Head elevation reduces head-rotation associated increased ICP in patients with intracranial tumours

PURPOSE: To quantify the effects of graded head rotation and elevation on intracranial pressure (ICP) in neurosurgical patients, before and after induction of general anesthesia. METHODS: Patients with supratentorial tumours (n=12), scheduled for craniotomy with planned ICP monitoring, underwent baseline ICP measurements awake and supine (0 degrees rotation and elevation). Incremental degrees of head rotation (15 degrees) and of head elevation (10 degrees) were performed independently and in combination. Paired measurements of ICP at all levels of head rotation and elevation were also performed before and after induction of general anesthesia (n=6). RESULTS: The baseline ICP was 12.3 +/- 6.4 mmHg (n=12). Changes of ICP were proportional to the degree of head rotation or elevation. Head rotation of 60 degrees maximally increased ICP to 24.8 +/- 14.3 mmHg (P < 0.05). Head elevation above 20 degrees reduced ICP with a maximal reduction to -0.2 +/- 5.5 mmHg at 40 degrees elevation (P < 0.01). Head elevation to 30 degrees reduced the intracranial hypertension associated with head rotation. No differences were observed between ICP measurements made before or after induction of general anesthesia (n=6). Three patients experienced headache with extreme head rotation (<60 degrees) and intracranial hypertension (ICP > 20 mmHg). CONCLUSION: Head rotation of 60 degrees caused an increase in ICP. Concomitant head elevation to 30 degrees reduced the intracranial hypertension associated with head rotation. Headache with head rotation may provide a useful clinical warning of elevated ICP.     

Local vascular response during organ elevation. A model for cerebral effects of upright position and dural puncture

BACKGROUND: Dural puncture can be followed by postural headache and, in patients with cerebral infections, by brain stem herniation. The present study evaluates whether these complications may be related to the changes in hydrostatic pressure generated by the spinal fluid column when the dural sac surrounding the cerebrospinal tissue has been punctured. METHOD: An isolated cat skeletal muscle enclosed in a plethysmograph connected to a tube served as a model imitating the brain, the cranium and the spinal canal. We investigated effects of organ elevation on tissue pressure, venous collapse (venous outflow resistance) and tissue volume with closed "spinal" tube (intact dural sac) and open "spinal" tube (dural puncture), and effects of compliance of the draining veins. RESULTS: Organ elevation with closed "spinal" tube induced a decreased tissue pressure, whereas tissue pressure remained unchanged if arterial inflow pressure to the muscle was kept constant. Organ elevation with the "spinal" tube opened distally caused a significantly larger decrease in tissue pressure, venous dilation and disappearance of venous outflow resistance. Transcapillary filtration increased, and the filtration rate was higher with high than with low venous compliance. CONCLUSION: If our results are applicable to the brain, changing to an upright position following a lumbar dural puncture may generate a negative hydrostatic force and a negative interstitial cerebral pressure, causing an increased transvascular pressure and dilation of the cerebral outflow veins. The corresponding increase in cerebral blood volume may induce post-spinal headache, and the increased transcapillary pressure may cause increased fluid filtration and brain oedema if the blood-brain barrier is disrupted.     

Effects of head posture on cerebral hemodynamics: its influences on intracranial pressure, cerebral perfusion pressure, and cerebral oxygenation

