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The effect of decompressive trepanation was compared to that of surgical resection of the traumatized tissue in the course of traumatic brain edema in standardized experimental brain trauma. Following a right parietal cold injury, the following parameters were monitored continuously in 12 cats: ventricular pressure, epidural pressure over both hemispheres, arterial and central venous pressure and heart rate. The EEG was evaluated continuously, using a computer (power spectra). After catheterization of the superior sagittal sinus, cerebral arteriovenous differences of glucose, lactate, O2 and CO2 were calculated. 6 animals were treated surgically when showing elevated intracranial pressure ICP and markedly altered EEG. In 3 animals, the right hemisphere was decompressed by extensive resection of bone and dura. In 3 further animals, the softened brain tissue of the cold lesion was resected and the skull defect closed. 6 untreated animals were used in controls. A decompression by skull hemiresection for ablation of the injured cortex abolished the high intracranial pressure, but only the latter method seemed to prevent further damage. This could be demonstrated by the EEG registration, and by the normalization of arteriovenous metabolite differences. Only animals treated with edema resection had a normal arousal reaction and survived the trauma. The results indicate, that only an ablation of the local injury will prevent further damage to the brain. After decompressive trepanation alone, the progression of tissue edema is not interrupted. As can be seen from the literature, the poor results obtained even from extensive decompressive operations in traumatic brain edema, indicate that the further development of edema is independent of the intracranial pressure, whereas the favorable results of resection of lobar contusions show an interruption of the spread of dysbolism.
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PMID:Comparison of the effects of surgical decompression and resection of local edema in the therapy of experimental brain trauma. Investigation of ICP, EEG and cerebral metabolism in cats. 47 64

The effects of sepsis on intracellular Na+ concentration ([Na+]i) and glucose metabolism were examined in rat red blood cells (RBCs) by using 23Na- and 2H-nuclear magnetic resonance (NMR) spectroscopy. Sepsis was induced in 15 halothane-anesthetized female Sprague-Dawley rats by using the cecal ligation and perforation technique; 14 control rats underwent cecal manipulation without ligation. The animals were fasted for 36 h, but allowed free access to water. At 36 h postsurgery, RBCs were examined by 23Na-NMR by using dysprosium tripolyphosphate as a chemical shift reagent. Human RBCs from 17 critically ill nonseptic patients and from 7 patients who were diagnosed as septic were also examined for [Na+]i. Five rat RBC specimens had [Na+]i determined by both 23Na-NMR and inductively coupled plasma-atomic emission spectroscopy (ICP-AES). For glucose metabolism studies, RBCs from septic and control rats were suspended in modified Krebs-Henseleit buffer containing [6,6-2H2]glucose and examined by 2H-NMR. No significant differences in [Na+]i or glucose utilization were found in RBCs from control or septic rats. There were no differences in [Na+]i in the two groups of patients. The [Na+]i determined by NMR spectroscopy agreed closely with measurements using ICP-AES and establish that 100% of the [Na+]i of the RBC is visible by NMR. Glucose measurements determined by 2H-NMR correlated closely (correlation coefficient = 0.93) with enzymatic analysis. These studies showed no evidence that sepsis disturbed RBC membrane function or metabolism.
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PMID:Sepsis does not alter red blood cell glucose metabolism or Na+ concentration: a 2H-, 23Na-NMR study. 230 34

