Minimum Cerebral Perfusion Pressure Research Articles

Progress of intracranial pressure and cerebral perfusion pressure in patients during the development of brain death

BackgroundClinical investigations of brain death are supposed to prove absence of cerebral perfusion. However, only limited data are available documenting intracranial pressure (ICP) and cerebral perfusion pressure (CPP) during the development of brain death. Our study presents additional data to understand the course of ICP and CPP in patients developing brain death. Material and methodsWe analyzed retrospective data of 18 patients with ICP monitoring during the development of brain death due to primary brain lesions. ICP and CPP values were continuously measured between two clinically defined time points: 1. non-reactive and widened pupils, 2. brain death determination. We analyzed ICP and CPP at the above-mentioned end points. Additionally, we investigated maximum ICP and minimal CPP values between these time points. ResultsPatients developed fixed and dilated pupils with a median of 38 h before brain death determination. During brain death determination median ICP and median CPP were 103.5 and –2.5 mmHg, respectively. Maximum ICP before brain death determination was significantly higher and minimal CPP values were significantly lower compared to the time point of brain death. During the investigation period all patients experienced ICP values >95 mmHg and CPP < 10 mmHg. All but one patient had documented CPP values of ≤0 mmHg. This single patient had a minimum CPP of 8 mmHg with a maximum ICP of 145 mmHg. ConclusionCerebral perfusion pressure during brain death determination may be positive in some patients. Our results showed variable values of ICP and CPP. However, extremely elevated ICP values before or during brain death in combination with low CPP values suggest absence of cerebral perfusion. The occurrence of positive CPP values during brain death determination therefore depends on the time point at which brain death determination is performed.

Early Craniectomy Improves Intracranial and Cerebral Perfusion Pressure after Severe Traumatic Brain Injury

After traumatic brain injury, decompressive craniectomy (DC) is a second-tier, late therapy for refractory intracranial hypertension. We hypothesize that early DC, based on CT evidence of intracranial hypertension, improves intracranial pressure (ICP) and cerebral perfusion pressure (CPP). From September 2008 to January 2015, 286 traumatic brain injury patients requiring invasive ICP monitoring at a single Level I trauma center were reviewed. DC and non-DC patients were propensity score matched 1:1, based on demographics, hemodynamics, injury severity score (ISS), Glasgow Coma Scale (GCS), transfusion requirements, and need for vasopressor therapy. Data are presented as M ± SD or median (IQR) and compared at P ≤ 0.05. The study population was 42 ± 17 years, 84 per cent male, ISS = 29 ± 11, GCS = 6(5), length of stay (LOS) = 32(40) days, and 28 per cent mortality. There were 116/286 (41%) DC, of which 105/116 (91%) were performed at the time of ICP placement. For 50 DC propensity matched to 50 non-DC patients, the midline shift was 7(11) versus 0(5) mm (P < 0.001), abnormal ICP (hours > 20 mm Hg) was 1(10) versus 8(16) (P = 0.017), abnormal CPP (hours < 60 mm Hg) was 0(6) versus 4(9) (P = 0.008), daily minimum CPP (mm Hg) was 67(13) versus 62(17) (P = 0.010), and daily maximum ICP (mm Hg) was 18(9) versus 22(11) (P < 0.001). However, LOS [33(37) versus 25(34) days], mortality (24 versus 30%), and Glasgow Outcome Score Extended [3.0(3.0) versus 3.0(4.0)] did not improve significantly. Early DC for CT evidence of intracranial hypertension decreased abnormal ICP and CPP time and improved ICP and CPP thresholds, but had no obvious effect on the outcome.

Rescue Decompressive Craniectomy in Children with Severe Traumatic Brain Injury.

Decompressive craniectomy (DC) is considered a rescue therapy in patients with traumatic brain injury (TBI) with increased intracranial pressure (ICP). In this retrospective study, we examined the impact of craniectomy on ICP in children with severe TBI and their neurological outcome. A total of 14 patients were enrolled. Peak ICP was significantly lower (31 ± 2.9 to 19 ± 4.6, p < 0.001) and minimum cerebral perfusion pressure (CPP) higher (41 ± 10.5 to 58 ± 11.4, p < 0.001) postcraniectomy. The survival rate was 71%. However, 57% of our cohort had a poor neurological outcome at 6 months postinjury. In conclusion, although rescue DC was effective in controlling ICP and CPP, the long-term neurological outcome remained poor.

