Cerebrospinal fluid lactate and lactate/pyruvate ratios in hydrocephalus

1976 ◽  
Vol 44 (3) ◽  
pp. 337-341 ◽  
Author(s):  
James E. Raisis ◽  
Glenn W. Kindt ◽  
John E. McGillicuddy ◽  
Carole A. Miller
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Perfusion ◽  
Inverse Relationship ◽  
Redox State ◽  
Anaerobic Metabolism ◽  
Perfusion Pressure ◽  
Cerebral Metabolism ◽  
Content Type ◽  
Lactate And Pyruvate ◽  
Fine Print

✓ Cerebral metabolism in 21 hydrocephalic patients was studied. Preoperative and postoperative specimens of cerebrospinal fluid (CSF) were obtained and the cerebral perfusion pressure (CPP) was calculated in each instance. The specimens of CSF were analyzed for lactate and pyruvate and the lactate/pyruvate (L/P) ratio was calculated for each sample. The L/P ratio, which reflects the redox state of the cell, was used to determine the extent of anaerobic metabolism. An inverse relationship was noted between CPP and lactate as well as the L/P ratio. In general, the level of anaerobic metabolism was decreased after insertion of a shunt.

The effect of cold-induced brain edema on cerebrospinal fluid formation rate

1980 ◽  
Vol 53 (5) ◽  
pp. 652-655 ◽  
Author(s):  
K. Gwan Go ◽  
Gerald M. Hochwald ◽  
Lenie Koster-Otte ◽  
Annie K. van Zanten ◽  
Mysore Gandhi
Keyword(s):  
Cerebrospinal Fluid ◽  
Brain Edema ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Formation Rate ◽  
Content Type ◽  
Ventriculocisternal Perfusion ◽  
Fluid Formation ◽  
Csf Formation Rate ◽  
Fine Print

✓ The net contribution of vasogenic brain edema to cerebrospinal fluid (CSF) formation was studied by ventriculocisternal perfusion. Individual cats were perfused both before and 2 ½ hours after a severe cold-induced injury to the cerebral cortex, and the results were compared. Although the edema had occupied the larger part of the hemispheric white matter and bordered the lateral ventricle, a decrease rather than an increase in CSF formation rate was observed. This decrease was related to a decrease in the cerebral perfusion pressure by a regression equation that was not affected by the cold injury.

Cerebral perfusion pressure: management protocol and clinical results

1995 ◽  
Vol 83 (6) ◽  
pp. 949-962 ◽  
Author(s):  
Michael J. Rosner ◽  
Sheila D. Rosner ◽  
Alice H. Johnson
Keyword(s):  
Cerebrospinal Fluid ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cerebrospinal Fluid Drainage ◽  
Content Type ◽  
Vasopressor Support ◽  
Management Techniques ◽  
Gcs Score ◽  
Fine Print

✓ 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 vegetative 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 χ2, p < 0.001). Better management could have improved outcome in as many as 35% to 50% of the deaths.

Intracranial hypertension and cerebral perfusion pressure: influence on neurological deterioration and outcome in severe head injury

2000 ◽  
Vol 92 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Niels Juul ◽  
Gabrielle F. Morris ◽  
Sharon B. Marshall ◽  
_ _ ◽  
Lawrence F. Marshall
Keyword(s):  
Head Injury ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Severe Head Injury ◽  
Perfusion Pressure ◽  
Neurological Deterioration ◽  
Double Blind ◽  
Content Type ◽  
Fine Print

