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Intracranial hypertension leading to brain stem herniation is a major cause of death in fulminant hepatic failure (FHF). Mannitol, barbiturates, and hyperventilation have been used to treat brain swelling, but most patients are either refractory to medical management or cannot be treated because of concurrent medical problems or side effects. In this study, we examined whether allogeneic hepatocellular transplantation may prevent development of intracranial hypertension in pigs with experimentally induced liver failure. Of the two preparations tested--total hepatectomy (n = 47), and liver devascularization (n = 16)--only pigs with liver ischemia developed brain edema provided, however, that animals were maintained normothermic throughout the postoperative period. This model was then used in transplantation studies, in which six pigs received intrasplenic injection of allogeneic hepatocytes (2.5 x 10(9) cells/pig) and 3 days later acute liver failure was induced. In both models (anhepatic state, liver devascularization), pigs allowed to become hypothermic had significantly longer survival compared to those maintained normothermic. Normothermic pigs with liver ischemia had, at all time points studied, ICP greater than 20 mmHg. Pigs that received hepatocellular transplants had ICP below 15 mmHg until death; at the same time, cerebral perfusion pressure (CPP) in transplanted pigs was consistently higher than in controls (45 +/- 11 mmHg vs. 16 +/- 18 mmHg; p < 0.05). Spleens of transplanted pigs contained clusters of viable hepatocytes (hematoxylin-eosin, CAM 5.2). It was concluded that removal of the liver does not result in intracranial hypertension; hypothermia prolongs survival time in both anhepatic pigs and pigs with liver devascularization, and intrasplenic transplantation of allogeneic hepatocytes prevents development of intracranial hypertension in pigs with acute ischemic liver failure.
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PMID:Transplantation of hepatocytes for prevention of intracranial hypertension in pigs with ischemic liver failure. 971 Mar 4

Ischemia causes secondary brain damage after severe head injury (SHI). Cerebral perfusion is commonly estimated by monitoring CPP, but the adequacy of cerebral oxygenation requires further measurements, such as jugular oxygen saturation or, more recently, PtiO2 monitoring. In 7 patients with severe head injury, ICP, MAP, CPP, SjO2 and PtiO2 were monitored for a mean time of 9.0 +/- 2.2 days. Most of the data were in a "normal" range. Focusing on values under the thresholds of 60 mm Hg for CPP and 20 mm Hg for PtiO2, we found a relationship between CPP and PtiO2. Looking at the PtiO2 time-course, we observed a quite constant increasing trend during the first 48 hours of monitoring, then the values remained relatively constant within a normal range. Our data show that decreases of PtiO2 are not uncommon after severe head injury and therefore it seems that monitoring of PtiO2 in SHI may be useful in order to minimize secondary insults.
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PMID:Effects of cerebral perfusion pressure on brain tissue PO2 in patients with severe head injury. 977 59

Elevated temperature is known to facilitate neuronal injury after ischemia. After head injury a gradient between temperature and body temperature of up to 3 degrees C higher in the brain has been reported. Hypothermia may limit some of the deleterious metabolic consequences of such increased temperature. In 20 patients who had suffered severe ischemic stroke in the middle cerebral artery (MCA) territory, intracerebral temperature combined with ICP monitoring was recorded using two different thermocouples, with epidural, and parenchymatous measurements. Mild hypothermia was induced using cooling blankets. Patients were kept at 33 degrees C core temperature for 48 to 72 hours. In all patients brain temperature exceeded body-core temperature by at least up to 1 degree C (range 1.0-2.1 degrees C). Systemic cooling was effective and sustained hypothermic (33-34 degrees C) brain temperatures. With mild hypothermia critically elevated ICP values could be controlled. 12 patients survived the hemispheric stroke with a mean Barthel index of 70. Severe side effects of hypothermia were not detected. After MCA stroke, human intracerebral temperature is higher than central body-core temperature. Mild hypothermia in the treatment of severe cerebral ischemia using cooling blankets is safe and does not lead to severe side effects. Mild hypothermia can help to control critically elevated ICP values in severe space-occupying stroke and may improve clinical outcome in these patients.
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PMID:Moderate hypothermia and brain temperature in patients with severe middle cerebral artery infarction. 977 65

