scholarly journals The Effect of Stable Xenon on ICP

1991 ◽  
Vol 11 (2) ◽  
pp. 347-350 ◽  
Author(s):  
Donald W. Marion ◽  
Kelly Crosby
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Xenon Ct ◽  
Correlation Test ◽  
Or Groups ◽  
Significant Difference ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients

Recent studies have suggested that under certain conditions, inhalation of stable xenon can cause an increase in CBF or intracranial pressure (ICP). We reviewed the ICP changes that occurred during 48 stable xenon/CT CBF studies in 23 comatose head-injured patients to determine if the concentration (32%) and duration of inhalation (4.5 min) of stable xenon we used caused an increase in ICP. In the group as a whole, there was no significant difference between the mean ICP at the start of xenon inhalation and the mean ICP immediately after completion of the studies. An increase in ICP also was not found in subgroups with low, normal, or high global CBF, or groups with or without intracranial hypertension. Changes in ICP that occurred during individual studies usually were related to corresponding changes in the arterial pco2 (p < 0.0001, Pearson's correlation test). Our data suggest that 32% stable xenon administered for 4.5 min does not cause a significant increase in ICP during xenon/CT CBF studies.

Effect of stable xenon inhalation on intracranial pressure during measurement of cerebral blood flow in head injury

1994 ◽  
Vol 81 (6) ◽  
pp. 822-828 ◽  
Author(s):  
Jan Plougmann ◽  
Jens Astrup ◽  
Jens Pedersen ◽  
Carsten Gyldensted
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Head Injury ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Stable Xenon ◽  
The Mean ◽  
Injured Patients ◽  
Fine Print

✓ Xenon-enhanced computerized tomography (CT) is well suited for measurements of cerebral blood flow (CBF) in head-injured patients. Previous studies indicated divergent results on whether inhalation of xenon may cause a clinically relevant increase in intracranial pressure (ICP). The authors employed Xe-enhanced CT/CBF measurements to study the effect of 20 minutes of inhalation of 33% xenon in oxygen on ICP, cerebral perfusion pressure (CPP), and arteriovenous oxygen difference (AVDO2) in 13 patients 3 days (mean 1 to 5 days) after severe head injury (Glasgow Coma Scale score ≤ 7). The patients were moderately hyperventilated (mean PaCO2 4.3 kPa or 32.3 mm Hg). Six patients were studied before and during additional hyperventilation. All 13 patients reacted with an increase in ICP and 11 with a decrease in CPP. The mean ICP increment was 6.9 ± 7.7 (range 2 to 17 mm Hg). The mean CPP decrement was −9.7 ± −14.6 (range 17 to 47 mm Hg). The time course of the ICP changes indicated that ICP increased rapidly during the first 5 to 6 minutes, then declined to a plateau (peak-plateau type in four of 13 patients), remained at a plateau (plateau type in six of 13), or continued to increase in three of 13, indicating individual variance in xenon reactivity. Additional hyperventilation had no effect on the xenon-induced increments in ICP but these occurred at lower ICP and higher CPP baseline levels. The AVDO2 values, an index of flow in relation to metabolism, indicated a complex effect of xenon on CBF as well as on metabolism. This study indicates that xenon inhalation for Xe-CT CBF measurements in head-injured patients according to our protocol causes clinically significant increments in ICP and decrements in CPP. It is suggested that the effect of xenon is analogous to anesthesia induction. Individual variations were observed indicating possible individual tolerance, possible influence of type and extent of the cerebral injury, disturbances in cerebrovascular reactivity, and possible influence of medication. These effects of xenon suggest that hyperventilation should be ensured in patients with evidence of reduced compliance or high ICP. On the other hand, inhalation of stable xenon is not believed to pose a risk because no signs of cerebral oligemia or ischemia were indicated in the AVDO2 values.

scholarly journals Intracranial Pressure during External Ventricular Drainage Weaning Is an Outcome Predictor of Traumatic Brain Injury

2020 ◽  
Vol 2020 ◽  
pp. 1-7
Author(s):  
Jia-cheng Gu ◽  
Hong Wu ◽  
Xing-zhao Chen ◽  
Jun-feng Feng ◽  
Guo-yi Gao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Intracranial Pressure ◽  
External Ventricular Drainage ◽  
Unfavorable Outcome ◽  
Ventricular Drainage ◽  
Outcome Group ◽  
Significant Difference ◽  
The Mean ◽  
The Relationship

External ventricular drainage (EVD) is widely used in patients with a traumatic brain injury (TBI). However, the EVD weaning trial protocol varies and insufficient studies focus on the intracranial pressure (ICP) during the weaning trial. We aimed to establish the relationship between ICP during an EVD weaning trial and the outcomes of TBI. We enrolled 37 patients with a TBI with an EVD from July 2018 to September 2019. Among them, 26 were allocated to the favorable outcome group and 11 to the unfavorable outcome group (death, post-traumatic hydrocephalus, persistent vegetative state, and severe disability). Groups were well matched for sex, pupil reactivity, admission Glasgow Coma Scale score, Marshall computed tomography score, modified Fisher score, intraventricular hemorrhage, EVD days, cerebrospinal fluid output before the weaning trial, and the complications. Before and during the weaning trial, we recorded the ICP at 1-hour intervals to calculate the mean ICP, delta ICP, and ICP burden, which was defined as the area under the ICP curve. There were significant between-group differences in the age, surgery types, and intensive care unit days (p=0.045, p=0.028, and p=0.004, respectively). During the weaning trial, 28 (75.7%) patients had an increased ICP. Although there was no significant difference in the mean ICP before and during the weaning trial, the delta ICP was higher in the unfavorable outcome group (p=0.001). Moreover, patients who experienced death and hydrocephalus had a higher ICP burden, which was above 20 mmHg (p=0.016). Receiver operating characteristic analyses demonstrated the predictive ability of these variables (area under the curve AUC=0.818 [p=0.002] for delta ICP and AUC=0.758 [p=0.038] for ICP burden>20 mmHg). ICP elevation is common during EVD weaning trials in patients with TBI. ICP-related parameters, including delta ICP and ICP burden, are significant outcome predictors. There is a need for larger prospective studies to further explore the relationship between ICP during EVD weaning trials and TBI outcomes.

