Trauma notebook 18. Intracranial pressure: intracranial pressure monitoring.
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Humans↗
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Cerebral perfusion pressure, intracranial pressure, and head elevation.
Previous investigations have suggested that intracranial pressure waves may be induced by reduction of cerebral perfusion pressure (CPP). Since pressure waves were noted to be more common in patients with their head elevated at a standard 20 degrees to 30 degrees, CPP was studied as a function of head position and its effect upon intracranial pressure (ICP). In 18 patients with varying degrees of intracranial hypertension, systemic arterial blood pressure (SABP) was monitored at the level of both the head and the heart. Intracranial pressure and central venous pressure were assessed at every 10 degrees of head elevation from 0 degree to 50 degrees. For every 10 degrees of head elevation, the average ICP decreased by 1 mm Hg associated with a reduction of 2 to 3 mm Hg CPP. The CPP was not beneficially affected by any degree of head elevation. Maximal CPP (73 +/- 3.4 mm Hg (mean +/- standard error of the mean] always occurred with the head in a horizontal position. Cerebrospinal fluid pressure waves occurred in four of the 18 patients studied as a function of reduced CPP caused by head elevation alone. Thus, elevation of the head of the bed was associated with the development of CPP decrements in all cases, and it precipitated pressure waves in some. In 15 of the 18 patients, CPP was maintained by spontaneous 10- to 20-mm Hg increases in SABP, and pressure waves did not occur if CPP was maintained at 70 to 75 mm Hg or above. It is concluded that 0 degree head elevation maximizes CPP and reduces the severity and frequency of pressure-wave occurrence. If the head of the bed is to be elevated, then adequate hydration and avoidance of pharmacological agents that reduce SABP or prevent its rise are required to maximize CPP.
Blood Pressure↗
Slow rhythmic oscillations of blood pressure, intracranial pressure, microcirculation, and cerebral oxygenation. Dynamic interrelation and time course in humans.
BACKGROUND AND PURPOSE: Various biological signals show nonpulsatile, slow rhythmic oscillations. These include arterial blood pressure (aBP), blood flow velocity in cerebral arteries, intracranial pressure (ICP), cerebral microflow, and cerebral tissue PO2. Generation and interrelations between these rhythmic fluctuations remained unclear. The aim of this study was to analyze whether stable dynamic interrelations in the low-frequency range exist between these different variables, and if they do, to analyze their exact time delay. METHODS: In a clinical study, 16 comatose patients with either higher-grade subarachnoid hemorrhage or severe traumatic brain injury were examined. A multimodal digital data acquisition system was used to simultaneously monitor aBP, flow velocity in the middle cerebral artery (FVMCA), ICP, cerebral microflow, and oxygen saturation in the jugular bulb (SjO2). Cross-correlation as a means to analyze time delay and correlation between two periodic signals was applied to a time series of 30 minutes' duration divided into four segments of 2048 data points (approximately 436 seconds) each. This resulted in four cross-correlations for each 30-minute time series. If the four cross-correlations were consistent and reproducible, averaging of the original cross-correlations was performed, resulting in a representative time delay and correlation for the complete 30-minute interval. RESULTS: Reproducible cross-correlations and stable dynamic interrelations were found between aBP, FVMCA, ICP, and SjO2. The mean time delay between aBP and ICP was 6.89 +/- 1.90 seconds, with a negative correlation in 81%. A mean time delay of 1.50 +/- 1.29 seconds (median, 0.85 seconds) was found between FVMCA and ICP, with a positive correlation in 94%. The mean delay between ICP and SjO2 was 9.47 +/- 2.21 seconds, with a positive correlation in 77%. Mean values of aBP and ICP did not influence the time delay and dynamic interrelation between the different parameters. CONCLUSIONS: These results strongly support Rosner's theory that ICP B-waves are the autoregulatory response of spontaneous fluctuations of cerebral perfusion pressure. There is casuistic evidence that failure of autoregulation significantly modifies time delay and the correlation between aBP and ICP.
Blood Pressure↗
[Effects of intravenous nitroglycerin on blood pressure, intracranial pressure and total and regional cerebral blood flow in cases of subarachnoid hemorrhage with vasospasm].