The objective was to examine the effect of the nitric oxide synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME) on leukocyte adhesion in the cerebral microcirculation during reperfusion following partial forebrain ischemia in the rat. Intravital fluorescence video-microscopy through a closed cranial window was used to visualize leukocyte-endothelium interaction in small pial veins of 15-100 microns diameter. Forebrain ischemia was produced by the ligation of both common carotid arteries plus elevation of the intracranial pressure to 20 mmHg for 60 min. The number of leukocytes adhering to the endothelium for longer than 3 sec was determined during ischemia (5 min and 60 min) and during reperfusion (5 min and 60 min). Two experimental groups were treated with either L-NAME or its inactive enantiomer D-NAME (20 mg kg-1 i.v.) 30 min prior to reperfusion. In a third group, also treated with D-NAME, post-ischemic hyperemia was prevented by lowering the ICP without removing the occlusion of common carotid arteries (partial reperfusion). The velocity of flow adjacent to the endothelial surface of pial veins was measured by tracking the movement of fluorescently labeled red blood cells as flow markers before and after ischemia. During ischemia, the number of adhering leukocytes increased approximately two-fold at 5 min, and three-fold at 60 min. In the D-NAME-treated group with complete reperfusion, leukocyte adhesion returned to the baseline level by 60 min of reperfusion. However, in the L-NAME-treated group, leukocyte adhesion remained elevated at 60 min of reperfusion. Post-ischemic flow velocity was significantly decreased (-66%) from control after L-NAME treatment whereas it was increased (+53%) in the D-NAME-treated group. In the partial reperfusion group, leukocyte adhesion continued to increase after the first hour of ischemia and reached a level 2.7-fold over baseline at 60 min reperfusion. Flow velocity remained below control (-26%) at 60 min reperfusion. Leukocyte adhesion was absent in pial arteries and no plugging by leukocytes was observed in cortical capillaries. The results suggest that leukocyte adhesion in small pial veins increases during 1 h forebrain ischemia and continues to increase during reperfusion if the velocity of flow or shear rate is low. The increase in leukocyte adhesion is reversible if flow velocity is elevated during reperfusion. L-NAME prevents post-ischemic hyperemia and augments leukocyte adhesion principally via a decrease in velocity or shear rate.
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PMID:Nitric oxide synthase inhibitor augments post-ischemic leukocyte adhesion in the cerebral microcirculation in vivo. 1040 10

The fundamental goals of resuscitation of the head-injured patient are the restoration of circulating volume, blood pressure, oxygenation, and ventilation. The physician should initiate maneuvers that serve to lower ICP and do not interfere with these aims as early as possible during resuscitation of any patient with a head injury. Treatment modalities such as hyperventilation and mannitol administration that have the potential of exacerbating intracranial ischemia or interfering with resuscitation should be reserved for patients who show signs of intracranial hypertension such as evidence of herniation or neurologic deterioration.
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PMID:The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Initial management. 1093 88

Chronic prophylactic hyperventilation therapy should be avoided during the first 5 days after severe TBI and particularly during the first 24 h. CBF measurements in patients with severe TBI demonstrate that blood flow early after injury is low and strongly suggest that in the first few hours after injury the absolute values approach those consistent with ischemia. These findings are corroborated by AVdO2 and SjO2 and brain tissue O2 measurements. Hyperventilation will reduce CBF values even further, but will not consistently cause a reduction of ICP and may cause loss of autoregulation. The cerebral vascular response to hypocapnia is reduced in those with the most severe injuries (subdural hematomas and diffuse contusions), and there is substantial local variability in perfusion. While the CBF level at which irreversible ischemia occurs has not been clearly established, ischemic cell change has been demonstrated in 90% of those who die following TBI, and there is PET evidence that such damage is likely to occur when CBF drops below 15-20 cc/100 g/min. A prospective randomized clinical trial has determined that outcomes are worse when TBI patients are treated with chronic prophylactic hyperventilation therapy. Within the standard, guideline, and options, specific paCO2 thresholds have been described that are different for each of the three parameters. These individual thresholds were selected based on the preponderance of literature supporting those thresholds in the contexts of the statements which included them. With the exception of the threshold included for the standard in this guideline, it is emphasized that the paCO2 threshold is not as important as the general concept of hyperventilation. The preponderance of the physiologic literature concludes that hyperventilation during the first few days following severe traumatic brain injury, whatever the threshold, is potentially deleterious in that it can promote cerebral ischemia.
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PMID:The Brain Trauma Foundation. The American Association of Neurological Surgeons. The Joint Section on Neurotrauma and Critical Care. Hyperventilation. 1093 94