OBJECTIVE: Severely head-injured patients have traditionally been maintained in the head-up position to ameliorate the effects of increased intracranial pressure (ICP). However, it has been reported that the supine position may improve cerebral perfusion pressure (CPP) and outcome. We sought to determine the impact of supine and 30 degrees semirecumbent postures on cerebrovascular dynamics and global as well as regional cerebral oxygenation within 24 hours of trauma. METHODS: Patients with a closed head injury and a Glasgow Coma Scale score of 8 or less were included in the study. On admission to the neurocritical care unit, a standardized protocol aimed at minimizing secondary insults was instituted, and the influences of head posture were evaluated after all acute necessary interventions had been performed. ICP, CPP, mean arterial pressure, global cerebral oxygenation, and regional cerebral oxygenation were noted at 0 and 30 degrees of head elevation. RESULTS: We studied 38 patients with severe closed head injury. The median Glasgow Coma Scale score was 7.0, and the mean age was 34.05 +/- 16.02 years. ICP was significantly lower at 30 degrees than at 0 degrees of head elevation (P = 0.0005). Mean arterial pressure remained relatively unchanged. CPP was slightly but not significantly higher at 30 degrees than at 0 degrees (P = 0.412). However, global venous cerebral oxygenation and regional cerebral oxygenation were not affected significantly by head elevation. All global venous cerebral oxygenation values were above the critical threshold for ischemia at 0 and 30 degrees. CONCLUSION: Routine nursing of patients with severe head injury at 30 degrees of head elevation within 24 hours after trauma leads to a consistent reduction of ICP (statistically significant) and an improvement in CPP (although not statistically significant) without concomitant deleterious changes in cerebral oxygenation.     

Effect of nitrous oxide on intracranial pressure after cranial-dural closure in patients undergoing craniotomy.

After cranial-dural closure, nitrous oxide (N2O) may diffuse into and expand an entrapped volume of intracranial air, thereby increasing intracranial pressure (ICP). We performed a prospective clinical study to determine the effect of continuation of N2O after dural closure on ICP in patients undergoing craniotomies. Patients were randomly assigned in a 1.5:1 ratio into a group in which N2O was continued after dural closure (N2O, n = 15) or a group in which N2O was discontinued and replaced with nitrogen (N2, n = 9) at the time of dural closure. PaCO2 was normal prior to closure, and end-tidal PCO2 was kept constant after dural closure. Ipsilateral ICP was recorded at 5-min intervals after dural closure until completion of skin closure and immediately postoperatively. Presence of intracranial air was determined by head computed tomography scan within the first postoperative hour. ICP at the time of dural closure did not differ between the groups (N2O: 3 +/- 2 mmHg vs. N2:5 +/- 1 mmHg). Intraoperatively, ICP did not change after dural closure, regardless of whether N2O was continued or discontinued. Postoperatively, ICP was reduced, with a significant decrease in ICP (P less than 0.01) observed only in the N2O group. Postoperative computed tomography scans demonstrated the presence of intracranial air in all patients, with most exhibiting a mild to moderate degree of pneumocephalus. We conclude that continuation of N2O after dural closure did not affect ICP during the craniotomy closure. These results suggest that it is not necessary to discontinue N2O prior to dural closure for reasons of avoiding expansion of intracranial air and increasing ICP.     

Mechanisms behind postspinal headache and brain stem compression following lumbar dural puncture--a physiological approach

BACKGROUND: The cause of postspinal headache and its specific characteristics are unknown, and whether lumbar dural puncture (LP) triggers brain-stem compression in patients with brain oedema is still controversial. METHODS: Hydrostatic effects of distal opening of the dural sac towards the atmosphere are described and applied to the normal brain and the brain with disrupted BBB. Analogue analyses from previous results using an isolated skeletal muscle enclosed in a rigid shell were applied to the brain in an attempt to simulate and verify the haemodynamic effects of distal opening of the spinal canal. RESULTS: The theoretical considerations and the experimental results are compatible with the hypothesis that hydrostatic effects of distal opening of the fluid-filled spinal canal may obliterate the normal subdural venous collapse after a change from the horizontal to vertical position, which may be compatible with postural postspinal headache as occurring close to pain-sensitive meningeal regions. The hydrostatic forces may also initiate transcapillary filtration and aggravate oedema when permeability is increased, which may cause a narrower situation in the brain stem region, perhaps aggravated by venous stasis and a Cushing reflex-induced increase in blood pressure. An magnetic resonance imaging (MRI) picture illustrates how this scenario may separate the subdural space into an upper high- and a lower low-pressure cavity, pressing the brain downwards with sagging of the brain. A life-threatening positive feedback situation for brain-stem compression may develop. CONCLUSION: The present study strongly suggests that postspinal headache and brain-stem compression and other LP-related effects are predictable following LP, without involving CSF leakage, and can be explained by hydrostatic effects triggered by distal opening of the normally closed dural space to the atmosphere.     