Object. Recently, a renewed emphasis has been placed on managing severe head injury by elevating cerebral perfusion pressure (CPP), which is defined as the mean arterial pressure minus the intracranial pressure (ICP). Some authors have suggested that CPP is more important in influencing outcome than is intracranial hypertension, a hypothesis that this study was designed to investigate.Methods. The authors examined the relative contribution of these two parameters to outcome in a series of 427 patients prospectively studied in an international, multicenter, randomized, double-blind trial of the N-methyl-d-aspartate antagonist Selfotel. Mortality rates rose from 9.6% in 292 patients who had no clinically defined episodes of neurological deterioration to 56.4% in 117 patients who suffered one or more of these episodes; 18 patients were lost to follow up. Correspondingly, favorable outcome, defined as good or moderate on the Glasgow Outcome Scale at 6 months, fell from 67.8% in patients without neurological deterioration to 29.1% in those with neurological deterioration. In patients who had clinical evidence of neurological deterioration, the relative influence of ICP and CPP on outcome was assessed. The most powerful predictor of neurological worsening was the presence of intracranial hypertension (ICP ≥ 20 mm Hg) either initially or during neurological deterioration. There was no correlation with the CPP as long as the CPP was greater than 60 mm Hg.Conclusions. Treatment protocols for the management of severe head injury should emphasize the immediate reduction of raised ICP to less than 20 mm Hg if possible. A CPP greater than 60 mm Hg appears to have little influence on the outcome of patients with severe head injury.

Pulmonary function and radiographic abnormalities related to neurological outcome after aneurysmal subarachnoid hemorrhage

1998 ◽  
Vol 88 (1) ◽  
pp. 28-37 ◽  
Author(s):  
Andreas Gruber ◽  
Andrea Reinprecht ◽  
Harald Görzer ◽  
Peter Fridrich ◽  
Thomas Czech ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Lung Injury ◽  
Pulmonary Function ◽  
Neurological Outcome ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Aneurysmal Subarachnoid Hemorrhage ◽  
Medical Complications ◽  
Content Type ◽  
Fine Print

Object. This observational study is based on a consecutive series of 207 patients with aneurysmal subarachnoid hemorrhage who were treated within 7 days of their most recent bleed. The purpose of the study was to evaluate the effect of respiratory failure on neurological outcome. Methods. Pulmonary function was assessed by determination of parameters describing pulmonary oxygen transport and exchange, by using composite scores for quantification of lung injury (lung injury score [LIS]) and mechanical ventilator settings (PIF score). Pulmonary function was related to the Hunt and Hess (H & H) grade assigned to the patient at hospital admission (p < 0.001). The pattern and time course of lung injury differed significantly between patients with H & H Grade I or II, Grade III, and Grade IV or V. Hunt and Hess grade, Fisher computerized tomography grade, intracranial pressure, cerebral perfusion pressure, LIS, ratio of PaO2 to the fraction of inspired oxygen (FiO2), and the ratio of the alveolar-minus-arterial oxygen tension difference (AaDO2) to FiO2 were related to neurological outcome (p < 0.001). The LIS on the day of maximum lung injury remained an independent predictor of outcome (p = 0.01) in a stepwise logistic regression analysis. The probability of poor neurological outcome significantly increased with both decreasing cerebral perfusion pressure and increasing severity of lung injury. Conclusions. The overall mortality rate was 22.2% (46 of 207 patients). Subarachnoid hemorrhage and its neurological sequelae accounted for the principal mortality in this series. Medical (nonneurological and nontreatment-related) complications accounted for 37% of all deaths. Systemic inflammatory response syndrome with associated multiple organ dysfunction syndrome was the leading cause of death from medical complications. The authors conclude that respiratory failure is related to neurological outcome, although it is not commonly the primary cause of death from medical complications.

Hyperacute measurement of intracranial pressure, cerebral perfusion pressure, jugular venous oxygen saturation, and laser Doppler flowmetry, before and during removal of traumatic acute subdural hematoma

2001 ◽  
Vol 95 (4) ◽  
pp. 569-572 ◽  
Author(s):  
Bon H. Verweij ◽  
J. Paul Muizelaar ◽  
Federico C. Vinas
Keyword(s):  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Laser Doppler ◽  
Bone Flap ◽  
Acute Subdural Hematoma ◽  
Laser Doppler Flow ◽  
Content Type ◽  
Venous Oxygen Saturation ◽  
Fine Print

