Changes in superior sagittal sinus pressure in children with head elevation, jugular venous compression, and PEEP

1986 ◽  
Vol 65 (2) ◽  
pp. 199-202 ◽  
Author(s):  
M. Sean Grady ◽  
Robert F. Bedford ◽  
T. S. Park

✓ Air embolism is a potential hazard during craniotomy whenever intracranial venous pressure is subatmospheric. In order to better understand both the risk of air embolism and its treatment in neurosurgical patients, the authors have investigated the relationship of superior sagittal sinus pressure (SSP) to head position in 15 children and examined the effects of both jugular venous compression and positive end-expiratory airway pressure (PEEP) on SSP. Progressive head elevation significantly decreased mean SSP and, in five patients, SSP was less than 0 mm Hg at 90° torso elevation. A PEEP of 10 cm H2O was ineffective in significantly increasing SSP at any degree of head elevation, whereas bilateral internal jugular compression always caused a significant increase in SSP. The authors conclude that children are at risk for venous air embolism when undergoing suboccipital craniectomy in the sitting position because intracranial venous pressure is often subatmospheric when the head is elevated. Furthermore, maintaining PEEP does not appear to be a reliable treatment for increasing SSP, whereas bilateral internal jugular compression is effective.

2019 ◽  
Vol 162 (5) ◽  
pp. 1001-1009 ◽  
Author(s):  
Afroditi-Despina Lalou ◽  
Marek Czosnyka ◽  
Zofia H. Czosnyka ◽  
Deepa Krishnakumar ◽  
John D. Pickard ◽  
...  

Abstract Objective Pseudotumour cerebri syndrome (PTCS including idiopathic intracranial hypertension) is characterised by the symptoms and signs of raised cerebrospinal fluid pressure (CSFp) in the absence of ventricular dilatation or an intracranial mass lesion. Its aetiology is unknown in the majority of cases but there is much evidence for impaired CSF absorption. Traditionally, sagittal sinus pressure has been considered to be independent of CSF pressure in adults. However, the discovery of stenoses of intracranial venous sinuses and introduction of venous sinus stenting has highlighted the importance of the venous drainage in PTCS. In this study, we have explored the relationship between CSFp and SSp before and during a CSF infusion test and during CSF drainage. Materials and methods Ten patients (9 females:1 male) with PTCS underwent infusion studies in parallel with direct retrograde cerebral venography. Both SSp and CSFp were recorded at a baseline and during CSFp elevation in a course of a CSF infusion test. The drainage of CSF after the CSF infusion was performed in 7 patients. In 5 cases, jugular venous pressure was also measured. Results CSFp and SSp including their amplitudes correlated significantly and strongly both at baseline (R = 0.96; p = 0.001) and during infusion (R = 0.92; p = 0.0026). During drainage, this correlation was maintained until SSp reached a stable value, whereas CSFp continued to decrease. Conclusions In this series of ten patients with PTCS, CSFp and SSp were coupled, both at baseline and during infusion. The implications of such coupling for the calculation of CSF outflow resistance are discussed.


1977 ◽  
Vol 46 (6) ◽  
pp. 804-810 ◽  
Author(s):  
Eduardo Lamas ◽  
Ramiro D. Lobato ◽  
Javier Esparza ◽  
Luis Escudero

✓ A patient with raised intracranial pressure secondary to a dural arteriovenous malformation (AVM) of the posterior fossa is presented. Direct shunting of arterial blood into the transverse sigmoid sinus caused a considerable increase of the sagittal sinus pressure (SSP) and elevation of intracranial pressure (ICP). Both ICP and SSP returned to normal values following obliteration of the dural AVM by selective embolization.


1974 ◽  
Vol 40 (5) ◽  
pp. 603-608 ◽  
Author(s):  
Albert N. Martins ◽  
Arthur I. Kobrine ◽  
Douglas F. Larsen

✓ Intracranial pressure (ICP) and sagittal sinus pressure (SSP) were measured simultaneously in 12 patients with brain tumors and secondary intracranial hypertension (ICH). In nine, the mean SSP was largely unaffected by changes in ICP. In three, SSP changed with the ICP. In all but one patient, the ICP remained higher than SSP and, as the ICP increased, the difference between the two also increased. Sinograms performed during ICH demonstrated partial collapse of the sinuses in some patients and not in others. The mean SSP in adults with brain tumors appears to respond unpredictably to changes in ICP. Since the rate of cerebrospinal fluid drainage depends upon the gradient between ICP and SSP, intracranial spatial compensation is probably influenced by the response of SSP to ICP. Individuals with gradients that rapidly increase because their sinuses do not collapse probably compensate more rapidly than those whose sinuses do collapse. This assumed difference in the rate of spatial compensation may account for some of the variability of the ICP response to an enlarging intracranial mass or a change in cerebral blood volume.


2017 ◽  
Vol 10 (1) ◽  
pp. 74-77 ◽  
Author(s):  
Daniel M S Raper ◽  
Thomas J Buell ◽  
Dale Ding ◽  
I Jonathan Pomeraniec ◽  
R Webster Crowley ◽  
...  

