Degree Of Intracranial Pressure Research Articles

Effect of caudal block using different volumes of local anaesthetic on optic nerve sheath diameter in children: a prospective, randomized trial

Background:Caudal block is commonly administered for postoperative analgesia in children. Although caudal block with 1.5 ml kg−1 local anaesthetic has been reported to reduce cerebral oxygenation in infants, the effect of caudal block on intracranial pressure (ICP) in children has not been well investigated. Optic nerve sheath diameter (ONSD) correlates with degree of ICP. This study aimed to estimate the effects of caudal block on ICP according to volume of local anaesthetic using ultrasonographic measurement of ONSD in children. Methods:Eighty patients, 6- to 48-months-old, were randomly allocated to the high-volume (HV) or low-volume (LV) groups for caudal block with ropivacaine 0.15%, 1.5 ml kg−1 or 1.0 ml kg−1, respectively. Measurement of ONSD was performed before (T0), immediately after (T1), and 10 min (T2) and 30 min (T3) after caudal block. Results:The two groups exhibited significant differences in ONSD according to time (PGroup x Time=0.003). The HV group exhibited significantly greater changes in ONSD from T0 to T2 and T3 than the LV group. However, in both groups, ONSDs at T1, T2 and T3 were significantly greater compared with those at T0, with the highest values at T2. Conclusions:Caudal block with a high volume of local anaesthetic can cause a greater increase in ICP than caudal block with a low volume of local anaesthetic. However, caudal block with 1.0 ml kg−1 of local anaesthetic can also result in a significant increase in ICP. Clinical trial registrationNCT02768493.

Is higher choroid plexus ‘load’ an aetiologic factor in idiopathic intracranial hypertension? A clinico-imaging morphometric correlative study

Idiopathic intracranial hypertension (IIH) is a condition of raised cerebrospinal fluid (CSF) pressure with normal ventricular size. Although the pathogenesis of IIH remains controversial, increased CSF formation may be important. We hypothesised that if increased CSF formation was an aetiologic factor, it might result in a macroscopic increase in size of the choroid plexus (CP). We retrospectively studied 50 patients with IIH. Total size of the CP was estimated on computed tomography (CT) venograms from the sum of axial areas measured at three locations. Results were compared with the CP load of 50 matched controls on post-contrast head CTs. Evans Index was measured to exclude ventriculomegaly. Results were analysed using a Student's t test for independent samples (p < 0.05), and the effect of ICP was tested on the dependent variable (area of CP) using regression analysis. There was no significant difference in the size of the CP glomus, total axial areas of the CP between IIH patients (183 mm(2)) and controls (178 mm(2)) and no correlation between the 'load' of CP and the degree of intracranial pressure (ICP) (R (2)< 0.02). If increased CSF formation is an aetiologic factor in IIH, this is not reflected in a corresponding raised 'load' of CP.

Relationship of “dose” of intracranial hypertension to outcome in severe traumatic brain injury

It has recently been suggested that the degree of intracranial pressure (ICP) above the treatment goal can be estimated by the area under the curve (AUC) of ICP versus time in patients with severe traumatic brain injury (TBI). The objective of this study was to determine whether the calculated "ICP dose"-the ICP AUC-is related to mortality rate, outcome, and Marshall CT classification. Of 135 patients (age range 1-82 years) with severe TBI treated during a 5-year period at the authors' institution, 113 patients underwent ICP monitoring (84%). Ninety-three patients with a monitoring time>24 hours were included for analysis of ICP AUC calculated using the trapezoidal method. Computed tomography scans were assessed according to the Marshall TBI classification. Patients with Glasgow Outcome Scale scores at 6 months and >3 years were separated into 2 groups based on outcome. Sixty patients (65%) had ICP values>20 mm Hg, and 12 (13%) developed severe intracranial hypertension and died secondary to herniation. A multiple regression analysis adjusting for Glasgow Coma Scale score, age, pupillary abnormalities and Injury Severity Scale score demonstrated that the ICP AUC was a significant predictor of poor outcome at 6 months (p=0.034) and of death (p=0.035). However, it did not predict long-term outcome (p=0.157). The ICP AUC was significantly higher in patients with Marshall head injury Categories 3 and 4 (24 patients) than in those with Category 2 (23 patients, p=0.025) and Category 5 (46 patients, p=0.021) TBIs using the worst CT scan obtained. The authors found a significant relationship between the dose of ICP, the worst Marshall CT score, and patient outcome, suggesting that the AUC method may be useful in refining and improving the treatment of ICP in patients with TBI.

