Hemodynamic characterization of intracranial pressure plateau waves in head-injured patients

1999 ◽  
Vol 91 (1) ◽  
pp. 11-19 ◽  
Author(s):  
Marek Czosnyka ◽  
Piotr Smielewski ◽  
Stefan Piechnik ◽  
Eric A. Schmidt ◽  
Pippa G. Al-Rawi ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Flow Velocity ◽  
Reduced Pressure ◽  
Content Type ◽  
Plateau Waves ◽  
Compensatory Reserve ◽  
Head Injured ◽  
Clinical Consequences ◽  
Injured Patients ◽  
Fine Print

Object. Plateau waves of intracranial pressure (ICP) are often recorded during intensive care monitoring of severely head injured patients. They are traditionally interpreted as meaningful secondary brain insults because of the dramatic decrease in cerebral perfusion pressure (CPP). The aim of this study was to investigate both the hemodynamic profile and the clinical consequences of plateau waves.Methods. One hundred sixty head-injured patients were studied using continuous monitoring of ICP; almost 20% of these patients exhibited plateau waves. In 96 patients arterial pressure, ICP, and transcranial Doppler (TCD) blood flow velocity were studied daily for 20 minutes to 3 hours. Sixteen episodes of plateau waves in eight patients were recorded and analyzed.The dramatic increase in ICP was followed by a profound fall in CPP (by 45%). In contrast, flow velocity fell by only 20%. Autoregulation was documented to be intact both before and after plateau but was disturbed during the wave (p < 0.05). Pressure-volume compensatory reserve was always depleted before the wave. Cerebrovascular resistance decreased during the wave by 60% (p <0.05) and TCD pulsatility increased (p <0.05). Plateau waves did not increase the probability of an unfavorable outcome following injury.Conclusions. The authors have confirmed that the plateau waves are a hemodynamic phenomenon associated with cerebrovascular vasodilation. They are observed in patients with preserved cerebral autoregulation but reduced pressure-volume compensatory reserve.

Little benefit from mild hypothermia therapy for severely head injured patients with low intracranial pressure

1999 ◽  
Vol 91 (2) ◽  
pp. 185-191 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Amami Kato ◽  
Mamoru Taneda ◽  
Toshiaki Hayakata ◽  
Naoyuki Hashiguchi ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Mild Hypothermia ◽  
Neurological Status ◽  
High Dose ◽  
Fluid Restriction ◽  
Content Type ◽  
Head Injured ◽  
Factor Α ◽  
Injured Patients ◽  
Fine Print

Object. This study was performed to determine whether mild hypothermia therapy is essential for the treatment of severely head injured patients in whom intracranial pressure (ICP) can be maintained below 20 mm Hg by using conventional therapies.Methods. Sixteen consecutive severely head injured patients fulfilled the following criteria: the patient's ICP was maintained below 20 mm Hg by using fluid restriction, hyperventilation, and high-dose barbiturate therapy; and the patient had a Glasgow Coma Scale score of 8 or less on admission. After conventional therapies had been applied, the patients were divided randomly into two groups: the mild hypothermia group (HT group; eight patients) and the normothermia group (NT group; eight patients). The HT group received mild hypothermia (intracranial temperature 34°C) therapy for 48 hours followed by rewarming at 1°C per day for 3 days, whereas the NT group received normothermia (intracranial temperature 37°C) therapy for 5 days. Specimens of cerebrospinal fluid (CSF) taken from an intraventricular catheter every 24 hours were analyzed for the presence of excitatory amino acids ([EAAs] glutamate, aspartate, and glycine) and cytokines (tumor necrosis factor—α, interleukin [IL]-1β, IL-6, IL-8, and IL-10). The two groups did not differ significantly in patient age, neurological status, or level of ICP. There were no significant differences in daily changes in CSF concentrations of EAAs and cytokines between the two groups. The incidence of pneumonia was slightly higher in the HT group compared with the NT group (p = 0.059). The incidence of diabetes insipidus associated with hypernatremia was significantly higher in the HT group compared with that in the NT group (p < 0.01). The two groups did not differ with respect to their clinical outcomes.Conclusions. The authors recommend normothermia therapy for the treatment of severely head injured patients in whom ICP can be maintained at lower than 20 mm Hg by using conventional therapies, because mild hypothermia therapy does not convey any advantage over normothermia therapy in such patients.