Intracranial pressure and cerebral perfusion pressure in patients developing brain death

PurposeWe investigated whether a critical rise of intracranial pressure (ICP) leading to a loss of cerebral perfusion pressure (CPP) could serve as a surrogate marker of brain death (BD). Materials and methodsWe retrospectively analyzed ICP and CPP of patients in whom BD was diagnosed (n = 32, 16-79 years). Intracranial pressure and CPP were recorded using parenchymal (n = 27) and ventricular probes (n = 5). Data were analyzed from admission until BD was diagnosed. ResultsIntracranial pressure was severely elevated (mean ± SD, 95.5 ± 9.8 mm Hg) in all patients when BD was diagnosed. In 28 patients, CPP was negative at the time of diagnosis (−8.2 ± 6.5 mm Hg). In 4 patients (12.5%), CPP was reduced but not negative. In these patients, minimal CPP was 4 to 18 mm Hg. In 1 patient, loss of CPP occurred 4 hours before apnea completed the BD syndrome. ConclusionsBrain death was universally preceded by a severe reduction of CPP, supporting loss of cerebral perfusion as a critical step in BD development. Our data show that a negative CPP is neither sufficient nor a prerequisite to diagnose BD. In BD cases with positive CPP, we speculate that arterial blood pressure dropped below a critical closing pressure, thereby causing cessation of cerebral blood flow.

Cerebral Perfusion Pressure and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage.

Whether delayed cerebral ischemia (DCI) mediates the relationship between Hunt and Hess grade and outcomes after aneurysmal subarachnoid hemorrhage remains unknown. To investigate the relationship between cerebral perfusion pressure, DCI, Hunt and Hess grade, and outcomes after aneurysmal subarachnoid hemorrhage. DCI was defined as neurological deterioration due to impaired cerebral blood flow. Relationships between minimum cerebral perfusion pressure and onset and occurrence of DCI were tested by using logistic regression and the accelerated failure time model. The mediation effect of DCI on relationships between Hunt and Hess grade and outcomes was tested by using the bootstrap confidence interval. Outcomes at 3 and 12 months included mortality and neuropsychological, functional, and physical outcomes. DCI occurred in 211 patients (42%). About one-third of the patients had poor functional outcome at 3 (32%) and 12 (30%) months. Impaired neuropsychological outcome was observed in 33% of patients at 3 months and 17% at 12 months. For every increase of 10 mm Hg in cerebral perfusion pressure, odds for DCI increased by 2.78 (95% CI, 2.00-3.87). High perfusion pressure was associated with earlier onset of DCI (P < .001). DCI does not mediate the relationship of Hunt and Hess grade to functional outcome or death. The relationship between cerebral perfusion pressure and DCI was most likely due to induced hypertension and hypervolemia. Clinical guidelines may need to include limits for induced hypertension.

Association of ICP, CPP, CT findings and S-100B and NSE in severe traumatic head injury. Prognostic value of the biomarkers

Objective: The association was studied of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) on S-100B and neuron-specific enolase (NSE) in severe traumatic brain injury (sTBI). The relationship was explored between biomarkers, ICP, CPP, CT-scan classifications and the clinical outcome.Materials and methods: Data were collected prospectively and consecutively in 48 patients with Glasgow Coma Scale score ≤ 8, age 15–70 years. NSE and S-100B were analysed during 5 consecutive days. The initial and follow-up CT-scans were classified according to the Marshall, Rotterdam and Morris-Marshall classifications. Outcome was evaluated with extended Glasgow outcome scale at 3 months.Results: Maximal ICP and minimal CPP correlated with S-100B and NSE levels. Complex relations between biomarkers and CT classifications were observed. S-100B bulk release (AUC = 0.8333, p = 0.0009), and NSE at 72 hours (AUC = 0.8476, p = 0.0045) had the highest prediction power of mortality. Combining Morris-Marshall score and S-100B bulk release improved the prediction of clinical outcome (AUC = 0.8929, p = 0.0008).Conclusion: Biomarker levels are associated with ICP and CPP and reflect different aspects of brain injury as evaluated by CT-scan. The biomarkers might predict mortality. There are several pitfalls influencing the interpretation of biomarker data in respect to ICP, CPP, CT-findings and clinical outcome.