Effet de la position sur la pression intracrânienne

The question as to whether the head and trunk of neurosurgery patients should be elevated remains controversial. This question is particularly important when intracranial hypertension is present. Head up position may have beneficial effects on intracranial pressure (ICP) via changes in mean arterial pressure (MAP), airway pressure, central venous pressure and cerebro spinal fluid displacement. However, in some circumstances, head up position may decrease MAP which in turn will result in a paradoxical rise in ICP through autoregulation mechanisms. Therefore, the degree of head elevation has to be titrated by evaluating the most adequate cerebral perfusion pressure (CPP) for each patient by means of transcranial Doppler or measurement of jugular venous blood oxygen saturation. Head elevation above 30° should be avoided in all cases. In most patients with intracranial hypertension, head and trunk elevation up to 30° is useful in helping to decrease ICP, providest that a safe CPP of at least 70 mmHg or even 80 mmHg is maintained. Patients in poor haemodynamic conditions are best nursed flat. CPP is thus the most important factor in assessment and monitoring when considering head elevation in patients with increased ICP.     

Position du patient en neurochirurgie

There is still controversy whether neurosurgical patients' head and trunc should be elevated or not, particularly in case of increased intracranial pressure (ICP). Head up position may have beneficial effects on ICP via changes in mean arterial pressure (MAP), airway pressure, central venous pressure and CSF displacement. However, in some circumstances, head up position may decrease MAP, which in turn will result in a paradoxical rise in ICP through autoregulation mechanisms. Therefore, the degree of head elevation has to be titrated by evaluating the most adequate cerebral perfusion pressure (CPP) for each patient by means of transcranial Doppler or measurement of jugular venous blood oxygen saturation. Head elevation above 30° should be avoided in all cases. In most patients with intracranial hypertension, head and trune elevation up to 30° is useful in helping to decrease ICP, providing that a safe CPP of a least 70 mmHg or even 80 mmHg is maintained. Patients in poor haemodynamic conditions are best nursed flat. CPP is thus a most important factor to evaluate and monitor while considering head elevation in patients with increased ICP.     

There is no transmantle pressure gradient in communicating or noncommunicating hydrocephalus

OBJECTIVE: To examine whether a transmantle pressure gradient exists in adult patients with communicating and noncommunicating hydrocephalus. METHODS: Ten patients participated in the study. The mean patient age was 57 +/- 18 years (range, 20-80 yr); seven patients had communicating hydrocephalus, and three had noncommunicating hydrocephalus. Microsensors were used to measure the intracranial pressure (ICP), for 17 to 24 hours during sleeping and waking periods, in the right lateral ventricle (ICP(IV)) and in the subarachnoid space (ICP(SAS)) over the right cerebral convexity simultaneously. Patient activities and body positions were documented. The hydrostatic pressure difference between the two sensors was calculated from cranial x-rays for four basic body positions and compared with the actual body positions of the patients and the measured difference between the two sensors. For three 10-minute periods, the exact transmantle pressure gradient was calculated for each patient as ICP(IV) - ICP(SAS), adjusted for the hydrostatic pressure difference. RESULTS: The measured pressure difference between the two sensors was always within the limits of the maximal possible hydrostatic pressure difference, and it correlated well with the expected difference for the various body positions: mean correlation coefficient, 0.79 +/- 0.10 (range, 0.65-0.92). The exact mean transmantle pressure was -0.01 +/- 0.24 mmHg (range, -0.4 to 0.4 mmHg). ICP waves caused by cardiac pulse, respiration, and B waves were identical in both spaces. CONCLUSION: This study demonstrates no factual support for existence of a transmantle pressure gradient in nonacute communicating or noncommunicating hydrocephalus.     

