Blood pressure and intracranial pressure-volume dynamics in severe head injury: relationship with cerebral blood flow

1992 ◽  
Vol 77 (1) ◽  
pp. 15-19 ◽  
Author(s):  
Gerrit J. Bouma ◽  
J. Paul Muizelaar ◽  
Kuniaki Bandoh ◽  
Anthony Marmarou
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Tissue Stiffness ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Increased brain tissue stiffness following severe traumatic brain injury is an important factor in the development of raised intracranial pressure (ICP). However, the mechanisms involved in brain tissue stiffness are not well understood, particularly the effect of changes in systemic blood pressure. Thus, controversy exists as to the optimum management of blood pressure in severe head injury, and diverging treatment strategies have been proposed. In the present study, the effect of induced alterations in blood pressure on ICP and brain stiffness as indicated by the pressure-volume index (PVI) was studied during 58 tests of autoregulation of cerebral blood flow in 47 comatose head-injured patients. In patients with intact autoregulation mechanisms, lowering the blood pressure caused a steep increase in ICP (from 20 ± 3 to 30 ± 2 mm Hg, mean ± standard error of the mean), while raising blood pressure did not change the ICP. When autoregulation was defective, ICP varied directly with blood pressure. Accordingly, with intact autoregulation, a weak positive correlation between PVI and cerebral perfusion pressure was found; however, with defective autoregulation, the PVI was inversely related to cerebral perfusion pressure. The various blood pressure manipulations did not significantly alter the cerebral metabolic rate of oxygen, irrespective of the status of autoregulation. It is concluded that the changes in ICP can be explained by changes in cerebral blood volume due to cerebral vasoconstriction or dilatation, while the changes in PVI can be largely attributed to alterations in transmural pressure, which may or may not be attenuated by cerebral arteriolar vasoconstriction, depending on the autoregulatory status. The data indicate that a decline in blood pressure should be avoided in head-injured patients, even when baseline blood pressure is high. On the other hand, induced hypertension did not consistently reduce ICP in patients with intact autoregulation and should only be attempted after thorough assessment of the cerebrovascular status and under careful monitoring of its effects.

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.

Dimethyl sulfoxide in experimental brain injury, with comparison to mannitol

1980 ◽  
Vol 53 (1) ◽  
pp. 58-62 ◽  
Author(s):  
Frederick D. Brown ◽  
Lydia M. Johns ◽  
Sean Mullan
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Brain Injury ◽  
Dimethyl Sulfoxide ◽  
Rhesus Monkeys ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Content Type ◽  
Missile Injury ◽  
Fine Print

✓ The effects of dimethyl sulfoxide therapy were studied in rhesus monkeys following a standardized occipitofrontal missile injury. This therapy resulted in substantially higher blood pressure, cerebral perfusion pressure, blood flow, and oxidative metabolism than those of a group of monkeys that had been treated similarly with mannitol, and than those of an untreated group.

Determination of threshold levels of cerebral perfusion pressure and intracranial pressure in severe head injury by using receiver operating—characteristic curves: an observational study in 291 patients

2001 ◽  
Vol 94 (3) ◽  
pp. 412-416 ◽  
Author(s):  
Iain Robert Chambers ◽  
Lynne Treadwell ◽  
A. David Mendelow
Keyword(s):  
Cerebral Perfusion ◽  
Operating Characteristic ◽  
Perfusion Pressure ◽  
Roc Curves ◽  
Content Type ◽  
Head Injured ◽  
Mass Lesions ◽  
Injured Patients ◽  
Fine Print

