < 0.001 for both). When the DCM reached zero, diastolic FV ceased for a short period during each heart cycle (R = 0.426, p < 0.001). CBF pressure passivity accelerated when DCM decreased below zero (from 1.51 ± 0.51 to 2.17 ± 1.17 % ΔLDF/ΔmmHg; mean ± SD; p = 0.010).

Conclusions

The disappearance of diastolic CBF below LLA can be explained by DCM reaching zero or negative values. Below this point the decrease in CBF accelerates with further decrements of CPP.     

Cerebrovascular Pressure Reactivity and Cerebral Oxygen Regulation After Severe Head Injury

Background

To investigate the relationship between cerebrovascular pressure reactivity and cerebral oxygen regulation after head injury.

Methods

Continuous monitoring of the partial pressure of brain tissue oxygen (P_brO₂), mean arterial blood pressure (MAP), and intracranial pressure (ICP) in 11 patients. The cerebrovascular pressure reactivity index (PRx) was calculated as the moving correlation coefficient between MAP and ICP. For assessment of the cerebral oxygen regulation system a brain tissue oxygen response (TOR) was calculated, where the response of P_brO₂ to an increase of the arterial oxygen through ventilation with 100 % oxygen for 15 min is tested. Arterial blood gas analysis was performed before and after changing ventilator settings.

Results

Arterial oxygen increased from 108 ± 6 mmHg to 494 ± 68 mmHg during ventilation with 100 % oxygen. P_brO₂ increased from 28 ± 7 mmHg to 78 ± 29 mmHg, resulting in a mean TOR of 0.48 ± 0.24. Mean PRx was 0.05 ± 0.22. The correlation between PRx and TOR was r = 0.69, P = 0.019. The correlation of PRx and TOR with the Glasgow outcome scale at 6 months was r = 0.47, P = 0.142; and r = ?0.33, P = 0.32, respectively.

Conclusions

The results suggest a strong link between cerebrovascular pressure reactivity and the brain’s ability to control for its extracellular oxygen content. Their simultaneous impairment indicates that their common actuating element for cerebral blood flow control, the cerebral resistance vessels, are equally impaired in their ability to regulate for MAP fluctuations and changes in brain oxygen.     

Goal Directed Brain Tissue Oxygen Monitoring Versus Conventional Management in Traumatic Brain Injury: An Analysis of In Hospital Recovery

Background

Brain tissue oxygen monitoring (pBtO2) has been advocated in the treatment of patients with severe traumatic brain injuries (TBI); however, controversy exists regarding the improvements that pBtO2 monitoring provides. The objective of our study was to evaluate our experience and effect on mortality with goal directed pBtO2 monitoring for severe TBI compared to traditional ICP/CPP monitoring.

Methods

All patients admitted with severe TBI (GCS < 8) to our Level 1 trauma center from June 2007 through June 2009 were retrospectively analyzed. All patients had ICP monitoring and pBtO2 monitors were placed based on the current practices of the attending neurosurgeon producing two temporally matched cohorts of patients with and without pBtO2 monitors. Exclusion criteria were age <18 years and survival <24 h. Goal-directed therapy was utilized in all patients to maintain ICP <20 mmHg and CPP >60 mmHg. Patients with pBtO2 monitors were managed to maintain a level >20 mmHg.

Results

74 patients were treated for severe TBI over the 2-year study period with 37 patients in each group. Both groups were similar in age, sex, and admission Glascow Coma Score(GCS).The pBtO2-monitored group did, however, have significantly lower injury severity score [26 (25–30) vs. 30 (26–36), p = 0.03] and AIS Chest [0 (0–0) vs. 2 (0–3), p = 0.02]. There was no survival difference found (64.9 vs. 54.1 %, p = 0.34). No difference with respect to discharge GCS or discharge Functional Independence Measure score was identified.

Conclusions

Compared with ICP/CPP-directed therapy alone, the addition of pBtO2 monitoring did not provide a survival or functional status improvement at discharge. The true clinical benefit of pBtO2 monitoring will require further study.     

Effects of Early Bedside Cycle Exercise on Intracranial Pressure and Systemic Hemodynamics in Critically Ill Patients in a Neurointensive Care Unit

Background

Physiotherapy is an important part of treatment after severe brain injuries and stroke, but its effect on intracranial and systemic hemodynamics is minimally investigated. Therefore, the aim of this study was to assess the effects of an early bedside cycle exercise on intracranial and systemic hemodynamics in critically ill patients when admitted to a neurointensive care unit (NICU).