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Blood Pressure↗
[The use of trans-cranial Doppler sonography in a neurosurgical intensive care unit. Intracranial pressure, intracranial circulatory arrest].
Transcranial Doppler Sonography (TCD) is a noninvasive simple bedside procedure to control continuously cerebral blood flow velocity in basal brain arteries in comatose patients of an intensive care unit (ICU). This measure can already be performed at ICU, to determine timing of angiography for confirming intracranial circulatory arrest when an organ explantation of patients judged clinically brain-dead is intended. TCD is also carried out to assess cerebral circulation in patients with intracranial hypertension. 64 patients are repeatedly evaluated by TCD and have been continuously monitored for ICP at the same time. According to our results a strong correlation between the flow parameters derived from TCD and the ICP exists when the ICP surpasses the level of 25 mmHg. Furthermore repeated control-TCD-examinations of 150 comatose patients in our ICU have elucidated the significant prognostic value of the pulsatility index representing the cerebrovascular resistance. Thereby important informations concerning further clinical course of patients suffering from intracranial hypertension are available. Additionally a clinical example of complete failure of cerebrovascular autoregulation shortly after hypoxic brain damage is demonstrated.
Blood Flow Velocity↗
[Monitoring and analysis of intracranial pressure: intracranial dynamics and signal processing].
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Cerebrovascular Circulation↗
[Relationship between the intracranial pressure, intracranial blood volume and total cerebral blood flow].
Studies in cats and in neurosurgical patients reveal that intraskull pressure, blood volume and total brain blood flow depend on the same factors, to a different extent though. This is determined by structural--functional organization of the intraskull circulation system, the analysis of which revealed a scheme of functional interrelationships among volumes and pressures of fluid media in the closed skull space. The features of interrelationships are not rigid and can have their own specifics in concrete situations.
Animals↗
Effects of varying levels of positive end-expiratory pressure on intracranial pressure and cerebral perfusion pressure.
OBJECTIVE: To determine the influence of positive end-expiratory pressure (PEEP) on intracranial pressure and cerebral perfusion pressure. DESIGN: Neurosurgical intensive care patients requiring intracranial pressure monitoring and mechanical ventilation were studied in a randomized, controlled study. SETTING: Tertiary care, neurosurgical intensive care unit. PATIENTS: Eighteen patients were enrolled in the study. Patients had posttraumatic head injuries (n = 9), subarachnoid hemorrhage (n = 7), obstructive hydrocephalus (n = 1), and intracerebral hemorrhage of unknown cause (n = 1). INTERVENTIONS: Patients had PEEP levels of 5, 10, and 15 cm H2O applied to their lungs. MEASUREMENTS AND MAIN RESULTS: Changes in intracranial pressure, mean arterial pressure, and cerebral perfusion pressure were measured. The results were analyzed separately for patients with normal and increased intracranial pressure (> 15 mm Hg). PEEP at 5 cm H2O had no effect on intracranial pressure in the group with normal intracranial pressure. However, PEEP at 10 and 15 cm H2O produced a significant (p < .05) increase in intracranial pressure (1.9 and 1.5 mm Hg, respectively). In the group with increased intracranial pressure, no significant change in intracranial pressure occurred at any of the PEEP levels used. In both groups, cerebral perfusion pressure was unchanged throughout. CONCLUSIONS: In patients with normal intracranial pressure, PEEP at 5 cm H2O did not significantly alter intracranial pressure. The clinical relevance of the intracranial pressure increase at PEEP levels of 10 and 15 cm H2O is questionable because cerebral perfusion pressure did not change and remained > 60 mm Hg. In patients with increased intracranial pressure, higher levels of PEEP did not significantly change intracranial pressure or cerebral perfusion pressure.
Adult↗
Development of a noninvasive technique for the measurement of intracranial pressure.
Intracranial pressure (ICP) dynamics are important for understanding adjustments to altered gravity. Previous flight observations document significant facial edema during exposure to microgravity, which suggests that ICP is elevated during microgravity. However, there are no experimental results obtained during space flight, primarily due to the invasiveness of currently available techniques. We have developed and refined a noninvasive technique to measure intracranial pressure noninvasively. The technique is based upon detecting skull movements of a few micrometers in association with altered intracranial pressure. We reported that the PPLL technique has enough sensitivity to detect changes in cranial distance associated with the pulsation of ICP in cadavera. In normal operations, however, we place a transducer on the scalp. Thus, we cannot rule out the possibility that the PPLL technique picks up cutaneous pulsation. The purpose of the present study was therefore to show that the PPLL technique has enough sensitivity to detect changes in cranial distance associated with cardiac cycles in vivo.
