ICP threshold in CPP management of severe head injury patients

BACKGROUND: Elevated intracranial pressure (ICP) is significantly associated with high mortality rate in severe head injury (SHI) patients. However, there is no absolute agreement regarding the level at which ICP must be treated. The objective of this study was to compare the outcomes of severe head injury patients treated by setting the ICP threshold at >or=20 mm Hg or >or=25 mm Hg. METHODS: Treatment protocol in this study consisted of therapeutic maneuvers designed to maximize cerebral profusion pressure (CPP) and control ICP. Twenty-seven patients with severe head injury and intracranial hypertension (ICP >or=20 mm Hg) were enrolled and fourteen cases were allocated to the group of ICP threshold >or=25 mm Hg. Six-month clinical outcomes were evaluated using the Glasgow Outcome Score (GOS). RESULTS: There were no statistically significant differences in clinical parameters between the groups. Logistic regression identified the presence of basal cisterns on the initial computed tomography (CT) scan as a significant predictor of good outcome. ICP threshold did not influence outcome. CONCLUSIONS: This study supported a recommended ICP threshold of 20 to 25 mm Hg in SHI management. However, in cases with an absence of basal cisterns on initial CT scan, the probability of good outcome may be higher using an ICP threshold of >or=20 mm Hg.     

Effect of positive end expiratory pressure ventilation on intracranial pressure in man.

THsi study was designed to define the effect of positive end expiratory pressure (PEEP) ventilation on intracranial pressure (ICP). In 25 patients with severe head trauma with and without associated pulmonary injury the following parameters were simultaneously monitored under mechanical ventilation with and without PEEP:ICP, arterial blood pressure, central venous pressure, arterial blood gases, and cardiac rate. In addition, the volume-pressure response (VPR) was evaluted in each patient to assess cerebral elastance. The results indicate a significant increase in ICP with the application of PEEP only in the 12 patients who manifested increased cerebral elastance by VPR. Half of this latter group manifested impairment of cerebral perfusion pressure to levels less than 60 mm Hg. Return to baseline CIP levels was observed with termination of PEEP. No significantly consistent changes in other parameters were noted.     

Effect of mannitol on cerebral blood flow and cerebral perfusion pressure in human head injury

Patients with severe head injury frequently have evidence of elevated intracranial pressure (ICP) and ischemic neuronal damage at autopsy. Mannitol has been used clinically to reduce ICP with varying success, and it is possible that it is more effective in some types of head injury than in others. The aim of the present study was to determine the effect of mannitol on ICP, cerebral perfusion pressure (CPP), and cerebral blood flow (CBF) in patients with severe head injury, and to discover if these effects differed in different types of injury. Measurements of CPP, ICP, and CBF were made in 55 patients with severe head injury. In general, the resting level of CBF was higher in patients with diffuse injury (mean 50.2 ml/100 gm/min) than in those with focal injury (mean 39.8 ml/100 gm/min). Mannitol consistently reduced ICP and increased CPP and CBF by 10 to 20 minutes after infusion. The lowest flows (31.8 ml/100 gm/min) were recorded from the most damaged hemispheres of patients with focal injuries and elevated ICP. The baseline levels of flow did not correlate with ICP, CPP, Glasgow Coma Scale score, or outcome. Only four of the 55 patients had a CBF of less than 20 ml/100 gm/min in either or both hemispheres. The few low CBF's in this and other studies may reflect the steady-state conditions under which measurements are made in intensive care units, and that these patients have entered a phase of reperfusion.     

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

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.     

