Initial Cerebral Perfusion Pressure Research Articles

Optimal Cerebral Perfusion Pressure Guided by Brain Oxygen Pressure Measurement.

Background: Although increasing cerebral perfusion pressure (CPP) is commonly accepted to improve brain tissue oxygen pressure (PbtO2), it remains unclear whether recommended CPP targets (i. e., >60 mmHg) would result in adequate brain oxygenation in brain injured patients. The aim of this study was to identify the target of CPP associated with normal brain oxygenation.Methods: Prospectively collected data including patients suffering from acute brain injury and monitored with PbtO2, in whom daily CPP challenge using vasopressors was performed. Initial CPP target was >60 mmHg; norepinephrine infusion was modified to have an increase in CPP of at least 10 mmHg at two different steps above the baseline values. Whenever possible, the same CPP challenge was performed for the following days, for a maximum of 5 days. CPP “responders” were patients with a relative increase in PbtO2 from baseline values > 20%.Results: A total of 53 patients were included. On the first day of assessment, CPP was progressively increased from 73 (70–76) to 83 (80–86), and 92 (90–96) mmHg, which resulted into a significant PbtO2 increase [from 20 (17–23) mmHg to 22 (20–24) mmHg and 24 (22–26) mmHg, respectively; p < 0.001]. Median CPP value corresponding to PbtO2 values > 20 mmHg was 79 (74–87) mmHg, with 2 (4%) patients who never achieved such target. Similar results of CPP targets were observed the following days. A total of 25 (47%) were PbtO2 responders during the CPP challenge on day 1, in particular if low PbtO2 was observed at baseline.Conclusions: PbtO2 monitoring can be an effective way to individualize CPP values to avoid tissue hypoxia. Low PbtO2 values at baseline can identify the responders to the CPP challenge.

Intravenous labetalol versus oral nifedipine for acute hypertension in pregnancy: effects on cerebral perfusion pressure

Pregnant women with preeclampsia have been found to have elevated cerebral perfusion pressure and impaired cerebral autoregulation compared with normal pregnant women. Transcranial Doppler is a noninvasive technique used to estimate cerebral perfusion pressure. The effects of different antihypertensive medications on cerebral perfusion pressure in preeclampsia are unknown. To compare the change in cerebral perfusion pressure before and after intravenous labetalol vs oral nifedipine in the setting of acute severe hypertension in pregnancy. This is a prospective cohort study of pregnant women between 24 and 42 weeks' gestation with severe hypertension (systolic blood pressure ≥160 mm Hg and/or diastolic blood pressure ≥110 mm Hg). Women who consented to the study and received either intravenous labetalol or oral nifedipine were included. Exclusion criteria included active labor or receipt of any antihypertensive medication within 2 hours of initial cerebral perfusion pressure measurement. Peripheral blood pressure and transcranial Doppler studies for middle cerebral artery hemodynamics were performed prior to the administration of antihypertensive medications and repeated 30 minutes after medication administration. A total of 16 women with acute severe hypertension were enrolled; 8 received intravenous labetalol and 8 received oral nifedipine. There were no significant differences between the labetalol and nifedipine groups in baseline characteristics such as maternal age, race and ethnicity, payment, hospital site, body mass index, nulliparity, gestational age, preexisting diabetes mellitus or chronic hypertension, fetal growth restriction, magnesium sulfate administration, and symptomatology (P>.05). When examined 30 minutes after the administration of either intravenous labetalol or oral nifedipine, there was a significantly greater decrease in systolic blood pressure (-9.8 mm Hg vs-39 mm Hg; P=.003), mean arterial pressure (-7.1 mm Hg vs-22.3 mm Hg; P=.02), and cerebral perfusion pressure (-2.5 mm Hg vs-27.7 mm Hg; P=.01) in the nifedipine group. There was no statistically significant decrease in diastolic blood pressure (-12.9 mm Hg vs-5.4 mm Hg; P=.15). The change in middle cerebral artery velocity by transcranial Doppler was compared between the groups and was not different (0.07 cm/s vs 0.16 cm/s; P=.64). Oral nifedipine resulted in a significant decrease incerebral perfusion pressure, whereas labetalol did not, after administration for acute severe hypertension among women with preeclampsia. This decrease seems to be driven by a decrease in peripheral arterial blood pressure rather than a direct change in cerebral blood flow.