Blood Pressure↗
The management of cerebral perfusion pressure and intracranial pressure after severe head injury.
Neurosurgical intervention attempts to minimize secondary central nervous system injury after severe head injury through the evacuation of mass lesions with subsequent manipulation of cerebral perfusion pressure and intracranial pressure. The normal brain couples blood flow to metabolic demand through autoregulation of the cerebral vasculature. After severe head trauma and its attendant increase in intracranial pressure, marked alterations in cerebral blood flow and perfusion may occur. Currently, intervention is based on maintenance of coronary perfusion pressure and aggressive management of intracranial pressure. Both may be impacted by manipulation of ventilation, systemic blood pressure and volume status, administration of osmotic diuretics, and head elevation. Such therapy in the patient with severe head injury attempts to maintain coronary perfusion pressure and adequate oxygen delivery in a damaged central nervous system with altered hemodynamics and raised intracranial pressure.
Brain↗
Relationship between intracranial pressure and intracranial volume in craniosynostosis.
Premature fusion of cranial sutures in craniosynostosis has been thought to lead to craniostenosis, which in turn may lead to increased intracranial pressures. In 41 consecutive patients with craniosynostosis, intracranial pressure and intracranial volume were measured. Of the 41 patients, 38 (92.6%) had raised intracranial pressure but only 4 (9.7%) had a decreased skull volume. In the present study, there is no correlation between intracranial volume and intracranial pressure. This study confirms that the measurement of intracranial volume, a non invasive procedure, cannot be used to assess intracranial pressure and to avoid an invasive procedure.
Aging↗
[The critical threshold of cerebral perfusion pressure in intracranial pressure circumstance of hydrocephalus during infancy].
In cases of brain insults in infants including those who are superimposed with increased intracranial pressure, the importance of management of cerebral hemodynamics has been stressed. As yet, minimal information is available on hydrocephalus. The aim of this clinical study is to clarify the circumstance of intracranial pressure in hydrocephalic infants with cerebrovascular compromise. Polygraphical and continuous intracranial pressure recordings were done in 20 hydrocephalic newborns and infants of various etiologies including 16 hydrocephalus of preshunted state, two cases of shunt dysfunction and two cases of slit ventricle syndrome. Analysis of intracranial pressure circumstance was done both quantitatively and qualitatively using newly devised microcomputer-aided analyzing system. As a cerebrovascularly compromised index of the intracranial pressure circumstance, the transmission ratio of systemic arterial pressure to intracranial pressure defined by Ikeyama, et al.: eta HB (PP of ICP/PP of SABP) was used. There exists bilinear correlation between ICP and eta HB, and more clearly, between CPP and eta HB. Thus, the correlation graph shows the breakpoint of ICP and CPP in relation to eta HB. Abnormal waves similar to Lundberg's A and B are recorded. They appear under the condition of high range of eta HB, and also, below the level of breakpoint of CPP or ICP, and show the characteristic features of pressure waves. During their appearance, the respiratory pattern shows a uniform sequential changes from dysrhythmia, ataxia to hyperventilation. The breakpoint of CPP in relation to eta HB, which is the critical level of CPP where the less tighter intracranial circumstance is maintained above this level, was clarified in hydrocephalus during infancy.(ABSTRACT TRUNCATED AT 250 WORDS)
Age Factors↗
Influences of phasic changes in systemic blood pressure on intracranial pressure.
In acute experiments on lambs, the effects of short-lasting induced modifications in arterial and venous systemic blood pressure on intracranial pressure have been studied. Haemodynamic changes have been provoked by increasing the cardiac venous return, by increasing or decreasing the arterial resistance and by stimulating the vagus nerve. Intracranial pressure modifications have been demonstrated to depend essentially on arterial influences. A direct venous influence is apparent only when the central venous pressure is increased, as occurs in the case of increased venous cardiac return.
