UMLS:C0268318 - FACTA Search

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The authors present the policy they have worked out for hydrocephalus patients with special reference to the pressure measurement and test methods and to rCBF, SPECT and transcranial Doppler sonography (TDC) studies. For diagnosis, the protocol proposed by Gjerris and Borgesen was followed in 75 cases: besides other methods (CT, radionuclide cisternography, MRI) the intracranial pressure waves routinely recorded and analyzed by means of ventricular catheters for 24 h. The patients were roughly divided into groups in terms of diagnosis, baseline pressure, compliance, results of infusion tests and of surgery. In 13 patients the investigations were supplemented by rCBF SPECT and in 42 patients by TCD studies before and after CSF shunting or withdrawal to analyze the acute effects on cerebral circulation. Clinical follow-up shows that need for shunting was indicated fairly well by the common results of baseline ICP, compliance and infusion loading. The rCBF SPECT studies revealed a significant increase of the cerebral perfusion at the basal ganglia after shunting while, on the basis of CBF velocity changes three types of vasoregulatory response could be defined with TCD. In our hands, monitoring of the pressure and craniospinal capacity has proved to be a valuable aid in decisions on surgery; however, for a more precise (and beneficial) appreciation of whether surgery is indicated the vasoregulatory responses should also be taken into account in future.
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PMID:Our policy in diagnosis and treatment of hydrocephalus. 775 7

Monitoring of ICP from the subarachnoid, intraparenchymal, or ventricular spaces can be accomplished easily and reliably. The risks and benefits of each approach should be considered when choosing the monitoring technique. The goal of ICP management is to prevent herniation and to optimize cerebral perfusion. Even transient episodes of post-traumatic cerebral ischemia due to inadequate CPP can quickly nullify all resuscitative efforts. The provision of sufficient CBF is complicated by the varying degree of disruption of pressure autoregulation commonly resulting from head trauma. Post-injury, there is a need to provide a CPP which is elevated to some extent with respect to that sufficient in uninjured brains. This generally requires a CPP of at least 70 mm Hg, which must be accomplished by maintaining an adequate MAP while controlling ICH. Although ICH can generally be controlled using methods commonly employed, the majority of these techniques have potential complications. Additionally, there is increasing evidence that significant variation exists in the pathologic processes driving ICH in individual patients. Therefore, goals such as the desired CPP and conditions such as the relative contribution of edema, cerebral hypervolemia, and ischemia to ICH should optimally be considered in a patient-specific fashion and allow a targeted approach to therapy.
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PMID:Intracranial pressure. Monitoring and management. 782 72

It is has been demonstrated that clinical outcome following head injury is correlated with the reactivity of the cerebrovasculature to carbon dioxide changes. Since CBF measurements are difficult to perform in these patients, a new technique is proposed utilizing the ICP response to capnic stimuli. In 40 head injured patients, the responses of ICP, pressure volume index (PVI) and middle cerebral artery velocities to hypocapnia and to hypercapnia were determined. Hypocapnia reduced ICP and MCA velocity while hypercapnia was followed by ICP and MCA velocity increases. Both changes were in the same magnitude supporting the concept the global ICP response reflects vascular reactivity. The fact that the velocity response to hypocapnia in lesioned hemispheres was less compared to the ICP response indicates the loss of ability to dilate in injured vessels and is consistent with earlier findings relating reduced reactivity to poor outcome.
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PMID:Measurement of vascular reactivity in head injured patients. 790 77

The possibility of measuring cerebral blood flow by mobile bedside units with the intravenous 133-Xenon technique increased the interest to monitor haemodynamic changes after head injury and subarachnoid haemorrhage in intensive care. Time course of resting CBF after trauma is variable (reduced CBF, hyperemia) and there is no strong correlation to clinical outcome. Additional studies of CBF/CO2 reactivity show normal and impaired CO2 response in the acute stage after trauma (day 1-8). A permanently impaired CO2 reactivity correlates with severe brain damage and bad outcome (GOS 1,2). A normal or improving CO2 reactivity indicates a favourable outcome (GOS 3-5). There was no significant correlation between CBF and ICP, nor between CBF and CPP. A CPP of more than 70 mmHg did not guarantee a sufficient CBF in every case indicating the variability of the limits of autoregulation. As therapeutic hyperventilation may lead to ischemia, mannitol was preferred to reduce ICP and increased low CBF to normal values. This fact should be considered in the treatment of patients with low CBF and normal CO2 reactivity. Delayed ischemic neurological deficits ("vasospasm") are well-known as significant complications of the clinical course following SAH. Immediately postoperatively performed CBF measurements enable to detect ischemia and allow to start early antiischemic therapy. During "vasospasm" CBF showed a better correlation to the neurological status than blood flow velocity in the basal arteries measured by transcranial doppler sonography. Furthermore hyperemia after SAH could only be verified by CBF measurements.
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PMID:Xenon 133--CBF measurements in severe head injury and subarachnoid haemorrhage. 790 78