APOE ε4 positive patients suffering severe traumatic head injury are more prone to undergo decompressive hemicraniectomy

ObjectIn this paper we tested the hypothesis if patients with severe traumatic brain injury and presence of the apolipoprotein E (APOE) ε4 allele are more prone to undergo the surgical procedure decompressive hemicraniectomy (DC) in order to bring the intracranial pressure (ICP) under control. MethodsIn this prospective consecutive study patients with sTBI were enrolled (n=48). Inclusion criteria were arrival to our level one trauma university hospital within 24h after trauma, patient age between 15 and 70years, Glasgow Coma Scale (GCS) score ≤8 at the time of intubation and sedation, an initial cerebral perfusion pressure >10mmHg.Venous blood was sampled for APOE genotype determination. Clinical outcome at 6months after injury was assessed with the Extended Glasgow Outcome Scale (GOSE).All surgical procedures needed for each patient were registered. ResultsPatients with the APOE ε4 allele were significantly overrepresented in the DC group.In the APOE ε4+DC group, ICPmax and ICPmean during the first 36h were significantly higher and GOSE was significantly worse at 6months. ConclusionOur data suggest that patients with the APOE ε4 allele are predisposed for the need of DC more often than patients without the APOE ε4 allele. Thus, it seems to be of importance to consider the APOE genotype in patients suffering severe traumatic brain injury in order to forecast the need for a more exquisite intensive care.

Relationship between Intracranial Pressure or Cerebral Perfusion Pressure and Prognosis in Patients with Severe Traumatic Brain Injury Treated with Mild Hypothermia

Aims: The purpose of this study was to predict the clinical course by intracranial pressure (ICP) or cerebral perfusion pressure (CPP) in the acute phase and prognosis in patients with severe head trauma who underwent therapeutic mild hypothermia (HT). Methods: A consecutive 143 patients treated with HT for intracranial hypertension (ICH) in two trauma centers were included in this study. The pressure measured after computed tomography scanning was defined as the initial ICP or CPP. Outcome was assessed at 6 months according to the Glasgow Outcome Scale. ROC analysis was performed to clarify the threshold value of ICP/CPP predictive of ICP uncontrollable by HT. Results: The cutoff value of ICP for uncontrollable ICP obtained from ROC analysis was 32.5 mmHg (sensitivity: 0.545, specificity: 0.875), and that for CPP was 56.5 mmHg (sensitivity: 0.813, specificity: 0.663). Fifty-three (96.4%) of 55 patients whose initial ICP was greater than 32.5 mmHg and 67 (95.7%) of 70 patients whose initial CPP was less than 56.5 mmHg had developed uncontrollable ICP. Conclusion: The cutoff values predictive of ICP uncontrollable by HT from ROC analysis were 32.5 mmHg for ICP and 56.5 mmHg for CPP. For those patients with initial ICP greater than the cutoff value or an initial CPP less than the cutoff value, it may be harmful to prolong HT. The knowledge obtained from this study may be useful for considering the treatment strategy for severe traumatic brain injury.