Decreased cerebrospinal fluid absorption during abdominal insufflation

BACKGROUND: Intracranial pressure (ICP) is known to rise during induced CO(2) pneumoperitoneum. This rise correlates with an increase in inferior vena caval pressure; therefore, it is probably associated with increased pressure in the lumbar venous plexus. Branches of this plexus communicate with arachnoid villi in the lumbar cistern and the dural sleeves of spinal nerve roots-areas where cerebrospinal fluid (CSF) absorption to normally takes place. The increased venous pressure in this area may impede CSF absorption. Because CSF is produced at a constant rate, decreased absorption will increase ICP. We hypothesized that increased ICP occurring during abdominal insufflation is due, at least in part, to decreased absorption of CSF. The purpose of this study is to show that CSF absorption is inhibited during abdominal insufflation. METHODS: After appropriate approval was obtained, 16 domestic swine were anesthetized and injected into the CSF with 100 microcuries (microCu) of I(131) radioactive iodinated human serum albumin (RISA) in 2 ml of normal saline. Eight subjects underwent CO(2) abdominal insufflation to 15 mmHg and were maintained for 4 h. A control group did not undergo insufflation. Blood levels of RISA were measured over a 4-h period to determine the rate of CSF absorption. RESULTS: Blood levels of RISA increased at a slower rate in the subjects undergoing abdominal insufflation than in the control group. The mean change over 2 h in the insufflated group was 15% compared to 34% in the control group (p = 0.02). This difference indicates decreased absorption of CSF in the insufflated group. CONCLUSIONS: These results demonstrate decreased absorption of CSF during abdominal insufflation and support the hypothesis that the increase in ICP pressure occurring during abdominal insufflation is caused, at least in part, by decreased absorption of CSF in the region of the lumbar cistern and the dural sleeves of spinal nerve roots.     

The effects of 10 degrees reverse Trendelenburg position on subdural intracranial pressure and cerebral perfusion pressure in patients subjected to craniotomy for cerebral aneurysm

The aim of the current study was to examine the effects of 10 degrees reverse Trendelenburg position (rTp) on subdural intracranial pressure (ICP), cerebral perfusion pressure (CPP), and dural tension. Additionally, the relationship between preoperative Hunt and Hess (H and H) grade and the subdural ICP in patients scheduled for cerebral aneurysm surgery was investigated. Twenty-eight consecutive patients with a cerebral aneurysm were subjected to craniotomy in propofol/fentanyl or propofol/remifentanil anesthesia. Subdural ICP was measured after opening of the bone flap and exposure of dura. After reference measurements of subdural ICP and mean arterial blood pressure (MABP), the measurements were repeated during 10 degrees rTp. No significant differences between the anesthetic groups were disclosed. During 10 degrees rTp, a significant decrease in MABP, ICP, and jugular bulb pressure was observed whereas CPP remained unchanged. In H and H 0 patients (unruptured aneurysm), the ICP decreased from 2.9 +/- 2.6 mmHg to 0.4 +/- 2.2 mmHg at 10 degrees rTp. In H and H I to II patients, the ICP decreased from 9.3 +/- 3.8 mmHg to 4.6 +/- 3.3 mmHg at 10 degrees rTp. A significant difference in the mean baseline subdural ICP and DeltaICP (change in ICP) was found between patients with unruptured aneurysm and patients with subarachnoid hemorrhage (H&H I and II). Furthermore, the relationship between the subdural ICP at neutral position and DeltaICP was significant. In patients without intracranial hypertension, 10 degrees rTp decreases subdural ICP and dural tension in patients with ruptured as well as patients with unruptured cerebral aneurysm; CPP is unchanged.     