ABSTRACT 351

Background and aims: A minimum cerebral perfusion pressure (CPP) of 40 mm Hg is acceptable in children with traumatic brain injury. Optimal CPP threshold in acute CNS infections remain undefined. Aims: To identify the impact of different CPP thresholds on mortality in children with acute CNS infections. Methods: Design: Retrospective analysis of prospectively collected data in level-III PICU. Subjects: 231 children, aged 1–12 years, with raised ICP and modified-GCS Score ≤ 8. Interventions: ICP monitoring using intraparenchymal microtransducer (Codman®). CPP was targeted by fluid boluses, vasopressors and anti-raised-ICP measures. Based on mean CPP in first 72 hours, patients were divided into Groups I (30–40) (n=25), II (41–50) (n=31), III (51–60) (n=56) and IV (≥60) (n=119). Outcomes: Primary: 90-day mortality. Secondary: 72-hour m-GCS score, length of mechanical ventilation, PICU stay, and functional status at 3 months. Statistics: Cox-regression adjusted for age, sex, diagnosis, PRISM-III, opening ICP, PRBC transfusion and osmotherapy. Department review committee approved the study. Results: 90-day-mortality was lower in Group IV (13.4%) than Groups I (96.2%; adjusted HR=16.75, 95% CI 8.75–32, p<0.001), II (64.5%; adjusted HR=7.38, 95% CI 3.8–14.35, p<0.001), III (32.7%; adjusted HR=2.4, 95% CI 1.41–5.37, p=0.003). Median m-GCS score was higher in Group IV (10; IQR 8–11) than others (<8) (p<0.001). Length of mechanical ventilation (Log-rank p<0.001) and PICU stay (Log-rank p<0.001) were lower in Group IV. Intact survival at 3 months was higher in Group-IV (54/103, 52.4%) than others (p<0.001). Conclusions: CPP ≥ 60 mm Hg is independently associated with lower mortality in children with acute CNS infections.

Dynamics of brain tissue changes induced by traumatic brain injury assessed with the Marshall, Morris–Marshall, and the Rotterdam classifications and its impact on outcome in a prostacyclin placebo-controlled study

The present study evaluates the types and dynamics of intracranial pathological changes in patients with severe traumatic brain injury (sTBI) who participated in a prospective, randomized, double-blinded study of add-on treatment with prostacyclin. Further, the changes of brain CT scan and their correlation to Glasgow Coma Scale score (GCS), maximal intracranial pressure (ICP(max)), minimal cerebral perfusion pressure (CPP(min)), and Glasgow Outcome Score (GOS) at 3, 6, and 12 months were studied. Forty-eight subjects with severe traumatic brain injury were treated according to an ICP-targeted therapy protocol based on the Lund concept with the addition of prostacyclin or placebo. The first available CT scans (CT(i)) and follow-up scans nearest to 24 h (CT(24)) were evaluated using the Marshall, Rotterdam, and Morris-Marshall classifications. There was a significant correlation of the initial Marshall, Rotterdam, Morris-Marshall classifications and GOS at 3 and 12 months. The CT(24) Marshall classification did not significantly correlate to GOS while the Rotterdam and the Morris-Marshall classification did. The CT(i) Rotterdam classification predicted outcome evaluated as GOS at 3 and 12 months. Prostacyclin treatment did not influence the dynamic of tissue changes. The Rotterdam classification seems to be appropriate for describing the evolution of the injuries on the CT scans and contributes in predicting of outcome in patients treated with an ICP-targeted therapy. The Morris-Marshall classification can also be used for prognostication of outcome but it describes only the impact of traumatic subarachnoid hemorrhage (tSAH).