Use of the CRASH study prognosis calculator in patients with severe traumatic brain injury treated with an intracranial pressure-targeted therapy

Based on the Corticosteroid Randomisation after Significant Head Injury (CRASH) trial database, a prognosis calculator has been developed for the prediction of outcome in an individual patient with a head injury. In 47 patients with severe traumatic brain injury (sTBI) prospectively treated using an intracranial pressure (ICP) targeted therapy, the individual prognosis for mortality at 14 days and unfavourable outcome at 6months was calculated and compared with the actual outcome. An overestimation of the risk of mortality and unfavourable outcome was found. The mean risk for mortality and unfavourable outcome were estimated to be 44.6±32.5% (95% confidence interval [CI], 35.1–54.2%) and 69.3±23.7% (95% CI, 62.3–76.2%). The actual outcome was 4.3% and 42.6% respectively. The absolute risk reduction (ARR) for mortality was 33.1% and for unfavourable outcome 29.8%. A logistic fit for outcome at 6months shows a statistically significant difference (p<0.01). A receiver operating characteristic (ROC) curve analysis shows an area under the curve (AUC) of 0.691. The CRASH prognosis calculator overestimates the risk of mortality and unfavourable outcome in patients with sTBI treated with an ICP-targeted therapy based on the Lund concept. We do not advocate the use of the calculator for treatment decisions in individual patients. We further conclude that patients with blunt sTBI admitted within 8hours of trauma should be treated regardless of their clinical status as long as the initial cerebral perfusion pressure is >10mmHg.

Acute neuro-endocrine profile and prediction of outcome after severe brain injury.

ObjectThe aim of the study was to evaluate the early changes in pituitary hormone levels after severe traumatic brain injury (sTBI) and compare hormone levels to basic neuro-intensive care data, a systematic scoring of the CT-findings and to evaluate whether hormone changes are related to outcome.MethodsProspective study, including consecutive patients, 15–70 years, with sTBI, Glasgow Coma Scale (GCS) score ≤ 8, initial cerebral perfusion pressure > 10 mm Hg, and arrival to our level one trauma university hospital within 24 hours after head trauma (n = 48). Serum samples were collected in the morning (08–10 am) day 1 and day 4 after sTBI for analysis of cortisol, growth hormone (GH), prolactin, insulin-like growth factor 1 (IGF-1), thyroid-stimulating hormone (TSH), free triiodothyronine (fT3), free thyroxine (fT4), follicular stimulating hormone (FSH), luteinizing hormone (LH), testosterone and sex hormone-binding globulin (SHBG) (men). Serum for cortisol and GH was also obtained in the evening (17–19 pm) at day 1 and day 4. The first CT of the brain was classified according to Marshall. Independent staff evaluated outcome at 3 months using GOS-E.ResultsProfound changes were found for most pituitary-dependent hormones in the acute phase after sTBI, i.e. low levels of thyroid hormones, strong suppression of the pituitary-gonadal axis and increased levels of prolactin. The main findings of this study were: 1) A large proportion (54% day 1 and 70% day 4) of the patients showed morning s-cortisol levels below the proposed cut-off levels for critical illness related corticosteroid insufficiency (CIRCI), i.e. <276 nmol/L (=10 ug/dL), 2) Low s-cortisol was not associated with higher mortality or worse outcome at 3 months, 3) There was a significant association between early (day 1) and strong suppression of the pituitary-gonadal axis and improved survival and favorable functional outcome 3 months after sTBI, 4) Significantly lower levels of fT3 and TSH at day 4 in patients with a poor outcome at 3 months. 5) A higher Marshall CT score was associated with higher day 1 LH/FSH- and lower day 4 TSH levels 6) In general no significant correlation between GCS, ICP or CPP and hormone levels were detected. Only ICPmax and LH day 1 in men was significantly correlated.ConclusionProfound dynamic changes in hormone levels are found in the acute phase of sTBI. This is consistent with previous findings in different groups of critically ill patients, most of which are likely to be attributed to physiological adaptation to acute illness. Low cortisol levels were a common finding, and not associated with unfavorable outcome. A retained ability to a dynamic hormonal response, i.e. fast and strong suppression of the pituitary-gonadal axis (day 1) and ability to restore activity in the pituitary-thyroid axis (day 4) was associated with less severe injury according to CT-findings and favorable outcome.