Intracerebral contusions can lead to regional ischemia caused by extensive release of excitotoxic aminoacids leading to increased cytotoxic brain edema and raised intracranial pressure. rCBF measurements might provide further information about the risk of ischemia within and around contusions. Therefore, the aim of the presented study was to compare the intra- and perilesional rCBF of hemorrhagic, non-hemorrhagic and mixed intracerebral contusions. In 44 patients, 60 stable Xenon-enhanced CT CBF-studies were performed (EtCO2 30 +/- 4 mmHg SD), initially 29 hours (39 studies) and subsequent 95 hours after injury (21 studies). All lesions were classified according to localization and lesion type using CT/MRI scans. The rCBF was calculated within and 1-cm adjacent to each lesion in CT-isodens brain. The rCBF within all contusions (n = 100) of 29 +/- 11 ml/100 g/min was significantly lower (p < 0.0001, Mann-Whitney U) compared to perilesional rCBF of 44 +/- 12 ml/100 g/min and intra/perilesional correlation was 0.4 (p < 0.0005). Hemorrhagic contusions showed an intra/perilesional rCBF of 31 +/- 11/44 +/- 13 ml/100 g/min (p < 0.005), non-hemorrhagic contusions 35 +/- 13/46 +/- 10 ml/100 g/min (p < 0.01). rCBF in mixed contusions (25 +/- 9/44 +/- 12 ml/100 g/min, p < 0.0001) was significantly lower compared to hemorrhagic and non-hemorrhagic contusions (p < 0.02). Intracontusional rCBF is significantly reduced to 29 +/- 11 ml/100 g/min but reduced below ischemic levels of 18 ml/100 g/min in only 16% of all contusions. Perilesional CBF in CT normal appearing brain closed to contusions is not critically reduced. Further differentiation of contusions demonstrates significantly lower rCBF in mixed contusions (defined by both hyper- and hypodense areas in the CT-scan) compared to hemorrhagic and non-hemorrhagic contusions. Mixed contusions may evolve from hemorrhagic contusions with secondary increased perilesional cytotoxic brain edema leading to reduced cerebral blood flow and altered brain metabolism. Therefore, the treatment of ICP might be individually modified by the measurement of intra- and pericontusional cerebral blood.
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PMID:rCBF in hemorrhagic, non-hemorrhagic and mixed contusions after severe head injury and its effect on perilesional cerebral blood flow. 1145 9

Caring for the patient with a brain injury is a dynamic process with the goal of providing therapy to prevent secondary injury. Until practitioners have a better understanding of the pathophysiology of ischemia and the response of therapies for treating increased ICP, they must use the tools that exist. ICP monitoring gives a rough index of the relationships and the response of the intracranial contents to changes in volume that may produce increases in pressure and further damage. Understanding the information supplied by ICP monitoring is imperative to successful management of increased ICP.
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PMID:Intracranial pressure monitoring and assessing intracranial compliance in brain injury. 1185 46

The aim of the present study was to assess the veno-arterial difference in pCO2 (delta pCO2) as an indicator of ischemia compared to the arteriovenous O2 difference (AVDO2). Staircase cerebral blood flow (CBF) reductions were obtained in seven domestic pigs by inducing intracranial hypertension: CBF 100%, 50-60% of baseline, 20-30% of baseline. ICP, MAP, CPP and CBF (Laser-Doppler method) were continuously recorded. The superior sagittal sinus was punctured to determine AVDO2 and delta pCO2. AVDO2 was 5.9 (+/- 1.78, range 3.3-7.4), 7.01 (+/- 1.31, range 5-8.9) and 8.17 (+/- 1.51, range 6.0-11.3) ml/100 ml in the three CBF steps (p = 0.001). CBF impairment was accompanied by the following increases in delta pCO2: from 10 (+/- 4, range 4-15) mmHg to 14.5 (+/- 4.11, range 10-27) mmHg, and to 31.2 (+/- 9.0, range 17-39) mmHg (p < 0.001). When CBF declines AVDO2 increases, indicating greater extraction of O2 to satisfy the aerobic metabolism. However, this mechanism can no longer compensate once a critical CBF threshold is reached. delta pCO2 rises slowly during moderate CBF reduction because of defective washout; the rise is impressive during marked CBF impairment when anaerobic metabolism takes place with proton buffering in CO2 and H2O. Therefore, when the brain's ability to compensate for low blood flow is exceeded, CO2 production outweighs O2 extraction.
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PMID:Cerebral veno-arterial pCO2 difference as an estimator of uncompensated cerebral hypoperfusion. 1216 4

We present a group of 29 consecutive head injured comatose patients with the syndrome of transtentorial herniation. All patients had urgent surgery and then continuous monitoring of ICP, CPP, blood pressure and jugular bulb oximetry was instituted. Two postoperative CT and SPECT examinations were performed in each patient. 15 patients had a normal CPP (> 70 mmHg) throughout the postoperative period, 80% of them had a favourable outcome. On the other hand 14 patients had decreased CPP lasting at least one hour and only 36% of them had a favourable outcome (p < 0.05). Similar relationships were found comparing GOS in patients with normal and increased ICP (> 20 mmHg) and normal and decreased SjO2 (< 55%). All but 3 patients had ischaemia on SPECT. Ischaemia improved on the 2nd SPECT in 11 patients and 10 (91%) of them had a favourable outcome. GOS (mean follow up 9 months) is: 12 patients good, 5 moderately disabled, 2 vegetative, 10 died. We conclude that SPECT is able to disclose even reversible ischaemic changes. In these patients all effort has to be made to keep CPP on normal levels. Improvement in cerebral perfusion is related to a better outcome.
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PMID:Cerebral perfusion pressure and spect in patients after craniocerebral injury with transtentorial herniation. 1216 62


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