Object. The poor prognosis for traumatic acute subdural hematoma (ASDH) might be due to underlying primary brain damage, ischemia, or both. Ischemia in ASDH is likely caused by increased intracranial pressure (ICP) leading to decreased cerebral perfusion pressure (CPP), but the degree to which these phenomena occur is unknown. The authors report data obtained before and during removal of ASDH in five cases. Methods. Five patients who underwent emergency evacuation of ASDH were monitored. In all patients, without delaying treatment, a separate surgical team (including the senior author) placed an ICP monitor and a jugular bulb catheter, and in two patients a laser Doppler probe was placed. The ICP prior to removing the bone flap in the five patients was 85, 85, 50, 59, and greater than 40 mm Hg, resulting in CPPs of 25, 3, 25, 56, and less than 50 mm Hg, respectively. Removing the bone flap as well as opening the dura and removing the blood clot produced a significant decrease in ICP and an increase in CPP. Jugular venous oxygen saturation (SjvO2) increased in four patients and decreased in the other during removal of the hematoma. Laser Doppler flow also increased, to 217% and 211% compared with preevacuation flow. Conclusions. Intracranial pressure is higher than previously suspected and CPP is very low in patients with ASDH. Removal of the bone flap yielded a significant reduction in ICP, which was further decreased by opening the dura and evacuating the hematoma. The SjvO2 as well as laser Doppler flow increased in all patients but one immediately after removal of the hematoma.

Adverse effects of pentobarbital on cerebral venous oxygenation of comatose patients with acute traumatic brain swelling: relationship to outcome

1996 ◽  
Vol 85 (5) ◽  
pp. 758-761 ◽  
Author(s):  
Julio Cruz
Keyword(s):  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Brain Swelling ◽  
Hemoglobin Content ◽  
Oxyhemoglobin Saturation ◽  
Content Type ◽  
Total Hemoglobin ◽  
Scale Scores ◽  
Before And After ◽  
Fine Print

✓ Global cerebrovenous oxygenation was evaluated before and after intravenous administration of pentobarbital sodium for the management of refractory intracranial hypertension in 151 comatose patients who had acute traumatic brain swelling. Two groups of patients were identified: a group in which the jugular oxyhemoglobin saturation (SjO2) remained at or above 45% after pentobarbital bolus, and a group in which the SjO2 dropped below 45%. The two groups were matched by predominant findings on computerized tomography scans of the head, as well as age, postresuscitation Glasgow Coma Scale scores, levels of total hemoglobin content, SjO2, intracranial pressure (ICP), and cerebral perfusion pressure (CPP) prior to pentobarbital bolus. Outcomes were significantly worse (p < 0.0001) in patients who developed decreases in SjO2 to levels below 45% than in those whose SjO2 remained at or above 45%, despite the fact that there were no significant differences between the two groups with regard to ICP and CPP after an intravenous bolus of pentobarbital.

Experimental cerebral oligemia and ischemia produced by intracranial hypertension

1975 ◽  
Vol 43 (3) ◽  
pp. 308-317 ◽  
Author(s):  
Lawrence F. Marshall ◽  
Felix Durity ◽  
Robert Lounsbury ◽  
David I. Graham ◽  
Frank Welsh ◽  
...  
Keyword(s):  
Blood Flow ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Neurological Function ◽  
Content Type ◽  
No Reflow ◽  
No Reflow Phenomenon ◽  
Complete Cerebral Ischemia ◽  
Fine Print

✓ Cerebral blood flow, electrical activity, and neurological function were studied in rabbits subjected to either 15 minutes of oligemia (20 torr cerebral perfusion pressure) or complete cerebral ischemia produced by cisterna magna infusion. During oligemia, flow was reduced from 68.4 ± 4.2 ml/100 gm/min to 26.3 ± 4.4 (p < .01), and during ischemia animals had no proven flow. By 5 minutes after oligemia or ischemia significant symmetrical hyperemia occurred and there was no evidence of the no-reflow phenomenon. The electroencephalogram became isoelectric significantly later and returned significantly sooner in oligemia than in ischemia. Oligemic animals had earlier and better return of neurological function than their ischemic counterparts, although postinsult hypocapnia improved functional recovery in both groups. These experiments do not support the concept that oligemia is a more severe insult than complete ischemia. In intracranial hypertension produced by this model, the no-reflow phenomenon does not occur.