The IMPACT prognosis calculator used in patients with severe traumatic brain injury treated with an ICP-targeted therapy

The prognosis of severe traumatic brain injury (sTBI) is important. The International Mission on Prognosis in Traumatic Brain Injury (IMPACT) study group has developed a prediction calculator for the outcome of patients with sTBI, and this has been made available on the World Wide Web. We have studied the use of the IMPACT calculator on sTBI patients treated with an ICP-targeted therapy based on the Lund concept. The individual clinical data of patients in a prospective sTBI protocol-driven trial of the treatment of sTBI using the Lund concept were entered into the prognosis calculator, and the individual prognosis for each patient was calculated and compared with the actual outcome at 6 months. The use of the IMPACT calculator led to an overestimation of mortality and of an unfavourable outcome. Compared with the IMPACT database, the absolute risk reduction (ARR) for mortality was 13.6 %. There is a statistically significant probability for the prediction of mortality and unfavourable outcome. A ROC curve analysis shows an area under the curve (AUC) in the Core model for mortality of 0.744 and of unfavourable outcome of 0.731, in the Extended model of 0.751 and 0.721 respectively, and in the Lab model of 0.779 and 0.810 respectively. The IMPACT prognosis calculator should be used with caution for the prediction of outcome for an individual patient with sTBI treated with an ICP-targeted therapy based on the Lund concept. We conclude that we have to initiate treatment in all patients with blunt sTBI and an initial cerebral perfusion pressure (CPP)≥10 mmHg [corrected]. It seems that the outcome in sTBI patients treated in this fashion is better than would have been expected from the IMPACT prognosis.

The release of S-100B and NSE in severe traumatic head injury is associated with APOE ε4

In this article we tested the hypothesis that the level of two biochemical markers of brain injury may be associated with the apolipoprotein E (APOE) ε4 allele. In this prospective consecutive study patients with sTBI were included (n = 48). Inclusion criteria were Glasgow Coma Scale (GCS) score ≤ 8 at the time of intubation and sedation, patient age between 15 and 70 years, an initial cerebral perfusion pressure > 10 mmHg, and arrival to our level-one trauma university hospital within 24 h after trauma. Blood samples for neuron-specific enolase (NSE) and S-100B were collected as soon as possibly after arrival, and then twice daily (12-h intervals) for 5 consecutive days. Venous blood was used for APOE genotype determination. Clinical outcome at 3 months after injury was assessed with the Extended Glasgow Outcome Scale (GOSE). Significantly higher levels of the maximal S-100B (S-100B(max)) and area under the curve (S-100B(AUC)) were found in subjects with the APOE ε4 allele compared to those with non-ε4. A similar tendency was observed for NSE(max) and NSE(AUC), though not statistically significant. Our data indicate that there might be a gene-induced susceptibility to severe traumatic brain injury and that patients with the APOE ε4 allele may be more predisposed to brain cellular damage measured as S-100B and NSE. Thus, it seems to be of importance to consider the APOE genotype in interpreting the levels of the biomarkers.

The apolipoprotein E ε4 allele and outcome in severe traumatic brain injury treated by an intracranial pressure–targeted therapy

In this paper, the authors' goal was to study the influence of the apolipoprotein E epsilon4 allele on the clinical outcome in patients treated for severe traumatic brain injury (TBI) with an intracranial pressure (ICP)-targeted therapy based on the Lund concept. The authors conducted a prospective double-blinded randomized trial in which they examined patients with severe TBI. Inclusion criteria consisted of a Glasgow Coma Scale (GCS) score < or = 8 at the time of intubation and sedation, patient age between 15 and 70 years, an initial cerebral perfusion pressure > 10 mm Hg, and arrival to the hospital < 24 hours after trauma. Blood samples for the analysis of apolipoprotein E allele types were collected. Independent staff members evaluated outcomes by obtaining Glasgow Outcome Scale (GOS) scores at 3, 12, and 24 months. The occurrence of the epsilon4 allele was analyzed in 46 patients (mean age 35 +/- 2.2 years with a median GCS score of 6 [range 3-8]). The epsilon4 allele was present in 39.1% of the patients. The ICP, cerebral perfusion pressure, and injury severity score were not statistically significantly different between the groups. The median GOS score at 3 months was 3.5, and at 12 and 24 months was 4 (range 1-5). Except for the GOS score at 3 months, which was dichotomized as favorable (GOS Score 4 or 5) and unfavorable (GOS Scores 1-3), no statistically significant differences in outcome, irrespective of GOS dichotomization used, were found between the patients with the epsilon4 allele and those without. The presence of the epsilon4 allele did not predict for clinical outcome, but GCS and ICP did. The presence of epsilon4 is not associated with long-term clinical outcome in patients with severe TBI treated with an ICP targeted therapy, based on the Lund concept.