Twelve dogs were anesthetized and instrumental for determination of CVP, arterial pressure, intracranial pressure, left atrial pressure, and frontal cerebral cortical blood flow (CCBF) by the thermal method. A catheter was introduced into the venous return of the cerebral confluence to allow determination of cerebral A-V oxygen saturation differences. The animals were placed on cardiac bypass using a circuit from the right atrium to the pulmonary artery and a second circuit from the left ventricular apex to the left femoral artery. A heat exchanger was used to maintain a constant blood temperature of 37 C in the output of the left side bypass circuit. All animals were heparinized during bypass. Ventricular fibrillation was induced after completion of the bypass surgery. Two dogs served as controls. Pre-arrest determinations of hemoglobin, glucose, CCBF, and cerebral A-V oxygen differences were taken. Full circulatory arrest was carried out for 20 minutes by shutting off the cardiac bypass. Resuscitation was achieved by resumption of bypass perfusion. Acid-base balance was corrected quickly, and pre-arrest perfusion pressure was achieved and maintained for 90 minutes. All pressure parameters were monitored continuously. All pre-arrest determinations were repeated at 20, 40, 60, and 90 minutes post resuscitation. Five dogs were treated with 6 microgram/kg flunarizine administered IV drip over 10 minutes immediately post reperfusion. Five dogs were not treated post arrest. Treated animals had a prompt return of CCBF rates equal to or greater than pre-arrest flow, which persisted throughout the period of post-arrest observation. Untreated animals had markedly reduced CCBF and increased resistance. CCBF uniformly proceeded to near zero flow by 90 minutes. The ICP was not significantly altered by treatment.
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PMID:Effect of flunarizine on canine cerebral cortical blood flow and vascular resistance post cardiac arrest. 706 84

The aim of this investigation was to assess the use of cerebral extracellular glucose as a parameter for microdialytic monitoring in neurosurgical critical care patients. Samples were collected from four patients with severe head injury and one with subarachnoid haemorrhage for periods of 4.5-67 h. Glucose and lactate were analysed in the dialysates. The ratios of glucose to lactate were calculated to partially allow for changes in microdialytic conditions over time. On-line pH was measured for up to 3 days in three patients. In experiments with spontaneous hypertensive rats we found that extracellular glucose became unmeasurable in the ischemic zone after middle cerebral artery occlusion. Similarly, in 3 patients glucose became undetectable for several hours, and glucose/lactate tended to decrease during measurement. This was accompanied by high ICP in one patient, and by a hypoxic episode in another. In the two other patients glucose/lactate ratios showed a rising trend. Findings indicate that glucose, and the glucose/lactate ratio show some correlations with clinical course and are promising parameters for cerebral monitoring and therapeutic decision making.
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PMID:Experimental and clinical monitoring of glucose by microdialysis. 765 89

We will report on our preliminary findings using microdialysis to monitor three patients in intensive care with either severe head injury (SHI) or severe subarachnoid hemorrhage (SAH) for up to 72 hours. In addition, basal levels in uninjured brain were assessed during an extra-intracranial bypass operation. Samples were collected hourly or half-hourly (flow rate 2 microliters/min, perfusion medium 0.9% saline). Parameters measured were the antioxidants ascorbic acid, uric acid, glutathione and cysteine. In 2 patients, the pH of the dialysate (pHD) was also measured on-line with a specially constructed flow-through meter, and glucose and lactate levels were assessed in the dialysate. In patient 1 (SHI), there was practically no cerebral perfusion pressure because of high ICP; cysteine and lactate levels were very high and glucose not measurable. In patient 2 (SAH) a hypoxic episode was accompanied by increased uric acid and decreased glucose. In patient 3 (SHI), the pHD reflected normalisation of blood gases after hyperventilation. Results indicate that parameters are in the range known from experimental studies, and can be correlated with clinical situations. The pHD as valuable indicator of metabolic changes is also feasible bedside.
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PMID:Neurochemical monitoring and on-line pH measurements using brain microdialysis in patients in intensive care. 797 24