Methods

Twenty critically ill patients suffering from brain injuries or stroke were included in this study performed in the NICU at Sahlgrenska University Hospital. One early implemented exercise session was performed using a bedside cycle ergometer for 20 min. Intracranial and hemodynamic variables were measured two times before, three times during, and two times after the bedside cycling exercise. Analyzed variables were intracranial pressure (ICP), cerebral perfusion pressure (CPP), mean arterial blood pressure (MAP), heart rate (HR), peripheral oxygen saturation (SpO₂), cardiac output (CO), stroke volume (SV), and stroke volume variation (SVV). The cycling intervention was conducted within 7 ± 5 days after admission to the NICU.

Results

Cycle exercise increased MAP (p = 0.029) and SV (p = 0.003) significantly. After exercise CO, SV, MAP, and CPP decreased significantly, while no changes in HR, SVV, SpO₂, or ICP were noted when compared to values obtained during exercise. There were no differences in data obtained before versus after exercise.

Conclusion

Early implemented exercise with a bedside cycle ergometer, for patients with severe brain injuries or stroke when admitted to a NICU, is considered to be a clinically safe procedure.

     

The Physiologic Effects of Indomethacin Test on CPP and ICP in Severe Traumatic Brain Injury (sTBI)

Background

Refractory intracranial hypertension (RICH) is associated with high mortality in severe traumatic brain injury (sTBI). Indomethacin (INDO) can decrease intracranial cerebral pressure (ICP) improving cerebral pressure perfusion (CPP). Our aim was to determine modifications in ICP and CPP following INDO in RICH secondary to sTBI.

Methods

INDO was administered in a loading dose (0.8 mg/kg/15 min), followed by continuous 2-h infusion period (0.5 mg/kg/h). Clinical outcome was assessed at 30 days according to Glasgow Outcome Scale (GOS). Differences in ICP and CPP values were assessed using repeated-measures ANOVA. Receiver operating characteristic curve (AUC) was used for discrimination in predicting 30-day survival and good functional outcome (GOS 4 or 5). Analysis of INDO safety profile was also conducted.

Results

Thirty-two patients were included. Median GCS score was 6 (interquartile range: 4–7). The most frequent CT finding was the evacuated mass lesion (EML) according to Marshall classification (28.1 %). Mortality rate was 34.4 %. Within 15 min of INDO infusion, ICP decreased (Δ%: ?54.6 %; P < 0.0001), CPP increased (Δ%: +44.0 %; P < 0.0001), and the remaining was stable during the entire infusion period. Patients with good outcome (n = 12) showed a greater increase of CPP during INDO test (P = 0.028). CPP response to INDO test discriminated moderately well surviving patients (AUC = 0.751; P = 0.0098) and those with good functional recovery (AUC = 0.763; P = 0.0035) from those who died and from those with worse functional outcome, respectively. No adverse events were observed.

Conclusions

INDO appears effective in reducing ICP and improving CPP in RICH. INDO test could be a useful tool in identifying RICH patients with favorable outcome. Future studies are needed.     

A National Trial on Differences in Cerebral Perfusion Pressure Values by Measurement Location

Background

Cerebral perfusion pressure (CPP) is a key parameter in management of brain injury with suspected impaired cerebral autoregulation. CPP is calculated by subtracting intracranial pressure (ICP) from mean arterial pressure (MAP). Despite consensus on importance of CPP monitoring, substantial variations exist on anatomical reference points used to measure arterial MAP when calculating CPP. This study aimed to identify differences in CPP values based on measurement location when using phlebostatic axis (PA) or tragus (Tg) as anatomical reference points. The secondary study aim was to determine impact of differences on patient outcomes at discharge.

Methods

This was a prospective, repeated measures, multi-site national trial. Adult ICU patients with neurological injury necessitating ICP and CPP monitoring were consecutively enrolled from seven sites. Daily MAP/ICP/CPP values were gathered with the arterial transducer at the PA, followed by the Tg as anatomical reference points.

Results

A total of 136 subjects were enrolled, resulting in 324 paired observations. There were significant differences for CPP when comparing values obtained at PA and Tg reference points (p < 0.000). Differences remained significant in repeated measures model when controlling for clinical factors (mean CPP-PA = 80.77, mean CPP-Tg = 70.61, p < 0.000). When categorizing CPP as binary endpoint, 18.8% of values were identified as adequate with PA values, yet inadequate with CPP values measured at the Tg.

Conclusion

Findings identify numerical differences for CPP based on anatomical reference location and highlight importance of a standard reference point for both clinical practice and future trials to limit practice variations and heterogeneity of findings.