Efficacy of hyperventilation, blood pressure elevation, and metabolic suppression therapy in controlling intracranial pressure after head injury

2002 ◽  
Vol 97 (5) ◽  
pp. 1045-1053 ◽  
Author(s):  
Matthias Oertel ◽  
Daniel F. Kelly ◽  
Jae Hong Lee ◽  
David L. McArthur ◽  
Thomas C. Glenn ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Content Type ◽  
Head Injured ◽  
Induced Hypertension ◽  
Metabolic Suppression ◽  
Gcs Score ◽  
Injured Patients ◽  
Fine Print

Object. Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. Methods. Thirty-three patients with a mean age of 33 ± 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 ± 5 to 27 ± 5 mm Hg and in ICP from 20 ± 11 to 13 ± 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 ± 5 mm Hg and ICP increased from 16 ± 9 to 19 ± 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 ± 10 to 16 ± 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. Conclusions Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.

Cerebrovascular carbon dioxide reactivity assessed by intracranial pressure dynamics in severely head injured patients

1995 ◽  
Vol 82 (3) ◽  
pp. 386-393 ◽  
Author(s):  
Masaaki Yoshihara ◽  
Kuniaki Bandoh ◽  
Anthony Marmarou
Keyword(s):  
Intracranial Pressure ◽  
Glasgow Coma Scale ◽  
Blood Volume ◽  
Volume Change ◽  
Volume Index ◽  
Content Type ◽  
Coma Scale ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Appropriate management of intracranial pressure (ICP) in severely head injured patients depends in part on the cerebral vessel reactivity to PCO2; loss of CO2 reactivity has been associated with poor outcome. This study describes a new method for evaluating vascular reactivity in head-injured patients by determining the sensitivity of ICP change to alterations in PCO2. This method was combined with measurements of the pressure volume index (PVI), which allowed calculation of blood volume change necessary to alter ICP. The objective of this study was to investigate the ICP response and the blood volume change corresponding to alterations in PCO2 and to examine the correlation of responsivity and outcome as measured on the Glasgow Outcome Scale. The PVI and ICP at different end-tidal PCO2 levels produced by mild hypo- and hyperventilation were obtained in 49 patients with Glasgow Coma Scale scores of less than 8 and over a wide range of PCO2 (25 to 40 mm Hg) in eight patients. Given the assumption that the PVI remained constant during alteration of PaCO2, the estimated blood volume change per torr change of PCO2 was calculated by the following equation: BVR = PVI × Δlog(ICP)/ΔPCO2, where BVR = blood volume reactivity. The data in this study showed that PVI remained stable with changes in PCO2, thus validating the assumption used in the blood volume estimates. Moreover, the response of ICP to PCO2 alterations followed an exponential curve that could be described in terms of the responsivity indices to capnic stimuli. It was found that responsivity to hypocapnia was reduced by 50% compared to responsivity to hypercapnia measured within 24 hours of injury (p < 0.01). The sensitivity of ICP to estimated blood volume changes in patients with a PVI of less than 15 ml was extremely high with only 4 ml of blood required to raise ICP by 10 mm Hg. The authors conclude from these data that, following traumatic injury, the resistance vessels are in a state of persistent vasoconstriction, possibly due to vasospasm or compression. Furthermore, BVR correlates with outcome on the Glasgow Coma Scale, indicating that assessment of cerebrovascular response within the first 24 hours of injury may be of prognostic value.

Interhemispheric supratentorial intracranial pressure gradients in head-injured patients: are they clinically important?