The Use of 23.4% Hypertonic Saline for the Management of Elevated Intracranial Pressure in Patients With Severe Traumatic Brain Injury: A Pilot Study

Oncotic agents are a therapeutic mainstay for the management of intracranial hypertension. Both mannitol and varied concentrations of hypertonic saline (HTS) have been shown to be effective at reducing elevated intracranial pressure (ICP). We compared the safety and efficacy of 23.4% HTS to mannitol for acute management of elevated ICP after traumatic brain injury (TBI). After approval from our institutional review board, the records of patients admitted with severe TBI who received mannitol or HTS were reviewed. Demographic and physiologic data were recorded. ICP, cerebral perfusion pressure, reduction of ICP after dose administration, serum sodium, osmolality, and magnitude of dose response during the subsequent 60 minutes were analyzed. Efficacy was determined by comparison of proportion of patients with any response and mean change in ICP after dosing with either agent. Safety was determined by recording any new postinfusion electrolyte or neurologic anomalies. Data were compared using chi2 test, accepting p < 0.05 as significant. Twenty-two patients with severe TBI received 210 doses of either mannitol or HTS. All patients suffered severe blunt injury (mean Injury Severity Score 28 +/- 11). HTS patients had a significantly higher ICP at the initiation of therapy than that of mannitol group (30.7 +/- 7.94 mm Hg vs. 28.3 +/- 8.07 mm Hg, respectively). There was no difference in initial cerebral perfusion pressure. Mean ICP reduction in the hour after administration of 102 doses of mannitol and 108 doses of HTS was greater for patients receiving HTS (9.3 +/- 7.37 mm Hg vs. 6.4 +/- 6.57 mm Hg, respectively; p = 0.0028, chi2). More patients responded to HTS (92.6% HTS vs. 74% mannitol; p = 0.0002, chi2). There was no significant difference between groups in the duration of ICP reduction after dose administration (4.1 hours vs. 3.8 hours, respectively). No adverse events after administration of either agent were identified. Based on this retrospective analysis, 23.4% HTS is more efficacious than mannitol in reducing ICP. If these results are confirmed in a prospective, randomized study, 23.4% HTS may become the agent of choice for the management of elevated ICP after TBI.

Frequency of Sustained Intracranial Pressure Elevation during Treatment of Severe Intraventricular Hemorrhage

Background: Elevated intracranial pressure (ICP) is an important marker of neurological deterioration. The occurrence and significance of elevated ICP and low cerebral perfusion pressure (CPP) in aggressively treated spontaneous intraventricular hemorrhage (IVH) are not defined. Methods: We performed a secondary longitudinal exploratory data analysis of a randomized multicenter trial of urokinase (UK) versus placebo (Pcb) as a treatment for IVH. Eleven IVH patients who required an external ventricular drain (EVD) were randomized to receive either intraventricular UK or Pcb every 12 h until clinical response permitted EVD removal. ICP and CPP were recorded every 4 or 6 h, as well as before and 1 h after EVD closure for administration of study agent. ICP, CPP and the proportion of ICP readings above 20, 30, 40 and 50 mm Hg were analyzed. Results: Six UK and 5 Pcb patients aged 39–74 years (mean ± standard deviation; 53 ± 11 years) were enrolled. Initial ICP ranged from 0 to 38 mm Hg (10.9 ± 11.0), initial CPP from 65 to 133 mm Hg (100.5 ± 17.7). We recorded 472 ICP readings over the entire monitoring period. Of these 65 (14%) were >20 mm Hg, 23 (5%) >30 mm Hg, 9 (2%) >40 mm Hg and 3 (<1%) >50 mm Hg. Only 2 of 141 intraventricular injections of study agent with EVD closure were not tolerated and required reopening of the EVD. Conclusions: In the intensive care unit, initial ICP measured with an EVD was uncommonly elevated (1/11 patients) in this group of severe IVH patients despite acute obstructive hydrocephalus. Frequent monitoring reveals ICP elevation >20 mm Hg in 14% of observations during use of EVD. ICP elevation, though it can occur, is not routinely associated with EVD closure for thrombolytic treatment with UK.