Chapter 4. Threshold for treatment of intracranial hypertension

Chapter 4. Threshold for treatment of intracranial hypertension

Pentobarbital Coma For Refractory Intra-Cranial Hypertension After Severe Traumatic Brain Injury: Mortality Predictions and One-Year Outcomes in 55 Patients

To identify predictors of mortality and long-term outcomes in survivors after pentobarbital coma (PBC) in patients failing current treatment standards for severe traumatic brain injuries (TBI). This is a retrospective cohort study of severe TBI patients receiving PBC at Level I Trauma Center and tertiary university hospital. Four thousand nine hundred thirty-four patients were admitted to the trauma intensive care unit with severe TBI (head Abbreviated Injury Scale >or= 3) between April 1998 and December 2004. Six hundred eleven received intracranial pressure (ICP) monitoring and 58 received PBC. Three patients underwent craniotomy for intracranial mass lesion and were excluded. The study group received standardized medical management for severe TBI including opiates, benzodiazepines, elevation of the head of bed, avoidance of hypotension and hypercapnia and hyperosmolar therapy (HOsmRx). In addition, 31 of 55 patients (56%) underwent placement of intraventricular catheters for cerebrospinal fluid drainage. If routine medical management and cerebrospinal fluid diversion failed to control ICP, then the patient was determined to have refractory intracranial hypertension (RICH) and PBC treatment was initiated. PBC was performed with pentobarbital infusion with continuous electroencephalogram monitoring to ensure adequate burst suppression. The measurements include serum sodium (Na) and osmolality (Osm) were assessed as indicators for initiation of PBC and to estimate the 50% mortality cut-points when controlling for ICP. Follow-up functional outcomes were assessed using the Glasgow Outcome Scale and stratified according to admission Glasgow Coma Scale score and Marshall computed tomography classification. Of the 55 PBC patients, 22 (40%) survived at discharge. 19 of 22 had long-term follow-up (1 year or more) available. Of these, 13 (68%) were normal or functionally independent (Glasgow Outcome Scale score 4 or 5). Serum Na and Osm were associated with death (p < 0.05) when controlling for ICP. The 50% mortality cut-points were Na of 160 mEq/L and Osm of 330 mOsm/kg H2O. Median minimum cerebral perfusion pressure after PBC was 42 mm Hg in survivors and 34 mm Hg in nonsurvivors (p = 0.013). In patients with severe TBI and RICH, survival at discharge of 40% with good functional outcomes in 68% of survivors at 1 year or more can be achieved with PBC after failure of HOsmRx. Based on 50% mortality cut-points, analysis suggests the limits of HOsmRx to be Na of 160 mEq/L and Osm of 330 mOsm/Kg H2O. Maintenance of higher cerebral perfusion pressure after PBC is associated with survival. PBC treatment of RIH may be even more important when other treatments of RIH, such as decompressive craniectomy, are not available.

BARBITURATE INFUSION FOR INTRACTABLE INTRACRANIAL HYPERTENSION AND ITS EFFECT ON BRAIN OXYGENATION

Barbiturate-induced coma can be used in patients to treat intractable intracranial hypertension when other therapies, such as osmotic therapy and sedation, have failed. Despite control of intracranial pressure, cerebral infarction may still occur in some patients, and the effect of barbiturates on outcome remains uncertain. In this study, we examined the relationship between barbiturate infusion and brain tissue oxygen (PbtO2). Ten volume-resuscitated brain-injured patients who were treated with pentobarbital infusion for intracranial hypertension and underwent PbtO2 monitoring were studied in a neurosurgical intensive care unit at a university-based Level I trauma center. PbtO2, intracranial pressure (ICP), mean arterial pressure, cerebral perfusion pressure (CPP), and brain temperature were continuously monitored and compared in settings in which barbiturates were or were not administered. Data were available from 1595 hours of PbtO2 monitoring. When pentobarbital administration began, the mean ICP, CPP, and PbtO2 were 18 +/- 10, 72 +/- 18, and 28 +/- 12 mm Hg, respectively. During the 3 hours before barbiturate infusion, the maximum ICP was 24 +/- 13 mm Hg and the minimum CPP was 65 +/- 20 mm Hg. In the majority of patients (70%), we observed an increase in PbtO2 associated with pentobarbital infusion. Within this group, logistic regression analysis demonstrated that a higher likelihood of compromised brain oxygen (PbtO2 < 20 mm Hg) was associated with a decrease in pentobarbital dose after controlling for ICP and other physiological parameters (P < 0.001). In the remaining 3 patients, pentobarbital was associated with lower PbtO2 levels. These patients had higher ICP, lower CPP, and later initiation of barbiturates compared with patients whose PbtO2 increased. Our preliminary findings suggest that pentobarbital administered for intractable intracranial hypertension is associated with a significant and independent increase in PbtO2 in the majority of patients. However, in some patients with more compromised brain physiology, pentobarbital may have a negative effect on PbtO2, particularly if administered late. Larger studies are needed to examine the relationship between barbiturates and cerebral oxygenation in brain-injured patients with refractory intracranial hypertension and to determine whether PbtO2 responses can help guide therapy.