Ventricular pressure monitoring during bilateral decompression with dural expansion

OBJECT: The management of massive brain swelling remains an unsolved problem in neurosurgery. Despite newly developed medical and pharmacological therapy, the rates of mortality and morbidity caused by massive brain swelling remain high. According to many recent reports, surgical decompression with dural expansion is superior to medical management in patients with massive brain swelling. To show the quantitative effect of decompressive surgery on intracranial pressure (ICP), the authors performed a ventricular puncture and measured the ventricular ICP continuously during decompressive surgery and the postoperative period. METHODS: Twenty patients with massive brain swelling who underwent bilateral decompressive craniectomy with dural expansion were included in this study. In all patients, ventricular puncture was performed at Kocher's point on the side opposite the massive brain swelling. The ventricular puncture tube was connected to the continuous monitor via a transducer device. The ventricular pressure was monitored continuously, during the bilateral decompressive procedures and postoperative period. The initial ventricular ICP was variable, ranging from 16 to 65.8 mm Hg. Immediately after the bilateral craniectomy, the mean ventricular ICP decreased to 50.2+/-16.6% of the initial ICP (range 5-51.5 mm Hg). Additional opening of the dura decreased the mean ICP by an additional 34.5% and reduced the ventricular pressure to 15.7+/-10.7% of the initial pressure (range 0-15 mm Hg). Ventricular pressure measured postoperatively in the neurosurgical intensive care unit was lowered to 15.1+/-16.5% of the initial ICP. The ventricular ICP trend in the first 24 hours after decompressive surgery was an important prognostic factor; if it was greater than 35 mm Hg, the mortality rate was 100%. CONCLUSIONS: Bilateral decompression with dural expansion is an effective therapeutic modality in the control of ICP. To obtain favorable clinical outcomes in patients with massive brain swelling, early decision making and proper patient selection are very important.     

Evaluation of mechanism of increased intracranial pressure with insufflation

Background: Previous studies have documented an increase in intracranial pressure with abdominal insufflation, but the mechanism has not been explained. Methods: Nine 30–35-kg domestic pigs underwent carbon dioxide insufflation at 1.5 l/min. Intracranial pressure (ICP), lumbar spinal pressure (LP), central venous pressure (CVP), inferior vena cava pressure (IVCP), heart rate, systemic arterial blood pressure, pulmonary arterial pressure, cardiac output, heart rate, respiratory rate, temperature, and end-tidal CO₂ were continuously measured. Mechanical ventilation was used to maintain a constant pCO₂. Measurements were recorded at 0, 5, 10, and 15 mmHg of abdominal pressure with animals in supine, Trendelenburg (T), and reverse Trendelenburg (RT) positions. Prior to recording measurements, the animals were allowed to stabilize for 40 min after each increase in abdominal pressure and for 20 min after each position change. Results: The animals showed a significant increase in ICP (mmHg) with each 5-mmHg increase in abdominal pressure (0 mmHg: 14 ± 1.7; 5 mmHg: 19.8 ± 2.3, p < 0.001; 10 mmHg: 24.8 ± 2.5, p < 0.001; 15 mmHg: 29.8 ± 4.7, p < 0.01). The ICP at 15 mmHg abdominal pressure increased further in the T position (39 ± 4, p < 0.01). Insufflating in the RT position did not significantly reduce the increase in ICP. The IVCP (mmHg) increased with increased abdominal pressure (0 mmHg: 11.5 ± 6.2, 15 mmHg: 22.1 ± 3.5, p < 0.01). This increase correlated with the increase in ICP and LP (r of mean pressures ≥0.95). There was no significant change in CVP. Conclusions: This study suggests that care may be needed with laparoscopy in patients at risk for increased ICP due to head injury or a space occupying lesion. The mechanism of increased ICP associated with insufflation is most likely impaired venous drainage of the lumbar venous plexus at increased intraabdominal pressure. Further studies of cerebral spinal fluid movement during insufflation are currently underway to confirm this hypothesis. Received: 28 March 1997/Accepted: 5 August 1997     

The mechanisms of intracranial pressure modulation by epidural blood and other injectates in a postdural puncture rat model