The Effect of Implementation of Guidelines for the Management of Severe Head Injury on Patient Treatment and Outcome

The authors retrospectively analysed two groups of consecutive patients who were similarly matched for brain injury severity. From a total of 39 severe head injury patients, 23 were treated according to the Guidelines for the Management of Severe Head Injury with intracranial pressure (ICP) monitoring ("Guidelines group"). Such an approach allowed the maintenance of ICP within normal values, especially in patients with intraventricular ICP monitoring allowing the release of cerebrospinal fluid (CSF) from the ventricular system. In the Guidelines group only two patients were administered barbiturates, after all other means of ICP lowering had been exhausted. The second group consisted of 16 patients who were not monitored for ICP ("non-Guidelines group"). In this group, management consisted of the prophylactic administration of barbiturates, high dose osmotic diuretics and hyperventilation usually at levels below 25 mm Hg. In the Guidelines group the mortality rate was 30% compared to 44% in the non-Guidelines group. Almost twice as many patients achieved a "favourable" (good recovery and moderate disability) outcome (49%) compared to the non-Guidelines treated patients (25%). Furthermore, there was a 32% decrease in severe neurological disabilities in those patients in the Guidelines group. It seems that the implementation of "Guidelines" in the treatment of severe head injury, based on the result of our clinical study, reduces death and disability rates in patients with severe head injury. The administration of therapy based on the "Guidelines principles" and monitoring of ICP, can minimise the application of those therapeutic modalities (barbiturate coma and prolonged hyperventilation) which, in addition to favourable effects, may also have harmful effects on patients with severe head injury.     

Intracranial pressure response to severe head injury induced apnea and catecholamine surge

BACKGROUND: Apnea and catecholamine surge have been known sequelae in the first few minutes of postexperimentally induced severe head injury for over a century. However, the intracranial pressure (ICP) response to these two pathophysiologic processes is poorly understood. METHODS: We used the rat fluid percussion head injury model to study apnea and catecholamine surge separately and in combination on measured ICP response RESULTS: The three experimental groups of apnea, hypertensive surge, and both combined revealed significantly different ICP responses with markedly elevated pressures correlating closely with mean arterial blood pressure. CONCLUSION: ICP and mean arterial blood pressure correlate closely in the first few minutes after head injury in the absence of space-occupying hematomas, and may initiate pathophysiologic sequelae that can only be treated by earlier medical intervention at the scene.     

Fentanyl and sufentanil increase intracranial pressure in head trauma patients.

Although opioids frequently are administered to patients with severe head trauma, the effects of such drugs on intracranial pressure are controversial. Nine patients with severe head trauma were studied for the effects of fentanyl and sufentanil on intracranial pressure (ICP). In all patients, ICP monitoring was instituted before the study. Full neuromuscular blockade was achieved with vecuronium bromide before the administration of either fentanyl (3 micrograms.kg-1) or sufentanil (0.6 microgram.kg-1) as an intravenous bolus over a 1-min period in a masked and random fashion. Patients received the other opioid in the same fashion 24 h later. Arterial blood pressure, heart rate, and ICP were recorded continuously for the 1 h after drug administration. Fentanyl was associated with an average ICP increase of 8 +/- 2 mmHg, and sufentanil with an increase of 6 +/- 1 mmHg. These increases were statistically significant. Both drugs produced clinically mild decreases in mean arterial blood pressure (fentanyl, 11 +/- 6 mmHg; sufentanil, 10 +/- 5 mmHg) that nevertheless were statistically significant. No significant changes in heart rate occurred. These results indicate that modest doses of potent opioids can significantly increase ICP in patients with severe head trauma.     

Posttraumatic cerebral hemispheric swelling. Analysis of 55 cases studied with computerized tomography