Animals↗
Headache caused by raised intracranial pressure and intracranial hypotension.
Extremes of intracranial pressure commonly cause headache. Benign intracranial hypertension is a rare syndrome of increased intracranial pressure manifesting as headache, intracranial noises, transient visual obscuration, and palsy of the sixth cranial nerve. Endocrine disorders such as obesity and hypoparathyroidism, hypervitaminosis A, tetracycline use and thyroid replacement are probable causes of benign intracranial hypertension. In the majority of cases, however, it is idiopathic. Benign intracranial hypertension is though to be caused by cerebral edema, high cerebrospinal fluid outflow resistance and high cerebral venous pressure, or a combination of the three. The management of benign intracranial hypertension includes, symptomatic headache relief, removal of offending risk factor(s), and medical or surgical reduction of intracranial pressure. Spontaneous intracranial hypotension is more rare than benign intracranial hypertension. Postural headache (worse in the upright position) is the hallmark of spontaneous intracranial hypotension. Typically, the cerebrospinal fluid pressure is less than 60 mm H2O. Diminished cerebrospinal fluid production, hyperabsorption, and leak are postulated mechanisms of spontaneous intracranial hypotension. Empirical treatment includes bed rest, administration of caffeine, corticosteroids or mineralocorticoids, epidural blood patch, and epidural saline infusion.
Brain Diseases↗
Anesthesia and subarachnoid intracranial pressure.
Intracranial pressure (ICP) was continuously monitored by the Richmond technic of Vries and Becker in 17 patients undergoing elective craniotomy. This method entails the placement, underlocal anesthesia, of a hollow screw through the cranium into the subarachnoid space. The screw was connected to a Statham P23Db pressure transducer with heavy vinyl tubing and with pressures recorded on a Beckman Dynograph. The effects of 3 anesthetic technice-halothane, enflurane, and nitrous oxide-narcotic-relaxant-on ICP during induction and maintenance were compared with preinduction control pressures. Control ICP in awake, lightly premedicated patients was 15 plus or minus 10 torr. Mask inductions with halothane and enflurane consistently caused significant increases in ICP from preinduction levels in the absence of excitement or airway obstruction. Induction with nitrous oxide-narcotic-relaxant did not increase ICP. Decreases in ICP following barbiturate administration were noted. Addition of halothane and enflurane to the inspired mixture of patients controlled and hyperventilated with nitrous oxide and oxygen caused consistent increases in ICP. With control hyperventilation (Paco2 25 plus or minus 5 torr), the ICP did not return toward preinduction values within 5 minutes with enflurane and halothane.
Anesthesia, Inhalation↗
Intracranial pressure and intracranial volume in children with craniosynostosis.
Intracranial volume and intracranial pressure have been measured in 66 children with craniosynostosis, 48 boys and 18 girls. The premature fusion of skull sutures is assumed to restrict skull growth and predispose to elevated intracranial pressure. Thirteen children (20 percent) had raised intracranial pressure and demonstrated a significant restriction of skull growth. In this series, volume measurement alone, however, did not serve as a reliable predictor that the intracranial pressure was raised.
Adolescent↗
Alfentanil increases intracranial pressure when intracranial compliance is low.
Intracranial pressure increases following the administration of alfentanil 1 mg are reported in five patients with suspected normal pressure hydrocephalus who were undergoing infusion of saline into a lateral ventricle to measure cerebrospinal fluid outflow resistance. The increase in intracranial pressure was accompanied by a fall in mean arterial pressure. These observations show that, when the intracranial compliance is reduced, alfentanil can cause considerable increases in intracranial pressure and decreases in cerebral perfusion pressure.
Aged↗
Influence of urapidil on intracranial pressure and intracranial compliance in dogs.
During induced hypotension with urapidil, measurements of intracranial pressure and of the ventricular volume-pressure response (intracranial compliance) were obtained in dogs with and without intracranial hypertension. A bolus of urapidil 50 mg plus an infusion of urapidil 8.2 +/- 1.2 mg min-1 decreased mean arterial pressure by 22 +/- 10% from control in group I (without intracranial hypertension) and by 24 +/- 8% in group II (with intracranial hypertension). In both groups there was no change in intracranial pressure or in intracranial compliance after the administration of urapidil.
Animals↗