The effects of acidosis on ischemic brain damage are unclear and probably diverse. To establish an in vivo model of acidosis, the authors assess changes in extracellular brain pH (pHe), CBF and ICP induced by hypercarbic ventilation, and discuss the reliability and short comings of this experimental model. Acidosis was induced by increasing the inspired CO2 concentration in mechanically ventilated rats. pHe was measured with a pH-sensitive electrode implanted into the cortical mantle. The rats were divided into five groups according to the CO2 concentrations inspired: G-1, 0% control; G-2, -5-% CO2; G-3, -10-% CO2; G-4, -20-% CO2; G-5, -25-% CO2. Cortical blood flow was measured using a laser Doppler flowmeter, and ICP was also determined in each of the experimental groups. pHe decreased rapidly after the CO2 supply was turned on and remained almost constant at fixed concentrations of inspired CO2. pHe values diminished as the concentration of inspired CO2 decreased, as follows: G-2, -0.10 +/- 0.03; G-3, -0.31 +/- 0.08; G-4, -0.49 +/- 0.09; G-5, -0.64 +/- 0.10. The changes in pHe almost perfectly paralleled the changes in blood pH. The percentage increase in CBF was more than 200% in the G-2 groups and minimal increases in CBF, probably due to changes in blood pressure, were observed in from G-2 to G-5. Changes in CBF paralleled changes in systemic blood pressure, especially after the CO2 supply was turned off. ICP also rose after increasing the CO2 supply, and the pattern of changes was similar to that of CBF.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Changes in cerebral extracellular pH, cerebral blood flow and intracranial pressure induced by hypercarbic ventilation--assessment as a potential in vivo model of cerebral acidosis]. 794 19

Focal contusions following head injury may be associated with focal or diffuse cerebral edema. Early global hyperemia and perifocal hyperemia may play a role in cerebral edema, although causal relationships have yet to be clearly been defined. We studied 27 patients with head injury (admission GCS 3-12) resulting in focal contusions (without evidence of subarachnoid, intraventricular or intraparenchymal hemorrhage by CT). Patients were studied with ICP monitors, head CTs, and intravenous 133Xenon regional cerebral perfusion studies serially over several days post injury. Low cortical blood flow and a low mean CBF15 flow were evident on the day of the injury. Additionally, F1 analysis indicated significantly (p < 0.05) greater cortical blood flow in the surrounding brain (mean 60 cc/100 g/min) compared to the contusion area (mean 43 cc/100 g/min) on the day of trauma. Mean regional CBF remained below normal in the contused areas (CBF15 < 35 cc/100 g/min), however the cortical flow increased in the first few days post-injury (peak F1 = 95 cc/100 g/min on day 3) then decreased to sub-normal levels. The mean CBF in the surrounding brain was low on the day of injury (CBF15 = 29 cc/100 g/min), although higher than the contused area, and increased to a peak of 45 cc/1009/min on day 3 posttrauma. Cortical flow in the surrounding brain, however, exhibited a different trend. The mean F1 was low on the day of trauma and significantly higher one day after trauma (mean 105 cc/100 g/min). Only 15 of the 27 patients with focal contusions had evidence of cerebral edema. Eleven of these exhibited focal edema and 4 exhibited diffuse edema. Focal edema developed over the first few days posttrauma as seen in followup CT, whereas patients with diffuse edema exhibited edema on the admission CT. Initial oligemia in the contused areas was associated with a subsequent hyperemic rim about the contusion. Focal hyperemia was associated with focal edema in 41% of the patients, whereas diffuse edema appeared to be independent of the hyperemic response in contusions.
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PMID:Regional cerebral blood flow trends in head injured patients with focal contusions and cerebral edema. 797 25

During the last few years continuous measurements of CBF by means of a thermal diffusion blood flow probe have been proposed as a possible means for monitoring the patient's CBF in a clinical setting. Also, it has been suggested that continuous CBF data from head injured patients can be correlated with other continuously recorded clinical parameters, such as ICP and blood pressure, in order to clarify pathophysiological mechanisms such as "plateau-waves". We measured regional cortical blood flow continuously with a thermal diffusion flow probe in 13 comatose head injured patients after undergoing craniotomy for evacuation of a traumatic intracranial mass lesion in order to assess the reliability and usefulness of the method. In seven patients stable Xenon-CT CBF studies were performed with the flow probe in place, in order to compare the two methods. The continuous blood flow values did not correlate with regional or global stable Xenon-CT values. These results indicate that continuous monitoring of CBF with the thermal diffusion method as currently used cannot be used in the clinical management of the patient. Further research will have to be directed to the question as to whether changes in CBF are reliably measured with this method. If this is true, the thermal diffusion flow probe with its high temporal resolution may still be useful in investigating pathophysiological mechanisms such as interaction between CBF, ICP, mean arterial blood pressure (MABP), and end-expiratory CO2 (etCO2).
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PMID:Monitoring of regional cerebral blood flow (CBF) in acute head injury by thermal diffusion. 831 Aug 62