In order to optimize therapy for the injured brain it is desirable to continuously monitor substrate delivery in the critically ill patient. Interruption of substrate delivery is a major factor of the great vulnerability to ischemic damage, which affects a majority of patients after severe head injury, stroke or subarachnoid hemorrhage. An approach to protecting the brain during ischemia is to increase the delivery of oxygen via residual blood flow through ischemic tissue. Hypothermia is also an important means of protecting brain cells from the deleterious effects of ischemia, after severe head injury, because it reduces metabolic demands. In this study we continuously measured brain oxygen, brain CO2, brain pH and brain temperature, as well as hourly brain glucose and lactate. A multiparameter sensor was inserted into brain tissue, via a three lumen bolt, along with a ventriculostomy catheter and a microdialysis probe in 60 severely head injured patients. Brain oxygen delivery was increased by stepwise increase of inspired oxygen (FiO2) from 30% to 60% to 100% over a period of 6 h, in order to test the effect of enhanced oxygen tension, on tissue oxygen. In most patients brain oxygen was initially low, and progressively increased, over the monitoring period, to a steady state level, around 30-40 mmHg. In those who died or remained vegetative, brain oxygen fell to anerobic levels. Episodes of increased ICP (n = 25), hypotension (n = 15), and respiratory difficulties (n = 9) caused an immediate increase in brain CO2. Multiple logistic regression analysis showed brain oxygen to be the strongest predictor for outcome in these patients. By increasing FiO2, an increase in oxygen delivery of more than 100%, and a simultaneous decline in lactate production was seen (p < 0.01). Brain temperature was closely related to rectal temperature, brain oxygen, and cerebral blood flow. Patients who were spontaneously hypothermic had a poor outcome (p < 0.01). A fuller understanding of dynamic factors affecting brain metabolism and substrate delivery may be obtained with extended neuromonitoring.
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PMID:Extended neuromonitoring: new therapeutic opportunities? 958 32

Intracranial pressure depends on cerebral tissue volume, cerebrospinal fluid volume (CSFV) and cerebral blood volume (CBV). Physiologically, their sum is constant (Monro-Kelly equation) and ICP remains stable. When the blood brain barrier (BBB) is intact, the volume of cerebral tissue depends on the osmotic pressure gradient. When it is injured, water movements across the BBB depend on the hydrostatic pressure gradient. CBV depends essentially on cerebral blood flow (CBF), which is strongly regulated by cerebral vascular resistances. In experimental studies, a decrease in oncotic pressure does not increase cerebral oedema and intracranial hypertension (ICHT). On the other hand, plasma hypoosmolarity increases cerebral water content and therefore ICP, if the BBB is intact. If it is injured, neither hypoosmolarity nor hypooncotic pressure modify cerebral oedema. Therefore, all hypotonic solutes may aggravate cerebral oedema and are contra-indicated in case of ICHT. On the other hand, hypooncotic solutes do not modify ICP. The osmotic therapy is one of the most important therapeutic tools for acute ICHT. Mannitol remains the treatment of choice. It acts very quickly. An i.v. perfusion of 0.25 g.kg-1 is administered over 20 minutes when ICP increases. Hypertonic saline solutes act in the same way, however they are not more efficient than mannitol. CO2 is the strongest modulating factor of CBF. Hypocapnia, by inducing cerebral vasoconstriction, decreases CBF and CBV. Hyperventilation is an efficient and rapid means for decreasing ICP. However, it cannot be used systematically without an adapted monitoring, as hypocapnia may aggravate cerebral ischaemia. Hyperthermia is an aggravating factor for ICHT, whereas moderate hypothermia seems to be beneficial both for ICP and cerebral metabolism. Hyperglycaemia has no direct effect on cerebral volume, but it may aggravate ICHT by inducing cerebral lactic acidosis and cytotoxic oedemia. Therefore, infusion of glucose solutes is contra-indicated in the first 24 hours following head trauma and blood glucose concentration must be closely monitored and controlled during ICHT episodes.
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PMID:[The internal environment and intracranial hypertension]. 975 May 95

To investigate the more effective route of oral administration of glycerol to decrease the raised ICP, two different routes were employed in the clinical practice. The one was through a Naso-Gastric tube, and the other was through an Entero-Duodenal tube. Pharmacokinetics of glycerol in relation to the decrease of ICP, and the changes of other parameters which could influence the serum osmotic pressure were sequentially monitored for initial 30 minutes. In the group of Entero-Duodenal route, the time to reach to the maximum glycerol concentration (Tmax) was faster, the maximum concentration of glycerol (Cmas) was higher, and ICP reduction rate was greater than these in the group of Naso-Gastric route. Other parameters (Na, K, BUN and Glucose) showed no significant difference between the two routes. It can be concluded that the Entero-Duodenal administration of glycerol is the more effective route to decrease the raised ICP, when it is administered orally.
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PMID:Pharmacokinetics of serum glycerol and changes of ICP: comparison of gastric and duodenal administration. 977 36