The authors have analyzed the clinical course and intracranial pressure (ICP) changes in 55 severely head-injured patients presenting with bulk enlargement of one cerebral hemisphere within a few hours after trauma. These patients represent 10.5% of a series of 520 patients with severe head injury studied with computerized tomography (CT). Cerebral hemispheric swelling has the highest mortality rate and the shortest survival period after trauma in all series of severe head injury. In this series, it was associated with an ipsilateral subdural hematoma of variable size in 47 patients (85%) or with a large epidural hematoma in five patients (9%); in three patients (5.4%) it occurred as an isolated lesion. Evacuation of an associated extracerebral hematoma, which was performed within 4 hours after injury in only 20% of cases, scarcely changed the patients' preoperative neurological status. The high incidence of arterial hypotension and/or hypoxemia at admission (47% of cases) and the severity of the clinical presentation (82% of patients scored 5 points or less on the Glasgow Coma Scale, 74% had unilateral or bilateral mydriasis, and 80% had an initial ICP above normal) correlated with a very poor final outcome (87% mortality). Only one of the 11 patients with normal initial ICP continued to have normal pressure throughout the course. High-dose thiopental failed to control severe intracranial hypertension in 24 patients (51%) who had a fulminant, malignant course. A transient decrease in ICP elevation was achieved in 15 patients (31.4%) and definitive control in eight patients (17%), among whom were the seven survivors in this series. In the authors' experience, once ICP is controlled, barbiturate administration should not be discontinued until a control CT scan shows complete disappearance of the mass effect.     

An analysis of the relationship between fluid and sodium administration and intracranial pressure after head injury.

Severe head injury is the leading cause of traumatic death. When a severe head injury is combined with hypotension the mortality doubles. The use of asanguineous salt solutions to maintain blood pressure, however, may contribute to cerebral swelling and intracranial hypertension. For this reason, restrictions of fluids (FLD) and sodium (Na) have been advocated. To our knowledge, however, there are no clinical data to support this recommendation. We hypothesized that in adult patients sustaining severe head injuries (Glasgow Coma Scale score less than or equal to 8) with or without associated injuries: (1) FLD balance and total Na administered during the initial 72 hours of hospital admission are positively and significantly correlated with each other, and (2) total FLD, FLD balance, and total Na administration during the initial 72 hours are significantly and positively correlated with changes in ICP and adverse outcome. We retrospectively studied 40 adult trauma patients with severe head injuries. We found a significant correlation between total Na and FLD balance (R2 = 0.54; p less than 0.05). However, we found no significant correlation between total FLD and maximum ICP (R2 = 0.081), ICP score (R2 = 0.01), or outcome (R2 = 0.066), no significant correlation between FLD balance and maximum ICP (R2 = 0.000), ICP score (R2 = 0.000), or outcome (R2 = 0.01), and no significant correlation between total Na and maximum ICP (R2 = 0.000), ICP score (R2 = 0.001), or outcome (R2 = 0.02). We conclude that Na and FLD administration are not independent determinants of ICP during the initial 72 hours after brain injury.     

Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation

OBJECTIVE: Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS: Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS: We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 +/- 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION: Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.     

Establishment of a blunt impact-induced brain injury model in rabbits

Objective: To establish an animal model to replicate the blunt impact brain injury in forensic medicine.Methods:Twenty-four New Zealand white rabbits were randomly divided into control group (n=4),mino...     

Intracranial pressure monitoring and outcomes after traumatic brain injury.

OBJECTIVE: Uncontrolled intracranial hypertension after traumatic brain injury (TBI) contributes significantly to the death rate and to poor functional outcome. There is no evidence that intracranial pressure (ICP) monitoring alters the outcome of TBI. The objective of this study was to test the hypothesis that insertion of ICP monitors in patients who have TBI is not associated with a decrease in the death rate. DESIGN: Study of case records. METHODS: The data files from the Ontario Trauma Registry from 1989 to 1995 were examined. Included were all cases with an Injury Severity Score (ISS) greater than 12 from the 14 trauma centres in Ontario. Cases identifying a Maximum Abbreviated Injury Scale score in the head region (MAIS head) greater than 3 were selected for further analysis. Logistic regression analyses were conducted to investigate the relationship between ICP and death. RESULTS: Of 9001 registered cases of TBI, an MAIS head greater than 3 was recorded in 5507. Of these patients, 541 (66.8% male, mean age 34.1 years) had an ICP monitor inserted. Their average ISS was 33.4 and 71.7% survived. There was wide variation among the institutions in the rate of insertion of ICP monitors in these patients (ranging from 0.4% to over 20%). Univariate logistic regression indicated that increased MAIS head, ISS, penetrating trauma and the insertion of an ICP monitor were each associated with an increased death rate. However, multivariate analyses controlling for MAIS head, ISS and injury mechanism indicated that ICP monitoring was associated with significantly improved survival (p < 0.015). CONCLUSIONS: ICP monitor insertion rates vary widely in Ontario's trauma hospitals. The insertion of an ICP monitor is associated with a statistically significant decrease in death rate among patients with severe TBI. This finding strongly supports the need for a prospective randomized trial of management protocols, including ICP monitoring, in patients with severe TBI.     