Responses to experimental subarachnoid hemorrhage in the spontaneously breathing primate

1980 ◽  
Vol 52 (3) ◽  
pp. 302-308 ◽  
Author(s):  
Charles Rothberg ◽  
Bryce Weir ◽  
Thomas Overton ◽  
Michael Grace
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Respiratory Pattern ◽  
Content Type ◽  
Cynomolgus Monkeys ◽  
Experimental Subarachnoid Hemorrhage ◽  
Subarachnoid Blood ◽  
Spontaneously Breathing ◽  
Fine Print

✓ The pathophysiological responses to experimental subarachnoid hemorrhage (SAH) were investigated in 20 spontaneously breathing cynomolgus monkeys. Four different volumes of fresh autogenous blood were used: 1.0, 1.33, 1.67, and 2.0 cc/kg. Five other animals had injection of 1.67 cc/kg of mock cerebrospinal fluid. Cerebral blood flow (CBF) was measured using the xenon-133 clearance technique. Respiratory rate and tidal volume were monitored by way of a Vertek pneumotach. The reduction of CBF after the SAH became more pronounced with increasing volumes of subarachnoid blood. The CBF remained reduced despite a return to normal of the cerebral perfusion pressure. Increasing SAH volumes were associated with greater abnormalities in the respiratory pattern, consisting of apnea and hyperventilation. These larger volumes were also associated with hypoxemia. Morbidity and mortality increased with increasing volumes of SAH, and are believed to be the result of a combination of decreased CBF, respiratory center disturbances, and pulmonary diffusion defects.

Increase in cerebral perfusion pressure by arterial hypertension in brain swelling

1975 ◽  
Vol 42 (3) ◽  
pp. 282-289 ◽  
Author(s):  
Frank Matakas ◽  
Rainer v. Waechter ◽  
Reent Knüpling ◽  
Samuel J. Potolicchio
Keyword(s):  
Vessel Wall ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Parietal Lobe ◽  
Systemic Arterial Pressure ◽  
Brain Swelling ◽  
Content Type ◽  
The Difference ◽  
The Relationship ◽  
Fine Print

✓ Brain swelling was produced in monkeys and cats by the inflation of an epidural balloon against the parietal lobe. Resulting changes in intracranial pressure (ICP) were correlated to variation in systemic arterial pressure (SAP). Intracranial perfusion pressure (ICPP) defined as the difference between SAP and ICP, was found to vary with the degree of arterial hyper- and hypotension. The relationship between SAP and ICP can be explained by an existing equilibrium between extramural pressure and vessel wall circumferential tension. A positive perfusion pressure can exist in brain swelling as long as vessel wall tension is preserved and the degree of expanding brain tissue volume is held below certain limits.

Effect of reduced cerebral perfusion pressure on cerebral blood flow following inhibition of nitric oxide synthesis

1998 ◽  
Vol 89 (3) ◽  
pp. 448-453 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Nitric Oxide Synthesis ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. The authors tested the hypothesis in a porcine model that inhibition of nitric oxide synthesis during reduced cerebral perfusion pressure (CPP) affected the relative cerebral blood flow (CBF) and the cerebrovascular resistance. Methods. The CPP was reduced by inducing high cerebrospinal fluid pressure and hemorrhagic hypotension. With continuous blood and intracranial pressure monitoring, relative CPP was estimated using the laser Doppler flowmetry technique in nine pigs that received 40 mg/kg nitro-l-arginine methyl ester (l-NAME) and in nine control animals. The l-NAME caused a decrease in relative CBF (p < 0.01) and increases in cerebrovascular resistance (p < 0.01), blood pressure (p < 0.05), and CPP (p < 0.001). During high intracranial pressure there were no significant differences between the treated animals and the controls. After hemorrhage, there was no significant difference between the groups initially, but 30 minutes later the cerebrovascular resistance was decreased in the control group and increased in the l-NAME group relative to baseline (p < 0.05). Combined hemorrhage and high intracranial pressure increased the difference between the two groups with regard to cerebrovascular resistance (p < 0.05). Conclusions. These results suggest that nitric oxide synthesis inhibition affects the autoregulatory response of the cerebral circulation after cardiovascular compensation has taken place. Nitric oxide synthesis inhibition enhanced the undesirable effects of high intracranial pressure during hypovolemia.

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