1999 ◽  
Vol 90 (1) ◽  
pp. 16-26 ◽  
Author(s):  
Juan Sahuquillo ◽  
Maria-Antonia Poca ◽  
Mercedes Arribas ◽  
Angel Garnacho ◽  
Enrique Rubio
Keyword(s):  
Intracranial Pressure ◽  
Clinical Significance ◽  
Focal Lesion ◽  
Entire Group ◽  
Midline Shift ◽  
Focal Lesions ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. It is generally accepted that the intracranial compartment behaves as a unicameral space in which intracranial pressure (ICP) is uniformly distributed. However, this concept has been challenged many times. Although there is general agreement on the existence of craniospinal and suprainfratentorial gradients, the existence of interhemispheric gradients is still a matter of debate. The object of this study was to reexamine the issue of interhemispheric supratentorial ICP gradients in patients with head injuries and the clinical significance of these gradients in their management.Methods. The authors present the results of a prospective study conducted in 50 head-injured patients to determine the clinical significance of supratentorial ICP gradients. In each case a concurrent bilateral frontal intraparenchymatous device was implanted within the 6-hour window after computerized tomography (CT) scanning. According to CT criteria, each patient was categorized into one of three different groups: 1) diffuse lesions, in which no unilaterally measured volumes greater than 25 ml were present and the midline shift was 3 mm or less; 2) Focal A, in which added hemispheric volumes were greater than 25 ml and midline shift was 3 mm or less; and 3) Focal B, in which all patients with a midline shift greater than 3 mm were included. From the results of the entire group the authors were able to distinguish four different patterns of supratentorial ICP. In Pattern I, the intracranial compartment behaved as a true unicameral space with similar mean ICPs and pulse amplitudes in both hemispheres; in Pattern II, different mean ICPs and amplitudes were observed although ICP increases or decreases were congruent; and in Pattern III, patients with different mean ICPs, different ICP amplitudes, and no congruent increases or decreases of ICP were included. All (15 cases) but one patient with a diffuse lesion presented with ICP Pattern I. Fifteen patients with focal lesions showed a Type II pattern, whereas only one patient presented with a Type III pattern. In 10 patients, of whom all but one presented with a focal lesion, transient gradients that disappeared in less than 4 hours were also observed.Conclusions. In many patients with focal lesions, clinically important interhemispheric ICP gradients exist. In this subset, transient gradients that disappear with time are frequently observed and may indicate an increase in the size of the lesion. The clinical relevance of such gradients is discussed and guidelines for adequately monitoring ICP are suggested to optimize head injury management and to avoid suboptimal or even harmful care in patients with mass lesions.

A multicenter prospective randomized controlled trial of the efficacy of mild hypothermia for severely head injured patients with low intracranial pressure

2001 ◽  
Vol 94 (1) ◽  
pp. 50-54 ◽  
Author(s):  
Tadahiko Shiozaki ◽  
Toshiaki Hayakata ◽  
Mamoru Taneda ◽  
Yoshikazu Nakajima ◽  
Naoyuki Hashiguchi ◽  
...  
Keyword(s):  
Randomized Controlled Trial ◽  
Intracranial Pressure ◽  
Mild Hypothermia ◽  
Controlled Trial ◽  
Content Type ◽  
Randomized Controlled ◽  
Prospective Randomized Controlled Trial ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The criteria for the use of mild hypothermia (34°C) in severely head injured patients have not been standardized. A prospective randomized controlled trial was conducted to determine whether mild hypothermia is essential in the treatment of severely head injured patients with low intracranial pressure (ICP). Methods. At 11 medical centers, 91 severely head injured patients with an admission Glasgow Coma Scale score of 8 or less in whom ICP could be maintained below 25 mm Hg by conventional therapies were divided randomly into two groups: the mild hypothermia group (HT group, 45 patients) and the normothermia group (NT group, 46 patients). Patients in the HT group were exposed to mild hypothermia (34°C) for 48 hours, followed by rewarming at 1°C per day for 3 days, whereas patients in the NT group were exposed to normothermia (37°C) for 5 days. The two groups were similar with respect to prognostic factors, and there was no difference in clinical outcome at 3 months postinjury. During treatment, there was a significantly greater use of neuromuscular blocking agents in the HT group (p = 0.011). During the initial 2 weeks postinjury, the incidences of pneumonia, meningitis, leukocytopenia, thrombocytopenia, hypernatremia, hypokalemia, and hyperamylasemia were significantly higher in the HT than in the NT group (p <0.05). Conclusions. Mild hypothermia should not be used for the treatment of severely head injured patients with low ICP because this therapy conveys no advantage over normothermia in such patients.