Effect of intracranial pressure monitoring and aggressive treatment on mortality in severe head injury

During 1977-1978, 127 patients with severe head injury were admitted and underwent intracranial pressure (ICP) monitoring. All patients had Glasgow Coma Scale (GCS) scores of 7 or less. All received identical initial treatment according to a standardized protocol. The patients' average age was 29 years; 60% had multiple trauma, and 35% needed emergency intracranial operations. Treatment for elevations of ICP was begun when ICP rose to 20 to 25 mm Hg, and included mannitol therapy and drainage of cerebrospinal fluid (CSF) when possible. Forty-three patients (34%) had ICP greater than or equal to 25 mm Hg; of these, 36 (84%) died. The mortality rate of the entire group was 46%. During 1979-1980, 106 patients with severe head injury were admitted and underwent ICP monitoring. Their average ager was 29 years; 51% had multiple trauma, and 31% underwent emergency intracranial surgery. All patients received the same standardized protocol as the previous series, with the exception of the treatment of ICP. In this present series: if ICP was 15 mm Hg or less (normal ICP), patients were continued on hyperventilation, steroids, and intensive care; if ICP was 16 to 24 mm Hg, mannitol was administered and CSF was drained; if ICP was 25 mm Hg or greater, the patients were randomized into a controlled barbiturate therapy study. Twenty-six patients (25%) had ICP's of 25 mm Hg or greater, compared to 34% in the previous series (p less than 0.05), and 18 of these 26 patients (69%) died. The overall mortality for this current series was 28% compared to 46% in the previous series (p less than 0.0005). This study reconfirms the high mortality rate if ICP is 25 mm Hg or greater; however, the data also document that early aggressive treatment based on ICP monitoring significantly lessens the incidence of ICP of 25 mm Hg or greater and reduces the overall mortality rate of severe head injury.     

Experience with Althesin in the management of persistently raised ICP following severe head injury

Of 243 patients who underwent intracranial pressure (ICP) monitoring after severe head injury, 42 (17%) were found to have severe persistently raised ICP, in spite of hyperventilation, mannitol, and surgical decompression. Althesin was infused to reduce ICP in these patients. This agent was shown to be effective and safe in reducing ICP, and a significant improvement in cerebral perfusion pressure was demonstrated. In this respect, Althesin may be more effective than barbiturates. However, no improvement in patient outcome was demonstrated in this series.     

Diffuse Axonal Injury (DAI) is not Associated with Elevated Intracranial Pressure (ICP)