The epidural blood patch is considered effective in treating postdural puncture headache. We have developed a postdural puncture model in rats for quantitative evaluation of the magnitude and duration of changes in cerebrospinal fluid (CSF) pressure in the cisterna magna in response to the administration of epidural blood or other moieties. This model was used to compare the efficacy of various methods of epidural injection for restoring and maintaining CSF pressure for up to 240 min. After lumbar dural puncture, CSF pressure declined 3.6 +/- 0.2 mm Hg. Epidural saline (100 microL) injected at the puncture site initially increased pressure by 7.2 +/- 0.7 mm Hg, but it rapidly (7.8 +/- 0.6 min) returned to postdural puncture baseline. A similar initial increase of CSF pressure was observed with equal volumes of all other epidural injectates, but the duration of pressure increase varied greatly. Hetastarch and dextran 40 produced results similar to saline. Only whole blood or fibrin glue consistently increased CSF pressure for the entire 240-min observation period. Whole blood mixed with anticoagulant or injected 20-mm cephalad to the puncture site did not sustain pressure. After laminectomy, direct application of blood or adhesive to the dural defect caused no pressure increase. Continuous infusion of saline after bolus could maintain pressure increase for 180 min, but within 60 min of stopping infusion, pressure returned to baseline. These results confirm the efficacy of the epidural administration of blood or fibrin glue to correct CSF hypotension after dural puncture and also provide insight into the mechanisms of intracranial pressure modulation. Sealing the dural defect does not effectively correct CSF pressure unless an epidural tamponade effect is also maintained. IMPLICATIONS: A rat model was developed to evaluate different drugs that may be injected epidurally to treat postdural puncture headache. Epidural injection of blood or fibrin glue was the most effective method of maintaining increased cerebrospinal fluid pressure after dural puncture. Sealing the dural defect does not effectively correct cerebrospinal fluid pressure unless an epidural tamponade effect is maintained.     

Posture-related changes in the pressure environment of the ventriculoperitoneal shunt system

OBJECT: The purpose of this study is to clarify the whole pressure environment of the ventriculoperitoneal (VP) shunt system in patients with successfully treated hydrocephalus and to determine which factor of the pressure environment has a preventive effect on overdrainage. METHODS: Thirteen patients with hydrocephalus who had been treated with VP shunt therapy by using a Codman-Hakim programmable valve without incidence of overdrainage were examined. The authors evaluated intracranial pressure (ICP), intraabdominal pressure (IAP), hydrostatic pressure (HP), and the perfusion pressure (PP) of the shunt system with the patients both supine and sitting. With patients supine, ICP, IAP, and HP were 4.6 +/- 3 mm Hg, 5.7 +/- 3.3 mm Hg, and 3.3 +/- 1 mm Hg, respectively. As a result, the PP was only 2.2 +/- 4.9 mm Hg. When the patients sat up, the IAP increased to 14.7 +/- 4.8 mm Hg, and ICP decreased to-- 14.2 +/- 4.5 mm Hg. The increased IAP and decreased ICP offset 67% of the HP (42.9 +/- 3.5 mm Hg), and consequently the PP (14 +/- 6.3 mm Hg) corresponded to only 33% of HP. CONCLUSIONS: The results observed in patients indicated that IAP as well as ICP play an important role in VP shunt therapy and that the increased IAP and the decreased ICP in patients placed in the upright position allow them to adapt to the siphoning effect and for overdrainage thereby to be avoided.     

Epidural Anesthesia and Acutely Increased Intracranial Pressure: Lumbar Epidural Space Hydrodynamics in a Porcine Model

Background: The effects of epidural injection on intracranial pressure (ICP), lumbar epidural pressure, cerebral blood flow (CBF), and spinal cord blood flow (SCBF) were studied after acutely increased ICP in swine.