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.

Cerebral perfusion pressure in head-injured patients: a noninvasive assessment using transcranial Doppler ultrasonography

1998 ◽  
Vol 88 (5) ◽  
pp. 802-808 ◽  
Author(s):  
Marek Czosnyka ◽  
Basil F. Matta ◽  
Piotr Smielewski ◽  
Peter J. Kirkpatrick ◽  
John D. Pickard
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Transcranial Doppler ◽  
Cerebral Perfusion ◽  
Doppler Ultrasonography ◽  
Perfusion Pressure ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

Object. The authors studied the reliability of a new method for noninvasive assessment of cerebral perfusion pressure (CPP) in head-injured patients in which mean arterial blood pressure (ABP) and transcranial Doppler middle cerebral artery mean and diastolic flow velocities are measured. Methods. Cerebral perfusion pressure was estimated (eCPP) over periods of continuous monitoring (20 minutes—2 hours, 421 daily examinations) in 96 head-injured patients (Glasgow Coma Scale score < 13) who were admitted to the intensive care unit. All patients were sedated, paralyzed, and ventilated. The eCPP and the measured CPP (ABP minus intracranial pressure, measured using an intraparenchymal microsensor) were compared. The correlation between eCPP and measured CPP was r = 0.73; p < 10−6. In 71% of the examinations, the estimation error was less than 10 mm Hg and in 84% of the examinations, the error was less than 15 mm Hg. The method had a high positive predictive power (94%) for detecting low CPP (< 60 mm Hg). The eCPP also accurately reflected changes in measured CPP over time (r > 0.8; p < 0.001) in situations such as plateau and B waves of intracranial pressure, arterial hypotension, and refractory intracranial hypertension. A good correlation was found between the average measured CPP and eCPP when day-by-day variability was assessed in a group of 41 patients (r = 0.71). Conclusions. Noninvasive estimation of CPP by using transcranial Doppler ultrasonography may be of value in situations in which monitoring relative changes in CPP is required without invasive measurement of intracranial pressure.

NINDS Traumatic Coma Data Bank: intracranial pressure monitoring methodology

1991 ◽  
Vol 75 (Supplement) ◽  
pp. S21-S27 ◽  
Author(s):  
Anthony Marmarou ◽  
Randy L. Anderson ◽  
John D. Ward ◽  
Sung C. Choi ◽  
Harold F. Young ◽  
...  
Keyword(s):  
Intracranial Pressure ◽  
Data Bank ◽  
The United States ◽  
Physiological Data ◽  
Intensity Level ◽  
Content Type ◽  
Head Injured ◽  
Traumatic Coma ◽  
Injured Patients ◽  
Fine Print

✓ This report describes the methods used by the Traumatic Coma Data Bank (TCDB) for acquisition and recording of intracranial pressure (ICP) data of severely head-injured patients. Direct computerization of physiological data from all four participating locations within the United States and transmission to a central data bank was found to be logistically complex and costly. A simple manual method for recording ICP, blood pressure, and concomitant ICP therapy at the bedside is described. The method documents the temporal course of these variables for the duration of monitoring. The importance of relating ICP to the therapy intensity level used for ICP management is emphasized. Concomitant analysis of the therapy intensity level is considered imperative in correlative patient studies. The methods described in this report have been in use among all four TCDB hospitals. Examples of ICP data retrieved from the TCDB are presented to illustrate the adequacy of the methods for assessing temporal trends. Of 1030 patients admitted to the TCDB, 654 severely head-injured patients had at least 4 hours of monitoring recorded; elevated ICP (> 20 mm Hg) was observed in 72% of these 654 patients.