     

Continuous Monitoring of Cerebrovascular Reactivity Using Pulse Waveform of Intracranial Pressure

Background

Guidelines for the management of traumatic brain injury (TBI) call for the development of accurate methods for assessment of the relationship between cerebral perfusion pressure (CPP) and cerebral autoregulation and to determine the influence of quantitative indices of pressure autoregulation on outcome. We investigated the relationship between slow fluctuations of arterial blood pressure (ABP) and intracranial pressure (ICP) pulse amplitude (an index called PAx) using a moving correlation technique to reflect the state of cerebral vasoreactivity and compared it to the index of pressure reactivity (PRx) as a moving correlation coefficient between averaged values of ABP and ICP.

Methods

A retrospective analysis of prospective 327 TBI patients (admitted on neurocritical care unit of a university hospital in the period 2003?C2009) with continuous ABP and ICP monitoring.

Results

PAx was worse in patients who died compared to those who survived (?0.04?±?0.15 vs. ?0.16?±?0.15, ??²?=?28, p?2?=?6, p?=?0.01).

Conclusions

PAx is a new modified index of cerebrovascular reactivity which performs equally well as established PRx in long-term monitoring in severe TBI patients, but importantly is potentially more robust at lower values of ICP. In view of establishing an autoregulation-oriented CPP therapy, continuous determination of PAx is feasible but its value has to be evaluated in a prospective controlled trail.     

Intermittent Versus Continuous Cerebrospinal Fluid Drainage Management in Adult Severe Traumatic Brain Injury: Assessment of Intracranial Pressure Burden

Introduction

There is clinical equipoise regarding whether neurointensive care unit management of external ventricular drains (EVD) in severe traumatic brain injury (TBI) should involve an open EVD, with continuous drainage of cerebrospinal fluid (CSF), versus a closed EVD, with intermittent opening as necessary to drain CSF. In a matched cohort design, we assessed the relative impact of continuous versus intermittent CSF drainage on intracranial pressure in the management of adult severe TBI.

Methods

Sixty-two severe TBI patients were assessed. Thirty-one patients managed by open EVD drainage were matched by age, sex, and injury severity (initial Glasgow Coma Scale (GCS) score) to 31 patients treated with a closed EVD drainage. Patients in the open EVD group also had a parenchymal intracranial pressure (ICP) monitor placed through an adjacent burr hole, allowing real-time recording of ICP. Hourly ICP and other pertinent data, such as length of stay in intensive care unit (LOS-ICU), Injury Severity Score, and survival status, were extracted from our prospective database.

Results

With age, injury severity (initial GCS score), and neurosurgical intervention adjusted for, there was a statistically significant difference of 5.66 mmHg in mean ICP (p < 0.0001) between the open and the closed EVD groups, with the closed EVD group exhibiting greater mean ICP. ICP burden (ICP ≥ 20 mmHg) was shown to be significantly higher in the intermittent EVD group (p = 0.0002) in comparison with the continuous EVD group.

Conclusion

Continuous CSF drainage via an open EVD seemed to be associated with more effective ICP control in the management of adult severe TBI.     

The Neurological Wake-up Test Does not Alter Cerebral Energy Metabolism and Oxygenation in Patients with Severe Traumatic Brain Injury

Background

The neurological wake-up test (NWT) is used to monitor the level of consciousness in patients with traumatic brain injury (TBI). However, it requires interruption of sedation and may elicit a stress response. We evaluated the effects of the NWT using cerebral microdialysis (MD), brain tissue oxygenation (Pb_tiO₂), jugular venous oxygen saturation (SjvO₂), and/or arterial-venous difference (AVD) for glucose, lactate, and oxygen in patients with severe TBI.

Methods

Seventeen intubated TBI patients (age 16–74 years) were sedated using continuous propofol infusion. All patients received intracranial pressure (ICP) and cerebral perfusion pressure (CPP) monitoring in addition to MD, Pb_tiO₂ and/or SjvO₂. Up to 10 days post-injury, ICP, CPP, Pb_tiO₂ (51 NWTs), MD (49 NWTs), and/or SjvO₂ (18 NWTs) levels during propofol sedation (baseline) and NWT were compared. MD was evaluated at a flow rate of 1.0 μL/min (28 NWTs) or the routine 0.3 μL/min rate (21 NWTs).

Results

The NWT increased ICP and CPP levels (p < 0.05). Compared to baseline, interstitial levels of glucose, lactate, pyruvate, glutamate, glycerol, and the lactate/pyruvate ratio were unaltered by the NWT. Pathological SjvO₂ (<50 % or >71 %; n = 2 NWTs) and Pb_tiO₂ (<10 mmHg; n = 3 NWTs) values were rare at baseline and did not change following NWT. Finally, the NWT did not alter the AVD of glucose, lactate, or oxygen.