Intracranial pressure and cerebral perfusion pressure as risk factors in children with traumatic brain injuries

The authors evaluated the initial intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as prognostic factors in severe head injury in children and tried to determine the optimal CPP range. The authors performed a 9-year retrospective review of all patients with severe traumatic brain injuries (TBIs) who required invasive ICP monitoring and were admitted to the pediatric intensive care unit at their institution between January 1995 and December 2003. These patients had Glasgow Coma Scale scores lower than 8 and/or required ICP monitoring due to worsening neurological status or neuroimaging results suggestive of cerebral hypertension. Clinical summaries and imaging studies were reviewed. Data for 156 pediatric patients who ranged in age from 1 to 18 years were obtained. Half of these patients presented with normal initial ICPs (< 20 mm Hg), and a good outcome was achieved in 80% of these children. An unfavorable outcome was observed in more than 60% of patients with an initial CPP lower than 40 mm Hg. The proportion of patients with an unfavorable outcome decreased to 10% with initial CPPs higher than 60 mm Hg, but patients with initial CPPs higher than 70 mm Hg did not improve. Initial ICP and CPP measurements were useful as prognostic factors in pediatric patients with severe TBIs: patients with initial CPPs between 40 and 70 mm Hg were found to have a better neurological prognosis than those with CPPs either higher or lower than that range.

Comportamento da pressão intracraniana, da perfusão cerebral e dos parâmetros hemodinâmicos durante a síndrome do compartimento abdominal em cães

OBJETIVO: Estudar as alterações hemodinâmicas e as repercussões sobre o sistema nervoso central ocasionados pela síndrome do compartimento abdominal. MÉTODO: Utilizou-se cães sem raça definida submetidos à anestesia geral e monitorização das pressões arterial média(PAM), intracraniana(PIC), de perfusão cerebral(PPC), da artéria pulmonar(PAP) e venosa central(PVC), do débito cardíaco(DC) e da freqüência cardíaca(FC). Aumentou-se a pressão intra-abdominal(PIA) para níveis de 10,20,30 e 40cmH2O . Após atingir-se nível PIA=40cmH2O realizou-se a descompressão cirúrgica da cavidade abdominal. Em cada etapa realizou-se a medida dos parâmetros PIA, PIC, PAM, PPC, PVC e DC. RESULTADOS: Observou-se que o aumento da PIA causou as seguintes alterações fisiológicas: aumento progressivo da PIC; aumento da PAM até PIA=20cmH2O e diminuição progressiva da mesma após PIA= 40cmH2O; aumento da PPC até PIA=10cmH2O e diminuição progressiva da mesma após PIA= 30cmH2O; aumento progressivo da PVC; diminuição progressiva do DC após PIA= 30cmH2O; Após a descompressão da cavidade, notou-se o retorno da PIC, PAM, PPC, PVC e do DC para valores próximos aos dos iniciais (antes do aumento da PIA). CONCLUSÕES: Concluímos que o aumento da PIA provocou alterações nos sistemas cardiovascular e nervoso central, que foram revertidas após a descompressão cirúrgica da cavidade abdominal.

Multimodal monitoring in patients with head injury: evaluation of the effects of treatment on cerebral oxygenation.