Somatosensory evoked potentials and intracranial pressure during chronic dilatation of an artificial extraparenchymal space-occupying lesion in cats.

Somatosensory evoked potentials (SEP) and intracranial pressure (ICP) were studied in cats, suffering from a chronic space-occupying lesion produced by enlargement of an epidural balloon over the left sensomotory cortex. Our study shows that latency alterations of SEP are not dependent on the degree of ICP. Additionally, the results obtained demonstrate that chronic space-occupying lesions cause continuous prolongation of SEP latencies, probably produced by atrophy of the compressed tissue. Regarding the clinical importance of SEP measurements, we concluded that they are not suitable for estimating the degree of ICP. However, they are useful to evaluate tissue damage caused by mass effects in the acute and chronic phase of various space-occupying processes.

Changes of somatosensory evoked potentials with increase of intracranial pressure in the rat's brain

Somatosensory evoked potentials (SEPs) to various combinations of two independent brain compression modalities (localized epidural pressure and intracerebral pressure evoked by an inserted balloon) were investigated in 24 rats. The SEP pattern in response to gradually expanding volume wihtout additional epidural pressure remained unchanged for a certain period. SEP changes occurred only shortly prior to death. On the other hand, remarkable SEP changes were observed in a gradually expanding intracerebral mass, when combined with epidural pressure application at about 50% of the lethal volume. SEP changes in response to intermittent and continuous epidural pressure, in addition to a small intracerebral mass, were investigated too. Intermittent application of minor epidural pressure led to specific P1 changes, which recovered after each pressure step. The same pressure, administered continuously, evoked SEP changes with only partial recovery in some instances. Severe epidural pressure, administered intermittently, gave rise to severe SEP changes with only partial recovery after each step. The same epidural pressure delivered continuously led to SEP changes with very small recovery. SEPs have proved to be a reliable method for signalling brain dysfunction corresponding to various modalities and degrees of intracranial pressure.

Reaction of the cerebral venous sinus system to acute intracranial hypertension.

A acute intracranial hypertension develops, the cerebral blood flow (CBF) invariably falls. Langfitt and coworkers 8 have shown that CBF reduction depends upon the degree of intracranial pressure (ICP) elevation and the rapidity with which it develops. The precise anatomical site of vascular obstruction or physiological alteration leading to failure of CBF in the presence of adequate arterial perfusing pressures has not, however, been conclusively demonstrated. Coincident with rising ICP and falling CBF, a separate and well-documented vascular phenomenon occurs. Cerebral vasodilation, as graphically demonstrated by Wolff and Forbes, 1~ can be observed through a cranial window concomitant with experimentally elevated ICP. The simultaneous occurrence of apparent dilation and falling CBF remains an unexplained vascular paradox. Conventional hemodynamic teaching would associate vasodilation with increased flow, and it has been explained as a physiological adjustment of the vascular bed to accumulated hypoxic acid metabolites. In the course of flow studies Marshall, et al., ~~ found that severe injury reduces or abolishes cerebral vasomotor tone and autoregulation. When the traumatized vascular system is subjeeCed to epinephrine-induced systemic hypertension the cerebral arterioles fail to constrict normally. This phenomenon may in part explain cerebral vasodilation, in which an increased blood mass may be presented to the capillary-venous system during arteriolar dilatation. However, faulty auto-regulation during intracranial hypertension does not explain falling CBF. Arteriolar failure should elevate the CBF in a manner analogous to that observed during hypercapneic states. T,~I Since the mechanism of falling CBF cannot be attributed to restriction of vascular