Significance of intracranial pressure and cerebral perfusion pressure in severe pediatric traumatic brain injury

The aim of the study was to evaluate outcome of children after severe traumatic brain injury treated according to intracranial pressure (ICP)-targeted protocol, to define threshold values of peak ICP and minimal cerebral perfusion pressure (CPP) for decompressive osteoplastic craniotomy, and to determine the relationship between ICP, CPP and long-term outcome in these children. All children admitted to Pediatric Intensive Care Unit of Kaunas University of Medicine Hospital after severe head injury from January 2004 to June 2006 and treated according to ICP-targeted protocol for the management of severe head trauma were prospectively included in the study. Raised ICP was defined as a level higher than 20 mmHg. Minimal CPP was considered to be at a level of 40 mmHg. Outcome was defined using Glasgow Outcome Scale (GOS) at discharge from the hospital and after 6 months. Forty-eight patients (32 boys and 16 girls) were included into the study. Favorable outcome (GOS score of 4 and 5) after 6 months was achieved in 43 (89.6%) cases. Mean peak ICP was 24.2+/-7.2 mmHg and mean minimal CPP - 53.1+/-14.7 mmHg. Decompressive craniotomy was performed in 13 cases. Threshold values of peak ICP and minimal CPP for decompressive craniotomy were 22.5 mmHg (area under the curve, 0.880) and 46.5 mmHg (area under the curve, 0.898), respectively. The differences in peak ICP and minimal CPP in groups of favorable and unfavorable outcomes were not statistically significant. Treating children after severe traumatic brain injury according to the ICP-targeted protocol for the management of severe pediatric traumatic brain injury resulted in a favorable long-term outcome.

ICP and CPP: excellent predictors of long term outcome in severely brain injured children

To determine the predictive powers of intracranial pressure (ICP) and cerebral perfusion pressure (CPP) amongst severely brain injured children. ICP and CPP were recorded from thirty-five severely brain injured children who were prospectively recruited after admission to paediatric intensive care. Twenty-five suffered traumatic brain injury (TBI) and ten suffered non-TBI. Peak ICP and minimum CPP recorded for each patient during their admission were related to 5 year Glasgow Outcome Scale outcome. Receiver operator characteristic curves determined that the optimum threshold for unfavourable outcome prediction was >or=40 mmHg for ICP and <or=49 mmHg for CPP. At these thresholds the sensitivity/specificity pairs for the prediction of unfavourable outcome were 33.3/100% and 55.6/100% for ICP and CPP, respectively, amongst patients suffering TBI and were 46.2/100% and 66.2/100% for ICP and CPP, respectively, amongst all patients. ICP and CPP are accurate predictors of unfavourable outcome.

Management of cerebral perfusion pressure after traumatic brain injury.