Recently, invasive intensive care unit monitoring of cerebral oxygenation has become feasible. The purpose of this study was to investigate the effects of standard therapeutic interventions used in the treatment of intracranial hypertension on cerebral oxygenation and other physiologic parameters in comatose patients. In the neurosurgical intensive care unit, Ptio2, and jugular bulb oxygen saturation (Sjvo2), arterial blood pressure, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were prospectively studied (0.1 Hz acquisition rate) with a multimodal monitoring system in 21 patients with severe traumatic brain injury during various treatment modalities: dopamine and mannitol infusion, head positioning, and induced arterial hypocapnia. For baseline CPP values below 40 mm Hg, dopamine infusion was more effective in decreasing ICP and improving Ptio2 and Sjvo2 than for initial CPP values above 60 mm Hg. Treatment with mannitol, although improving CPP and lowering ICP, did not affect Ptio2 and Sjvo2. CPP in this group, however, was always above 60 mm Hg. Forced hyperventilation to an end-tidal Pco2 of 21 mm Hg normalized ICP and CPP, but significantly reduced cerebral oxygenation. A CPP > 60 mm Hg emerges as the crucial factor guaranteeing sufficient brain oxygenation. Any intervention used to further elevate CPP does not improve cerebral oxygenation, to the contrary, forced hyperventilation even bears the risk of inducing brain ischemia.

Neurogenic pulmonary edema in fatal and nonfatal head injuries.

Impaired pulmonary function is a frequent but poorly understood complication of acute head injury (HI). A potential early contributor to the pulmonary dysfunction seen in HI patients is neurogenic pulmonary edema (NPE). We hypothesized that NPE would occur early after HI and that it would have a continuum of clinical severity depending on the severity of the HI and associated intracranial hypertension. A large autopsy data base and inpatient HI data base were used to search for cases of NPE. Patients in the autopsy data base were stratified according to injury type and whether they died at the scene or within 96 hours of injury. There were significant (p < 0.0001, analysis of variance) elevations in lung weights in patients dying at the scene and within 96 hours from HI, compared with those dying from other noncentral nervous system injuries. No other organs studied showed significant weight increases. The incidence of NPE in isolated HI patients dying at the scene was 32%. In patients with isolated HI dying within 96 hours, the incidence of NPE was 50%. We found an inverse correlation (r = 0.62; p < 0.0014) between the initial cerebral perfusion pressure and the PaO2/FIO2 ratio despite a normal-appearing chest x-ray film. We conclude that NPE occurs frequently in HI patients. The process of edema formation begins early in the clinical course and is isolated to the lung.(ABSTRACT TRUNCATED AT 250 WORDS)

Large hemispheric infarction, deterioration, and intracranial pressure.

Neurologic deterioration from large hemispheric infarction with edema (LHIE) often leads to the use of therapies directed at decreasing intracranial pressure (ICP). Many of these ICP therapies can potentially accentuate tissue shifts from unilateral mass lesions and lead to rebound ICP elevations. We sought to determine whether ICP elevation is a common cause of deterioration from LHIE by measuring the initial ICP and cerebral perfusion pressure (CPP) in 19 patients deteriorating to stupor from LHIE within 3 hours of deterioration, after ruling out metabolic aberrations, medication side effects, infection, and seizures and prior to commencement of any ICP-lowering therapies. We evaluated 19 patients aged 23 to 77 years--14 with complete middle cerebral artery and five with complete internal carotid artery territory infarctions. Stupor began 59 +/- 37 hours after the stroke onset. ICP monitoring (12 ipsilateral Camino, five contralateral ventriculostomy, and two ipsilateral epidural) demonstrated elevation of ICP (> 15 mm Hg) in only five patients (26.3%), with group mean initial ICP = 13.4 +/- 10 mm Hg. Similarly, the initial CPP was diminished (< 55 mm Hg) in only two patients (10.5%), with group mean initial CPP = 74.9 +/- 14 mm Hg. Globally elevated ICP is not a common cause of initial neurologic deterioration from LHIE mass effect.