Contribution of CSF and vascular factors to elevation of ICP in severely head-injured patients

1987 ◽  
Vol 66 (6) ◽  
pp. 883-890 ◽  
Author(s):  
Anthony Marmarou ◽  
Angelo L. Maset ◽  
John D. Ward ◽  
Sung Choi ◽  
Danny Brooks ◽  
...  
Keyword(s):  
Severe Head Injury ◽  
Ventricular Catheter ◽  
Outflow Resistance ◽  
Content Type ◽  
Relative Contribution ◽  
Temporal Course ◽  
Head Injured ◽  
Predominant Factor ◽  
Injured Patients ◽  
Fine Print

✓ The authors studied the relative contribution of cerebrospinal fluid (CSF) and vascular parameters to the level of intracranial pressure (ICP) in 34 severely head-injured patients with a Glasgow Coma Scale score of less than 8. This was accomplished by first characterizing the temporal course of CSF formation and outflow resistance during the 5-day period postinjury. The CSF formation and outflow resistance were obtained from pressure responses to bolus addition and removal of fluid from an indwelling ventricular catheter. The vascular contribution to the level of ICP was assessed by withdrawing fluid at its rate of formation and observing the resultant change in equilibrium ICP level. It was found that, with the exception of patients with subarachnoid hemorrhage, CSF parameters accounted for approximately one-third of the ICP rise after severe head injury, and that a vascular mechanism may be the predominant factor in elevation of ICP.

Impairment of helper T-cell function and lymphokineactivated killer cytotoxicity following severe head injury

1991 ◽  
Vol 75 (5) ◽  
pp. 766-773 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Edmund H. Frank ◽  
Claramae H. Miller ◽  
Asim Amin ◽  
Bernardo W. Issel ◽  
...  
Keyword(s):  
T Cell ◽  
Head Injury ◽  
Severe Head Injury ◽  
Cell Cytotoxicity ◽  
Content Type ◽  
Lak Cell ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Infection is a major complication of severe head injury, occurring in 50% to 75% of patients who survive to hospitalization. Previous investigations of immune activity following head injury have demonstrated suppression of helper T-cell activation. In this study, the in vitro production of interferon-gamma (INF-γ), interleukin-1 (IL-1), and interleukin-2 (IL-2) was determined in 25 head-injured patients following incubation of peripheral blood lymphocytes (PBL's) with the lymphocyte mitogen phytohemagglutinin (PHA). In order to elucidate the functional status of cellular cytotoxicity, lymphokine-activated killer (LAK) cell cytotoxicity assays were performed both prior to and following incubation of PBL's with IL-2 in five patients with severe head injury. The production of INF-γ and IL-2 by PHA-stimulated PBL's was maximally depressed within 24 hours of injury (p < 0.001 for INF-γ, p = 0.035 for IL-2) and partially normalized within 21 days of injury. There was no change in the production of IL-1. When comparing the in vitro LAK cell cytotoxicity of PBL's from head-injured patients and normal subjects, there was a significant depression in LAK cell cytotoxicity both prior to (p = 0.010) and following (p < 0.001) incubation of PBL's with IL-2. The results of this study indicate that IL-2 and INF-γ production, normally required for inducing cell-mediated immunity, is suppressed following severe head injury. The failure of IL-2 to enhance LAK cell cytotoxicity suggests that factors other than decreased IL-2 production, such as inhibitory soluble mediators or suppressor lymphocytes, may be responsible for the reduction in cellular immune activity following severe head injury. These findings may have significant implications in designing clinical studies aimed at reducing the incidence of infection following severe head injury.

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