Conclusions

The NWT-induced stress response resulted in increased ICP and CPP levels although it did not negatively alter focal neurochemistry or cerebral oxygenation in TBI patients.     

Brain Tissue Oxygenation and Cerebral Perfusion Pressure Thresholds of Ischemia in a Standardized Pig Brain Death Model

Background

Neurointensive care of traumatic brain injury (TBI) patients is currently based on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) targeted protocols. Monitoring brain tissue oxygenation (B_tipO₂) is of considerable clinical interest, but the exact threshold level of ischemia has been difficult to establish due to the complexity of the clinical situation. The objective of this study was to use the Neurovent-PTO (NV) probe, and to define critical cerebral oxygenation- and CPP threshold levels of cerebral ischemia in a standardized brain death model caused by increasing the ICP in pig. Ischemia was defined by a severe increase of cerebral microdialysis (MD) lactate/pyruvate ratio (L/P ratio?>?30).

Methods

B_tipO₂, L/P ratio, Glucose, Glutamate, Glycerol and CPP were recorded using NV and MD probes during gradual increase of ICP by inflation of an epidural balloon catheter with saline until brain death was achieved.

Results

Baseline level of B_tipO₂ was 22.9?±?6.2?mmHg, the L/P ratio 17.7?±?6.1 and CPP 73?±?17?mmHg. B_tipO₂ and CPP decreased when intracranial volume was added. The L/P ratio increased above its ischemic levels, (>30) when CPP decreased below 30?mmHg and B_tipO₂ to <10?mmHg.

Conclusions

A severe increase of ICP leading to CPP below 30?mmHg and B_tipO₂ below 10?mmHg is associated with an increase of the L/P ratio, thus seems to be critical thresholds for cerebral ischemia under these conditions.     

Effect of Percutaneous Tracheostomy on Intracerebral Pressure and Perfusion Pressure in Patients with Acute Cerebral Dysfunction (TIP Trial): An Observational Study

Background

Bedside percutaneous tracheostomy (PT) is very commonly used for patients who require prolonged mechanical ventilation. The effect of tracheostomy on intracranial pressure (ICP) is currently a subject of controversy. The aim of our study is to clarify the relation between PT and its effect on ICP and cerebral perfusion pressure.

Methods

38 patients on our intensive care unit were included prospectively in an observational study. We examined mean values of HF, SpO₂, ICP, CPP, and MAP for changes over five different phases of the procedure using paired Mann?CWhitney U tests. A p value of <0.05 was considered significant. p values were Bonferroni corrected for multiple testing.

Results

PT was performed on 38 patients (f?=?19, m?=?19; mean?=?56?years). Median ICP before intervention was 9?mmHg. During positioning of the patient, ICP had risen to 14, during bronchoscopy to 16, and during tracheostomy to 18?mmHg, all being significantly higher than baseline level. Monitoring of MAP showed a significant increase to 101?mmHg only during tracheostomy. SpO₂ and HF did not show any significant changes. Mean duration of positioning, bronchoscopy and tracheostomy was 19, 10, and 17?min. 8 patients received osmotherapy due to a rise of ICP of more than 30?mmHg.

Conclusion

PT only leads to a significant rise of ICP during the procedure. Nevertheless, therapy of ICP is necessary in some patients. From our point of view, therefore, tracheostomy should only be performed under continuous monitoring of ICP and CPP in patients with severe cerebral dysfunctions and critically elevated ICP.     

Consideration of the Intracranial Pressure Threshold Value for the Initiation of Traumatic Brain Injury Treatment: A Xenon CT and Perfusion CT Study

Background

Monitoring of intracranial pressure (ICP) is considered to be fundamental for the care of patients with severe traumatic brain injury (TBI) and is routinely used to direct medical and surgical therapy. Accordingly, some guidelines for the management of severe TBI recommend that treatment be initiated for ICP values >20 mmHg. However, it remained to be accounted whether there is a scientific basis to this instruction. The purpose of the present study was to clarify whether the basis of ICP values >20 mmHg is appropriate.

Subject and Methods

We retrospectively reviewed 25 patients with severe TBI who underwent neuroimaging during ICP monitoring within the first 7 days. We measured cerebral blood flow (CBF), mean transit time (MTT), cerebral blood volume (CBV), and ICP 71 times within the first 7 days.