ObjectiveSafety and efficacy of superior sagittal sinus (SSS) stenting for non-thrombotic intracranial venous occlusive disease (VOD) is unknown. The aim of this retrospective cohort study is to evaluate outcomes after SSS stenting.MethodsWe evaluated an institutional database to identify patients who underwent SSS stenting. Radiographic and clinical outcomes were analyzed and a novel angiographic classification of the SSS was proposed.ResultsWe identified 19 patients; 42% developed SSS stenosis after transverse sinus stenting. Pre-stent maximum mean venous pressure (MVP) in the SSS of 16.2 mm Hg decreased to 13.1 mm Hg after stenting (p=0.037). Preoperative trans-stenosis pressure gradient of 4.2 mm Hg decreased to 1.5 mm Hg after stenting (p<0.001). No intraprocedural complication or junctional SSS stenosis distal to the stent construct was noted. Improvement in headache, tinnitus, and visual obscurations was reported by 66.7%, 63.6%, and 50% of affected patients, respectively, at mean follow-up of 5.2 months. We divided the SSS into four anatomically equal segments, numbered S1–S4, from the torcula to frontal pole. SSS stenosis typically occurs in the S1 segment, and the anterior extent of SSS stents was deployed at the S1–S2 junction in all but one case.ConclusionsSSS stenting is reasonably safe, may improve clinical symptoms, and significantly reduces maximum MVP and trans-stenosis pressure gradients in patients with VOD with SSS stenosis. The S1 segment is most commonly stenotic, and minimum pressure gradients for symptomatic SSS stenosis may be lower than for transverse or sigmoid stenosis. Additional studies and follow-up are necessary to better elucidate appropriate clinical indications and long-term efficacy of SSS stenting.


2000 ◽  
Vol 88 (2) ◽  
pp. 655-661 ◽  
Author(s):  
Thomas J. K. Toung ◽  
H. Aizawa ◽  
Richard J. Traystman

Mechanical ventilation with positive end-expiratory pressure (PEEP) may prevent venous air embolism in the sitting position because cerebral venous pressure (Pcev) could be increased by the PEEP-induced increase in right atrial pressure (Pra). Whereas it is clear that there is a linear transmission of the PEEP-induced increase in Pra to Pcev while the dog is in the prone position, the mechanism of the transmission with the dog in the head-elevated position is unclear. We tested the hypothesis that a Starling resistor-type mechanism exists in the jugular veins when the head is elevated. In one group of dogs, increasing PEEP linearly increased Pcev with the dog in the prone position (head at heart level, slope = 0.851) but did not increase Pcev when the head was elevated. In another group of dogs, an external chest binder was used to produce a larger PEEP-induced increase in Pra. Further increasing Pra increased Pcev only after Pra exceeded a pressure of 19 mmHg (break pressure). This sharp inflection in the upstream (Pcev)-downstream (Pra) relationship suggests that this may be caused by a Starling resistor-type mechanism. We conclude that jugular venous collapse serves as a significant resistance in the transmission of Pra to Pcev in the head-elevated position.


1997 ◽  
Vol 111 (8) ◽  
pp. 757-759 ◽  
Author(s):  
A. Tomkinson ◽  
R. G. S. Mills ◽  
P. J. Cantrell

AbstractThe pathophysiology of otitic hydrocephalus remains controversial. It has been argued that involvement of the superior sagittal sinus, by, at least, a mural thrombus is a necessary component of this disease.We present a case of otitic hydrocephalus where on magnetic resonance imaging (MRI) normal luminal and mural flow within the superior sagittal sinus is demonstrated. The presence of thrombus in the lateral venous sinus alone appears sufficient in this case to impede venous drainage of the intracranial contents into the neck and produce a rise in the cerebral venous pressure and a subsequent increase in the CSF pressure. The presence of a superior sagittal sinus mural thrombus is not required.


2015 ◽  
Vol 2015 ◽  
pp. 1-3
Author(s):  
Ai Hosaka ◽  
Tetsuto Yamaguchi ◽  
Fumiko Yamamoto ◽  
Yasuro Shibagaki

Cerebral venous air embolism is sometimes caused by head trauma. One of the paths of air entry is considered a skull fracture. We report a case of cerebral venous air embolism following head trauma. The patient was a 55-year-old man who fell and hit his head. A head computed tomography (CT) scan showed the air in the superior sagittal sinus; however, no skull fractures were detected. Follow-up CT revealed a fracture line in the right temporal bone. Cerebral venous air embolism following head trauma might have occult skull fractures even if CT could not show the skull fractures.


1974 ◽  
Vol 41 (4) ◽  
pp. 427-434 ◽  
Author(s):  
Yoku Nakagawa ◽  
Mitsuo Tsuru ◽  
Kenzoh Yada

✓ The pressure gradient of the venous pathway between the cortical vein and superior sagittal sinus was measured in adult mongrel dogs by recording the pressures of the bridging vein, lateral lacuna (proximal portion), and superior sagittal sinus, together with the systemic blood pressure while gradually increasing the intracranial pressure up to the level of mean systemic blood pressure. The pressure gradient between the lateral lacuna and the superior sagittal sinus was also measured under increased intracranial pressure. Pressures of the bridging vein and lateral lacuna were constantly 50 to 250 mm H2O higher than the intracranial pressure, regardless of the level of intracranial pressure. An abrupt drop in the intraluminal pressure was observed at a point 1 to 2 mm proximal to the junction of the lateral lacuna and the superior sagittal sinus, regardless of the level of intracranial pressure. It is concluded that gradual stenosis of the parasagittal venous pathways took place 1 to 2 mm proximal to the junction between the lacuna and the superior sagittal sinus, and thus cortical venous pressure was maintained 50 to 250 mm H2O higher than intracranial pressure. The authors believe that an “intracranial venous pressure regulation mechanism” exists at the junction of the lateral lacuna and the superior sagittal sinus.


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