IN 1996, the Brain Trauma Foundation sponsored the development of guidelines for the management of severe traumatic brain injury (TBI). The method used for development of the guidelines was evidence based, and probably the most significant contribution of the guidelines has been to highlight the remarkable lack of class I evidence available for many current management practices. Recently, revisions to the guidelines were published, and little has been changed in the recommendations. 1 From all of the aspects of management that were reviewed for the guidelines, the authors were only able to provide three standards based on class I evidence (randomized clinical trials) and only eight guidelines based on class II evidence (table 1). Furthermore, the randomized clinical trials that have supported the three guideline standards showed ineffectiveness of certain long-standing management practices (prophylactic hyperventilation, steroid administration, prophylactic anticonvulsants) rather than showing that any practices are

Should Induced Hypertension Be Beneficial After Traumatic Brain Injury?

Should Induced Hypertension Be Beneficial After Traumatic Brain Injury?

Cerebral perfusion pressure: management protocol and clinical results

Early results using cerebral perfusion pressure (CPP) management techniques in persons with traumatic brain injury indicate that treatment directed at CPP is superior to traditional techniques focused on intracranial pressure (ICP) management. The authors have continued to refine management techniques directed at CPP maintenance. One hundred fifty-eight patients with Glasgow Coma Scale (GCS) scores of 7 or lower were managed using vascular volume expansion, cerebrospinal fluid drainage via ventriculostomy, systemic vasopressors (phenylephrine or norepinephrine), and mannitol to maintain a minimum CPP of at least 70 mm Hg. Detailed outcomes and follow-up data bases were maintained. Barbiturates, hyperventilation, and hypothermia were not used. Cerebral perfusion pressure averaged 83 +/- 14 mm Hg; ICP averaged 27 +/- 12 mm Hg; and mean systemic arterial blood pressure averaged 109 +/- 14 mm Hg. Cerebrospinal fluid drainage averaged 100 +/- 98 cc per day. Intake (6040 +/- 4150 cc per day) was carefully titrated to output (5460 +/- 4000 cc per day); mannitol averaged 188 +/- 247 g per day. Approximately 40% of these patients required vasopressor support. Patients requiring vasopressor support had lower GCS scores than those not requiring vasopressors (4.7 +/- 1.3 vs. 5.4 +/- 1.2, respectively). Patients with vasopressor support required larger amounts of mannitol, and their admission ICP was 28.7 +/- 20.7 versus 17.5 +/- 8.6 mm Hg for the nonvasopressor group. Although the death rate in the former group was higher, the outcome quality of the survivors was the same (Glasgow Outcome Scale scores 4.3 +/- 0.9 vs. 4.5 +/- 0.7). Surgical mass lesion patients had outcomes equal to those of the closed head-injury group. Mortality ranged from 52% of patients with a GCS score of 3 to 12% of those with a GCS score of 7; overall mortality was 29% across GCS categories. Favorable outcomes ranged from 35% of patients with a GCS score of 3 to 75% of those with a GCS score of 7. Only 2% of the patients in the series remained vegatative and if patients survived, the likelihood of their having a favorable recovery was approximately 80%. These results are significantly better than other reported series across GCS categories in comparisons of death rates, survival versus dead or vegetative, or favorable versus nonfavorable outcome classifications (Mantel-Haenszel chi 2, p < 0.001). Better management could have improved outcome in as many as 35% to 50% of the deaths.

Monitoring in non-traumatic coma. Part II: Electroencephalography.

Forty eight comatose children had electroencephalograms (EEG) recorded during the acute phase of their illnesses. These were classified according to a simple grading system and the findings correlated with the presence of seizures, deep coma, minimum cerebral perfusion pressure, and eventual neurological outcome. Serial EEGs proved important, particularly when slow activity was seen initially. None of the 20 patients who showed low amplitude EEG activity or electrocerebral silence at any stage of the acute illness did well. Discharges were seen in only 13 of the 29 patients with seizures and their presence did not correlate with outcome except in five patients with a distinctive pattern of discharges, none of whom had a good outcome. EEG findings associated with poor outcome did not always correlate with the clinical assessment of deep coma, emphasising the difficulties of neurological evaluation in these patients. Five of the patients with cerebral perfusion pressures greater than 42 mm Hg had a poor outcome that was predicted by serial EEGs. In nine patients with a minimum cerebral perfusion pressure in the borderline range 38-42 mm Hg the EEG was useful as an indication of the outcome. The EEG reflects changes in cerebral function which may be due to multifactorial or repeated insults. An EEG is therefore important in both the initial assessment and as an indicator of the neurological outcome, particularly in those patients in whom the cerebral perfusion pressure has apparently been adequate or within the borderline range.