Continuous measurements of mean arterial pressure (MAP), ICP, and jugular venous oxygen saturation (SjO2) were performed in 11 patients with severe head injury (GCS 3-7) to assess the dependence of SjO2 from the cerebral perfusion pressure (CPP), trying to establish an indirect measure of cerebrovascular autoregulation. Changes in CPP resulting from spontaneous fluctuations in MAP or ICP induced highly significant alterations in SjO2 in the range of 0.14-0.56% SjO2 mmHg-1 CPP in all patients and all periods after trauma. The analysis of the distribution of the SjO2:CPP-ratios showed the highest frequency of values in the range of 0.0-0.25% SjO2 mmHg-1 CPP in 9 of the 11 patients. Within the first 2 days after trauma, a more pronounced dependency of SjO2 from changes in CPP was found, but this was not statistically significant. No predictable relationship of the SjO2:CPP-ratio to the level of ICP could be demonstrated in the patients. Because changes in SjO2 induced by alterations in CPP were found in all patients and throughout the acute phase of severe head injury, these changes more probably reflect physiological alterations in CBF with varying perfusion pressure rather than impaired autoregulation after head trauma. Although assessment of cerebral autoregulation by estimation of the SjO2:CPP-ratio offers new possibilities for monitoring of these patients, the high frequency of erroneous readings or irregular fluctuations of the SjO2-signal from the fibreoptic catheter limits the usefulness of the SjO2-dependency from CPP for practical use in the intensive care unit.
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PMID:Correlation of jugular venous oxygen saturation to spontaneous fluctuations of cerebral perfusion pressure in patients with severe head injury. 858 22

The normal cerebral circulation has the ability to maintain a stable cerebral blood flow over a wide range of cerebral perfusion pressures and this is known as cerebral autoregulation. This autoregulation may be impaired in the injured brain. Closed head injury was induced in 28 Sprague-Dawley rats weighing 400-450 g. Four groups were studied: control group, head injured rat from meter height using 350 g, 400 g and 450 g respectively. CBF, volume velocity was monitored using laser-Doppler flowmetry together with monitoring of ICP and arterial blood pressure. Correlation to assess the relationship between CBF and CPP was done in each animal every hour. If correlation coefficient was > 0.85 and CPP was within normal range, loss of autoregulation was hypothesized. Chi square test, ANOVA test and unpaired Student's t-test were done and significant level of p < 0.05 was established. Mean CBF in injured rats was significantly lower than controls (p = 0.028) at the fifth hour. CBV was lower in the group of 450 g 1 m impact than in controls at 3 h (p = 0.04). Velocity in the group of all injured rats, was significantly lower than in controls at 3 h (p = 0.032) and at 4 h (p = 0.027). Loss of autoregulation was seen during first four hours after trauma in all groups of rats who sustained injury. Statistical significant difference (p = 0.041) in loss of autoregulation between injured and control animals was seen. No loss of autoregulation was observed in the control group. In conclusion CBF and CPP provide information about loss of autoregulation in diffuse brain injury. Decrease in CBF and increase of ICP is observed as a result of loss of cerebral autoregulation. Knowledge of loss of autoregulation could give important information and help in the management of head injured patients.
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PMID:Evaluation of cerebral autoregulation following diffuse brain injury in rats. 926 20

The normal cerebral circulation has the ability to maintain a stable cerebral blood flow over a wide range of cerebral perfusion pressures and this is known as cerebral autoregulation. Autoregulation may be impaired in the injured brain. Closed head injury was induced in 28 Sprague-Dawley rats weighing 400-450 g. Four groups were studied: control and groups, head injured by weight drop from one meter height using 350 g, 400 g and 450 g respectively. CBF was monitored using laser-Doppler flowmetry along with monitoring of ICP and arterial blood pressure. If the correlation coefficient between CBF and CPP was > 0.85 and CPP was within normal range, loss of autoregulation was hypothesized. Loss of autoregulation was seen in all groups of injured rats during first four hours. A statistically significant difference (p = 0.041) was seen in the trequency of loss of autoregulation between injured and control animals. No loss of autoregulation was observed in the control group. In conclusion CBF and CPP provide information about loss of autoregulation in diffuse brain injury. Decrease in CBF and increase of ICP is observed as a result of loss of cerebral autoregulation. Knowledge of loss of autoregulation could help in the management of head injured patients.
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PMID:Failure of cerebral autoregulation in an experimental diffuse brain injury model. 977 63

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