Object. Intracranial pressure (ICP) and cerebral perfusion pressure (CPP) are frequently monitored in severely head injured patients. To establish which one (ICP or CPP) is more predictive of outcome and to examine whether there are significant threshold levels in the determination of outcome, receiver—operating characteristic (ROC) curves were used to analyze data in a large series of head-injured patients. Methods. Data were obtained from a total of 291 severely head injured patients (207 adults and 84 children). Outcome was categorized as either independent (good recovery or moderate disability) or poor (severely disabled, vegetative, or dead) by using the Glasgow Outcome Scale; patients were also grouped according to the Marshall computerized tomography scan classification. Conclusions. The maximum value of a 2-minute rolling average of ICP readings (defined as ICPmax) and the minimum value of the CPP readings (CPPmin) were then used to calculate the sensitivity and specificity of the ROC curves over a range of values. Using ROC curves, a threshold value for CPPmin of 55 mm Hg and for ICPmax of 35 mm Hg appear to be the best predictors in adults. For children the levels appear to be 43 to 45 mm Hg for CPPmin and 35 mm Hg for ICPmax. Higher levels of CPPmin seem important in adults with mass lesions. These CPP thresholds (45 mm Hg for children and 55 mm Hg for adults) are lower than previously predicted and may be clinically important, especially in children, in whom a lower blood pressure level is normal. Also, CPP management at higher levels may be more important in adults with mass lesions. A larger observational series would improve the accuracy of these predictions.

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.

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.

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.

Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury

2000 ◽  
Vol 92 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Niels Juul ◽  
Gabrielle F. Morris ◽  
Sharon B. Marshall ◽  
_ _ ◽  
Lawrence F. Marshall
Keyword(s):  
Head Injury ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neurological Deterioration ◽  
Double Blind ◽  
Content Type ◽  
Fine Print

Object. Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.Methods. The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-d-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP ≥ 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.Conclusions. Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Cell-mediated immunity in severely head-injured patients: the role of suppressor lymphocytes and serum factors

1992 ◽  
Vol 77 (5) ◽  
pp. 694-699 ◽  
Author(s):  
Keith B. Quattrocchi ◽  
Claramae H. Miller ◽  
Franklin C. Wagner ◽  
Sally J. DeNardo ◽  
Gerald L. DeNardo ◽  
...  
Keyword(s):  
Head Injury ◽  
Cellular Immunity ◽  
Severe Head Injury ◽  
Normal Subjects ◽  
Lymphocyte Function ◽  
Serum Factors ◽  
Content Type ◽  
Head Injured ◽  
Injured Patients ◽  
Fine Print

✓ Severe head injury results in suppression of cellular immunity associated with defective in vitro functioning of effector lymphocytes, such as helper T cells and cytotoxic T cells. It is not known whether this suppression in effector lymphocyte function is due to intrinsic lymphocyte dysfunction, to suppressor peripheral blood mononuclear cells (PBMC's) such as suppressor lymphocytes or suppressor monocytes, or to serum factors capable of inhibiting effector lymphocyte function. The purpose of this study was to determine whether a subpopulation of PBMC's and/or serum factors) are responsible for this observed suppression in cell-mediated immunity. Cell-mediated immune activity was determined measuring in vitro lymphokine-activated killer (LAK) cytotoxicity following incubation of PBMC's from 15 head-injured patients with those from 15 heterologous normal subjects. The PBMC's were separated into lymphocyte-enriched and monocyte-enriched subpopulations by plastic adherence techniques, and the effect of each population on LAK cytotoxicity was determined. Additionally, the effect on cytotoxicity of serum from the head-injured patients was determined in a dose-response fashion. There was significant depression in LAK cytotoxicity when: 1) PBMC's from normal subjects were incubated with PBMC's from head-injured patients (p < 0.001); 2) lymphocytes (PBMC's depleted of monocytes) from head-injured patients were incubated with PBMC's from normal subjects (p < 0.001); and 3) PBMC's from normal subjects were incubated with serum from head-injured patients (p < 0.001). No suppression in cellular immunity was noted when lymphocytes from normal subjects were incubated with monocytes from head-injured patients. The results indicate that lymphocytes rather than monocytes actively inhibit cellular immunity following severe head injury. The detection of immmunosuppressive serum factors suggests a mechanism by which lymphocytes might be modulated by severe head injury.

Sign in / Sign up

Export Citation Format

Share Document