Summary Objective. Traditionally, intracranial pressure (ICP) monitoring has been utilized in all patients with severe head injury (Glasgow coma score of 3–8). Ventriculostomy placement, however, does carry a 4 to 10 percent complication rate consisting mostly of hematoma and infection. The authors propose that a subgroup of patients presenting with severe head trauma and diffuse axonal injury without associated mass lesion, do not need ICP monitoring. Additionally, the monitoring data from ICP, MAP, and CPP for a comparison severe head injury group, and subgroups of DAI would be presented. Materials and methods. Thirty-six patients sustaining blunt head trauma and fitting our strict clinical and radiographic diagnosis of DAI were enrolled in our study. Inclusion criteria were severe head injury patients who did not regain consciousness after the initial impact, and whose CT scan demonstrated characteristic punctate hemorrhages of <10 mm diameter at the greywhite junction, basal ganglia, corpus callosum, upper brainstem, or a combination of the above. Patients with significant mass lesions and documented anoxia were excluded. Their intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were compared to a control group of 36 consecutive patients with severe non-penetrating non-operative head injury, using the Analysis for Variance method. Results. Eighteen (50.0%), six (16.7%), and twelve (33.3%) patients had types I, II, and III DAI, respectively. The admission Glasgow Coma Score (GCS) was higher for types I and II than for type III DAI. ICP was monitored from 23 to 165 hours, with a mean ICP for 36 patients of 11.70 mmHg (SEM=75) and a range from 4.3 to 17.3 mmHg. Of all ICP recordings, of which 89.7% (2421/2698) were ≤20 mmHg. Average mean arterial pressure (MAP) was 96.08 mmHg (SEM=1.69), and 94.6% (2038/2154) of all MAP readings were greater than 80 mmHg. Average cerebral perfusion pressure (CPP) was 85.16 mmHg (SEM=1.68), and 90.1% (1941/2154) of all CPP readings were greater than 70 mmHg. This is compared to the control group mean ICP, MAP, and CPP of 16.84 mmHg (p=0.000021), 92.80 mmHg (p=0.18), and 76.49 mmHg (p=0.0012). No treatment for sustained elevated ICP>20 mmHg was needed for DAI patients except in two; one with extensive intraventricular and subarachnoid hemorrhage who developed communicating hydrocephalus, and another with ventriculitis requiring intrathecal and intravenous antibiotic treatments. Two complications, one from a catheter tract hematoma, and another with Staph epidermidis ventriculitis, were encountered. All patients, except type III DAI, generally demonstrated marked clinical improvement with time. The outcome, as measured by Glasgow Coma Score (GCS) and Glasgow Outcome Score (GOS) was similarly better with types I and II than type III DAI. Conclusion. The authors conclude that ICP elevation in DAI patients without associated mass lesions is not as prevalent as other severe head injured patients, therefore ICP monitoring may not be as critical. The presence of an ICP monitoring device may contribute to increased morbidity. Of key importance, however, is an accurate clinical history and interpretation of the CT scan.     

Threshold levels of intracranial pressure as determinants of survival from diffuse brain injury. An observational study

OBJECTIVE: Intracranial pressure (ICP) is frequently monitored in patients with severe head injuries. In this study of a series of diffuse brain injury patients, we investigated whether there are significant threshold levels that determine the outcome. METHOD: Data were obtained from 17 patients with severe head injuries (adults aged ≥ 15-years-old). The outcome was categorized using the Glasgow Outcome Scale and survival or death. Patients were also grouped according to the Traumatic Coma Data Bank (TCDB) CT classification for diffuse injury: type I (n=0); II (n=5); III (n=10); IV (n=2). CONCLUSION AND RESULT: The mortality rate was 29% (5 of 17 patients). The average initial ICP within 24 hours (14.08 mmHg) and the peak ICP (26.75 mmHg) were lower in the survivors than that in the patients who died (57.60 mmHg and 91.00 mmHg, respectively; p=0.0006 and 0.0002, respectively). Patients with an initial ICP score>35 mmHg did not survive, and patients with a peak ICP<35 mmHg, except one who died of a traumatic brainstem hemorrhage, did survive. Using an X-bar chart, a threshold value for the initial ICP within 24 hours of 27 mmHg and for the peak ICP 46 mmHg appear to be the survival predictors in patients with diffuse brain injury.     