This study was carried out to elucidate the pathophysiologic mechanism of cerebral hyperemia observed during the early phase of bacterial meningitis. We tested the hypothesis that microbial invasion through the blood-brain barrier is responsible for cerebral vasodilation and hyperemia in meningitis. Escherichia coli was given either intravenously (i.v.) or intracisternally (i.c.) to closely mimic the primary or secondary bacterial invasion occurring in meningitis and newborn piglets were grouped according to their invasion results (+ or -); 12 in the i.v. (+) group, 14 in the i.v. (-) group, 13 in the i.c. (+) group, 15 in the i.c. (-) group. The results were compared with eight animals in the control group. Near infrared spectroscopy (NIRS) was employed to monitor changes in total hemoglobin (HbT), oxygenated hemoglobin (HbO), deoxygenated hemoglobin (Hb), deduced hemoglobin (HbD), and oxidized cytochrome aa3 (Cyt aa3). HbT, as an index of cerebral blood volume, increased progressively in both i.v. (+) and i.v. (-) groups and became significantly different from control and baseline values at 2 h. Hb significantly increased only in i.v. (+) group. HbD, as an index of cerebral blood flow, decreased significantly in i.v. (+), i.v.(-) and i.c. (-) groups and this change was mitigated in i.c. (+) group, HbO was reduced in i.c. (-) group and this decrease was attenuated in i.c. (+) group. Increased Cyt aa3 was observed in all experimental groups after bacterial inoculation. Changes in ICP, blood pressure, cerebral perfusion pressure, blood or CSF glucose or lactate, CSF TNF-alpha level, or CSF leukocytes number were not associated with changes in NIRS findings. These findings suggest that primary or secondary bacterial invasion across the blood-brain barrier is primarily responsible for cerebral vasodilation and hyperemia observed during the early phase of bacterial meningitis.
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PMID:Effects of microbial invasion on cerebral hemodynamics and oxygenation monitored by near infrared spectroscopy in experimental Escherichia coli meningitis in the newborn piglet. 1040 12

In the management of severe pediatric brain injury, attention has previously been paid to brain edema, ICP elevation and low cerebral perfusion pressure (CPP). However, in the acute stage within 3-6 hours after trauma, brain hypoxia and hyperglycemia associated with diffuse brain injury are often observed. We have pointed out brain thermo-pooling (elevation of brain tissue temperature) and brain hypoxia caused by defective release of oxygen from hemoglobin (due to decrease in red blood cell enzyme (DPG)) as a new mechanism of brain injury. To treat these pathologic changes, we have developed a brain hypothermia treatment, the major purpose of which is to prevent brain hypoxia, brain thermo-pooling, neurohormonal changes causing cytokine encephalopathy, and a selective, radical-mediated damage of the dopamine A10 nervous system. The brain tissue temperature is initially adjusted to 35 degrees C with adequate cerebral oxygenation, followed by brain hypothermia at 34 degrees C for 1 weeks to prevent brain hypoxia, free radical reactions, brain edema and ICP elevation. What is most difficult in the pediatric brain hypothermia treatment is to maintain metabolic balance in the injured brain tissue and pulmonary infections associated with an immune crisis. When a rapid elevation of serum glucose is noted it is critical to lower the value because glucose quickly penetrates the blood-brain barrier and increases pyruvate and lactate by inhibiting the TCA cycle metabolism. Thus, hyperglycemia during brain hypothermia treatment is one of the major target of management. Another problem is immune crisis associated with secondary pulmonary infections. To prevent them, early enteral nutrition and replacement of L-arginine were most useful, as well as preconditioning for rewarming as follows: serum albumin > 3.0 g/dl; lymphocyte > 1500/mm3; T-H (CD4) lymphocytes > 55%; serum glucose, 120-140 mg/dl; vitamin A > 50 mg/dl; Hb > 12 g/dl and 2,3 DPG, 10-15 mumol/gHb; O2 ER, 23-25% and AT-III, > 100%. The clinical benefit of this therapy is still controversial.
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PMID:[Brain hypothermia treatment for the management of severe pediatric brain injury]. 1072 86


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