Monitoring in non-traumatic coma. Part I: Invasive intracranial measurements.

The arterial blood pressure, intracranial pressure, and organ system failure scores were reviewed for 49 infants and children with non-traumatic coma from various causes. The neurological outcome was good in 21 patients, moderate in five, and poor in 23. There was no significant difference in maximum intracranial pressures between patients with a good outcome and those with a poor one, but patients with a poor outcome had significantly lower minimum cerebral perfusion pressures. During the period of admission 18 patients had cardiovascular failure, none had renal failure, and two developed severe coagulopathy. Seventeen of the 19 patients in whom at least one of these systems failed died. Our findings emphasise the diversity of illnesses associated with raised intracranial pressure in children and the number who develop multiple organ failure, and the values and limitations of using minimum cerebral perfusion pressure and the organ system failure scores as guides to severity of illness and prognosis.

Variables affecting outcome from severe brain injury in children

This study evaluates the outcome of 56 severely brain injured children (mean age 6.2 +/- 2.1 years) and relates the Initial Glasgow Coma Scale (IGCS), initial intracranial pressure (ICP int), maximal intracranial pressure (ICP max) and minimal cerebral perfusion pressure (CPP min) to quality of survival. Forty-one children sustained head trauma, five severe central nervous system infections and 10 were of miscellaneous etiology. Therapy consisted of mechanical hyperventilation, moderate fluid restriction, dexamethasone and diagnosis specific measures when indicated. Outcome was categorized according to the Glasgow outcome scale at discharge from the hospital. An IGCS of 3 was associated with 100% mortality, 7 and above resulted in 72% good recovery, 28% poor outcome and no mortality. ICP int of less than 20 torr was noted in (67%) of the patients, and did not correlate with ICP max or outcome. Conversely, ICP int in excess of 40 torr correlated well with ICP max and outcome. ICP max of less than 20 torr resulted in 57% good recovery, 36% poor outcome and 7% mortality. ICP max greater than 40 torr resulted in 7% poor outcome and 93% mortality (p less than 0.001). In head trauma, 32 patients (78%) were alive with mean ICP max 16.9 +/- 3.1 and CPP min 65.5 +/- 8.5 torr compared to 9 patients (22%) who died with mean ICP max 53.7 +/- 10.8 and CPP min 6 +/- 3.9 torr, (p less than 0.01). In children with infectious etiology 60% survived with mean ICP max 16 +/- 3 and CPP min 96 +/- 16 torr.(ABSTRACT TRUNCATED AT 250 WORDS)

Value of intracranial pressure monitoring of asphyxiated newborn infants.

Twenty-three infants suffering the effects of moderate or severe hypoxic-ischaemic encephalopathy were continuously monitored for intracranial pressure (ICP) by means of a subarachnoid catheter for a total of 1083 hours. Cerebral perfusion pressure (CPP) was also continuously monitored for 21 of the infants. The median age at the start of ICP monitoring was 17 hours, and the opening pressure correlated poorly with maximum sustained pressures. Maximum sustained ICP allowed the infants to be divided into three groups: (1) those with no elevation of ICP (nine), of whom two died and five had a normal outcome; (2) those with sustained rises in ICP which were resistent to treatment (nine), of whom seven died and two survivors are severely handicapped; and (3) those in whom the pressure was elevated but could be controlled medically (five), of whom two survived to be quite normal. No infant with a sustained elevation of ICP of 15mmHg or more survived to be normal, nor any who had had a CPP below 20mmHg for one hour or more. Hypotension was the cause of low CPP in most cases. There was a highly significant correlation between sustained elevation of ICP above 10mmHg and poor outcome, but no correlation between outcome and minimum CPP. It was not possible to predict clinically which infants would develop intracranial hypertension, and some infants with very severe perinatal asphyxia did not develop intracranial hypertension, and some infants with very severe perinatal asphyxia did not develop raised intracranial pressure at any time.