The metabolic response to severe head injury

1984 ◽  
Vol 60 (4) ◽  
pp. 687-696 ◽  
Author(s):  
Guy L. Clifton ◽  
Claudia S. Robertson ◽  
Robert G. Grossman ◽  
Susan Hodge ◽  
Richard Foltz ◽  
...  
Keyword(s):  
Body Surface ◽  
Nitrogen Balance ◽  
Metabolic Response ◽  
The Body ◽  
Nitrogen Excretion ◽  
Content Type ◽  
Head Injured ◽  
The Mean ◽  
Metabolic Expenditure ◽  
Injured Patients

✓ Caloric expenditure and nitrogen balance were measured in 14 steroid-treated comatose head-injured patients acutely and up to 28 days after injury. During this period patients were fed with a continuous enteral infusion of a formula containing 2 Kcal/cc and 10 gm nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated nonparalyzed patients was 138% ± 37% of that expected for an uninjured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 135 patient-days. The mean excretion was 20.2 ± 6.4 gm/day. The mean protein caloric contribution was 23.9% ± 6.7% and was greater than 25% for six patients, compared to normal values of 10% to 15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with enterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20% to 40% of the body surface.

Role of intracranial pressure monitoring in severely head-injured patients without signs of intracranial hypertension on initial computerized tomography

1994 ◽  
Vol 80 (1) ◽  
pp. 46-50 ◽  
Author(s):  
Michael G. O'Sullivan ◽  
Patrick F. Statham ◽  
Patricia A. Jones ◽  
J. Douglas Miller ◽  
N. Mark Dearden ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Ct Scan ◽  
Intracranial Hypertension ◽  
Mass Lesion ◽  
Midline Shift ◽  
Pressure Monitoring ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Previous studies have suggested that only a small proportion (< 15%) of comatose head-injured patients whose initial computerized tomography (CT) scan was normal or did not show a mass lesion, midline shift, or abnormal basal cisterns develop intracranial hypertension. The aim of the present study was to re-examine this finding against a background of more intensive monitoring and data acquisition. Eight severely head-injured patients with a Glasgow Coma Scale score of 8 or less, whose admission CT scan did not show a mass lesion, midline shift, or effaced basal cisterns, underwent minute-to-minute recordings of arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) derived from blood pressure minus ICP. Intracranial hypertension (ICP ≥ 20 mm Hg lasting longer than 5 minutes) was recorded in seven of the eight patients; in five cases the rise was pronounced in terms of both magnitude (ICP ≥ 30 mm Hg) and duration. Reduced CPP (≤ 60 mm Hg lasting longer than 5 minutes) was recorded in five patients. Severely head-injured (comatose) patients whose initial CT scan is normal or does not show a mass lesion, midline shift, or abnormal cisterns nevertheless remain at substantial risk of developing significant secondary cerebral insults due to elevated ICP and reduced CPP. The authors recommend continuous ICP and blood pressure monitoring with derivation of CPP in all comatose head-injured patients.

Venous sinus stenting shortens the duration of medical therapy for increased intracranial pressure secondary to venous sinus stenosis

2017 ◽  
Vol 10 (3) ◽  
pp. 310-314 ◽  
Author(s):  
Tarek A Shazly ◽  
Ashutosh P Jadhav ◽  
Amin Aghaebrahim ◽  
Andrew F Ducruet ◽  
Brian T Jankowitz ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Intracranial Hypertension ◽  
Medical Therapy ◽  
Venous Sinus ◽  
Increased Intracranial Pressure ◽  
Rnfl Thickness ◽  
Group A ◽  
Sinus Stenosis ◽  
The Mean ◽  
Group B

IntroductionMedical treatment, cerebrospinal fluid (CSF) shunting, and optic nerve sheath fenestration are standard treatments for increased intracranial pressure (ICP) in patients with idiopathic intracranial hypertension (IIH). Venous sinus stenting provides a novel alternative surgical treatment in cases of venous sinus stenosis with elevated ICP.Methods12 consecutive subjects with papilledema, increased ICP, and radiological signs of dural sinus stenosis underwent cerebral venography and manometry. All subjects had papilledema and demonstrated radiological evidence of dural venous sinus stenosis.ResultsSix subjects chose venous stenting (Group A) and six declined and were managed conservatively with oral acetazolamide (Group B). The relative pressure gradient across the venous narrowing was 29±16.3 mm Hg in Group A and 17.6±9.3 mm Hg in Group B (p=0.09). The mean lumbar puncture opening pressure was 40.4±7.6 cm H2O in Group A and 35.6±10.6 cm H2O in Group B (p=0.4). Spectral domain optical coherence tomography (SD-OCT) showed mean average retinal nerve fiber layer (RNFL) thickness of 210±44.8 µm in Group A and 235±124.7 µm in Group B. However, the mean average RNFL thickness at 6 months was 85±9 µm in Group A and 95±24 µm in Group B (p=0.6). The total duration of acetazolamide treatment was 188±209 days in Group A compared with 571±544 days in Group B (p=0.07).ConclusionsIn subjects with venous sinuses stenosis, endovascular stenting offers an effective treatment option for intracranial hypertension which may shorten the duration of medical therapy.

Sign in / Sign up

Export Citation Format

Share Document