Results

Although the CBF, MTT, and CBV values were not correlated with the ICP value at ICP values ≤20 mmHg, the CBF value was significantly negatively correlated with the ICP value (r = ?0.381, P < 0.05) at ICP values >20 mmHg. The MTT value was also significantly positively correlated with the ICP value (r = 0.638, P < 0.05) at ICP values >20 mmHg.

Conclusion

The cerebral circulation disturbance increased with the ICP value. We demonstrated the cerebral circulation disturbance at ICP values >20 mmHg. This study suggests that an ICP >20 mmHg is the threshold to initiate treatments. An active treatment intervention would be required for severe TBI when the ICP was >20 mmHg.

     

Intracranial Pressure During Pressure Control and Pressure-Regulated Volume Control Ventilation in Patients with Traumatic Brain Injury: A Randomized Crossover trial

Introduction

Mechanical ventilation with control of partial arterial CO₂ pressures (PaCO₂) is used to treat or stabilize intracranial pressure (ICP) in patients with traumatic brain injury (TBI). Pressure-regulated volume control (PRVC) is a ventilator mode where inspiratory pressures are automatically adjusted to deliver the patient a pre-set stable tidal volume (TV). This may result in a more stable PaCO₂ and thus a more stable ICP compared with conventional pressure control (PC) ventilation. The aim of this study was to compare PC and PRVC ventilation in TBI patients with respect to ICP and PaCO₂.

Methods

This is a randomized crossover trial including eleven patients with a moderate or severe TBI who were mechanically ventilated and had ICP monitoring. Each patient was administered alternating 2-h periods of PC and PRVC ventilation. The outcome variables were ICP and PaCO₂.

Results

Fifty-two (26 PC, 26 PRVC) study periods were included. Mean ICP was 10.8 mmHg with PC and 10.3 mmHg with PRVC ventilation (p = 0.38). Mean PaCO₂ was 36.5 mmHg (4.87 kPa) with PC and 36.1 mmHg (4.81 kPa) with PRVC (p = 0.38). There were less fluctuations in ICP (p = 0.02) and PaCO₂ (p = 0.05) with PRVC ventilation.

Conclusions

Mean ICP and PaCO₂ were similar for PC and PRVC ventilation in TBI patients, but PRVC ventilation resulted in less fluctuation in both ICP and PaCO₂. We cannot exclude that the two ventilatory modes would have impact on ICP in patients with higher ICP values; however, the similar PaCO₂ observations argue against this.

     

Effect of Prolonged Therapeutic Hypothermia on Intracranial Pressure,Organ Function,and Hospital Outcomes Among Patients with Aneurysmal Subarachnoid Hemorrhage

Background

Global cerebral edema (GCE) with subsequent refractory intracranial hypertension complicates some cases of aneurysmal subarachnoid hemorrhage (aSAH), and typically is associated with poorer outcome. Treatment options for refractory intracranial pressure (ICP) cases are limited to decompressive hemicraniectomy (DHC) and targeted temperature management (TTM) with induced hypothermia (32–34 °C). No outcomes comparison between patients treated with either or both forms of refractory ICP therapy exists, and data on the effect of prolonged hypothermia on ICP and organ function among patients with aSAH are limited.

Methods

This is a retrospective study of aSAH patients who underwent DHC and/or prolonged hypothermia (greater than 48 h) for refractory ICP (i.e., ICP >20 mmHg after osmotherapy) in the intensive care unit of a single, tertiary-care academic center.

Results

Nineteen individuals with aSAH underwent TTM with or without DHC; sixteen patients underwent DHC alone. The patients in TTM group were younger (median age 44 years) than the DHC without TTM population (median age 60 years). TTM was started on median day 2 with a median duration of 7 days. There were no significant group differences in survival to discharge (59 % vs. 69 %) or in the mean modified Rankin score on follow-up (3.6 vs. 3.7), despite the TTM group having longer hospital length of stay (24 vs. 19 days, p = 0.03), longer duration of mechanical ventilation (20 vs. 9 days, p = 0.04), a higher cumulative fluid balance (12.8 vs. 5.1 L, p = 0.01), and higher APACHEII scores. The median maximal ICP decreased from 23.5 to 21 mmHg within 24 h of hypothermia initiation. There were no significant differences in other markers of end-organ function (respiratory, hematologic, renal, liver, and cardiac), infection rate, or adverse events between groups.

Conclusions

Use of prolonged TTM among aSAH patients with GCE and refractory ICP elevations is associated with a longer duration of mechanical ventilation but is not different in terms of neurological outcomes measured by modified Rankin score or organ function outcomes compared to patients who received DHC alone.