Head injury,subarachnoid hemorrhage and intracranial pressure monitoring in Italy

Background. Intracranial pressure monitoring is recommended for the management of severe head injury and is increasingly used during intensive care for other pathologies, such as subarachnoid hemorrhage. However, it is still not uniformly applied in different centers. The objectives of this paper are to summarize the frequency and the modalities of intracranial pressure (ICP) monitoring in different centers in Italy; to describe its use in traumatic brain injury (TBI) and in subarachnoid hemorrhage (SAH); and to identify areas for improvement. Method. The medical directors of either the neurosurgical department or the intensive care unit, or both, of every Italian neurosurgical center were personally interviewed. They answered specific questions about TBI and SAH patients admitted, and ICP monitoring used, in their units. Data were cleared of any obvious inconsistencies and entered in a database for analysis. All analyses were based simply on the data declared. Findings. The clinical information was obtained from 9137 TBI cases, of whom 4240 severe, and 3151 SAH patients. Among the 106 participating centers, 15 did not use ICP monitoring at all. The remaining 91 had used 3293 ICP devices during the year 2001; 146 were used in tumor cases, 2009 in TBI, and 1138 in SAH. Twenty-two percent of TBI cases admitted to centers with ICP equipment were monitored. Restricting this analysis to severe cases, 47% of TBI with a GCS <8 had ICP. On average, 36% of SAH underwent ICP monitoring. The proportions of head injury and SAH cases who underwent ICP monitoring varied widely in the different centers. Dividing the country into three main areas (north, center and south), there were considerable differences both in the rate of admissions per million inhabitants and in the frequency of ICP monitoring. Interpretation. ICP monitoring in Italy is used in most, but not all, centers. ICP is measured fairly extensively in head injury cases, but a significant proportion of SAH patients is monitored as well. There are substantial differences in the frequency of ICP monitoring in different parts of the country. The use of ICP for both these indications, and the rates of admission to specialized centers, could be improved.Published online July 31, 2003     

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

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.     

High-dose barbiturate control of elevated intracranial pressure in patients with severe head injury

In a five-center study, 73 patients with severe head injury and elevated intracranial pressure (ICP) were randomly assigned to receive either a regimen that included high-dose pentobarbital or one that was otherwise similar but did not include pentobarbital. The results indicated a 2:1 benefit for those treated with the drug with regard to ICP control. When patients were stratified by prerandomization cardiac complications, the advantage increased to 4:1. A multiple logistic model considering treatment and selected baseline variables indicated a significant positive treatment effect of barbiturates, a significant effect of time from injury to randomization, and an interaction of treatment with cardiovascular complications. However, of 925 patients potentially eligible for randomization, only 12% met ICP randomization criteria. The results support the hypothesis that high-dose pentobarbital is an effective adjunctive therapy, but that it is indicated in only a small subset of patients with severe head injury.     

Failure of high-dose steroid therapy to influence intracranial pressure in patients with severe head injury.

While corticosteroids in standard neurosurgical dosage do not appear to influence recovery from severe head injury or elevated intracranial pressure (ICP), some reports claim that a much higher dose is effective. A resultant hypothesis is that an abrupt increase in corticosteroid dosage in patients with severe head injury should cause a detectable reduction in ICP and in cerebral elastance within 48 hours. To test this hypothesis 20 consecutive patients with severe head injury, 12 of whom had had surgical decompression of mass lesions, were studied. All patients were artificially ventilated, and had continuous monitoring of ICP and intermittent testing of elastance by measurement of the volume-pressure response (VPR). For the first 12 hours after admission, patients received methylprednisolone, 40 mg every 6 hours. The dose was then increased abruptly by giving a single dose of 2 gm and 500 mg every 6 hours for the next 24 hours, then tapering rapidly. No significant change in ICP or VPR could be detected after 24 or 48 hours of high-dose steroid therapy. Of the 20 patients, 50% had good recovery or were moderately disabled, 15% were severely disabled or vegetative, and 35% had died. The course of ICP and the outcomes in these patients were not significantly different from those observed in a previous group of 262 patients managed in the same way for the high-dose regimen. There was, however, high incidence of gastric hemorrhage (50%) and of hyperglycemia with glucosuria (85%) in these 20 patients. These negative results in patients with head injury stand in marked contrast to our experience of the benefit of methylprednisolone in patients with brain tumors.