Methods: Twenty pigs, anesthetized with isoflurane and mechanically ventilated to maintain normocarbia, had two Tuohy needles placed in the lumbar epidural space. The ICP, lumbar epidural pressure, heart rate, mean arterial pressure, and central venous pressure were monitored. All animals had a Fogarty catheter placed in the parietal epidural space. Six pigs were randomized to a normal ICP group (group N) and eight pigs to an increased ICP group by inflation of the Fogarty catheter balloon (group R). Each pig had 0.33 ml [centered dot] kg sup -1 of 2.0% carbonated lidocaine injected over 20 s via an epidural needle placed at L3. The ICP and lumbar epidural pressure were then monitored continuously for 30 min. Pressure-time data were fit to traditional compartmental models. Epidural elastance and resistance were calculated using a derivation of the Windkessel theory. An additional six pigs had ICP elevated as in group R and CBF and SCBF measured using radioactive microspheres at five time periods: baseline, 0-60 s, 100-160 s, 200-260 s, and at 30 min after epidural injection.

Results: The animals did not differ with respect to heart rate, central venous pressure, or mean arterial pressure at baseline. The ICP was 10 +/- 2 mmHg in group N, and 24 +/- 2 mmHg after balloon inflation in group R. After epidural injection, peak ICP was significantly greater in group R (76 +/- 22 vs. 54 +/- 17 mmHg) but not different by 30 min (17 +/- 5 vs. 11 +/- 1 mmHg). Epidural elastance in group N was 8.3 +/- 3.1 mmHg [centered dot] ml sup -1 and 12.8 +/- 3.0 mmHg [centered dot] ml sup -1 in group R (P = 0.045). Epidural resistance was 1,330 +/- 590 mmHg [centered dot] s [centered dot] ml sup -1 in group N and 2,220 +/- 600 mmHg [centered dot] s [centered dot] ml sup -1 in group R (P = 0.038). The CBF and SCBF were less than 10% of baseline during the 0- to 60-s time period after epidural injection. Thereafter, CBF and SCBF did not differ from baseline values.     

The effects of head and body positioning on upper airway collapsibility in normal subjects who received midazolam sedation

STUDY OBJECTIVE: To test the hypothesis that the change of body and head position affects upper airway patency during midazolam sedation. DESIGN: Clinical study using 30 healthy subjects. SETTING: Research unit for sleep study. INTERVENTIONS: We used a pressure-flow relationship to evaluate critical closing pressure (Pcrit) and upper airway resistance (Rua) in different condition of body and head position. A pressure-flow relationship was obtained in 3 body postures (supine, 15 degrees elevation, and 30 degrees elevation) and was obtained in 3 head positions (supine with the head in the neutral, supine with head extension, and supine position with head rotated). MEASUREMENTS: The pressure and inspiratory flow at subjects' nose mask were recorded. Polysomnographic parameters (electroencephalograms, electrooculograms, submental electromyograms, upper esophageal pressure, and plethysmogram) were also recorded. MAIN RESULTS: In experiment 1, 30 degrees elevation of the body significantly decreased Pcrit (P < 0.05) to -13.3 +/- 1.3 cm H(2)O compared with -8.2 +/- 1.4 cm H(2)O in supine condition without changing the slope (1/Rua). In experiment 2, head extension significantly decreased Pcrit (-12.5 +/- 1.3 cm H(2)O) (P < 0.05) compared with the value (-8.2 +/- 1.0 cm H(2)O) in supine condition without changing the slope (1/Rua). CONCLUSIONS: Our findings indicate that 30 degrees body elevation and head extension significantly decreased upper airway collapsibility during midazolam sedation and established the relative potency of maneuvers that maintain upper airway patency.     

Effect of the skull and dura on neural axis pressure-volume relationships and CSF hydrodynamics

The pressure-volume index (PVI) technique of bolus manipulation of cerebrospinal fluid (CSF) was used to measure changes of neural axis volume buffering-capacity and CSF dynamics produced by different conditions of the skull and dura. Twenty-eight cats were studied in the intact state, after bilateral craniectomy, and with the dura opened. At each stage of altering the container of the brain, the following parameters were obtained: steady-state intracranial pressure (ICP), sagittal sinus venous pressure, PVI, and the resistance to the absorption of CSF. The resistance to absorption of CSF was determined using both the bolus injection and the continuous infusion of fluid. After craniectomy, PVI increased from 0.76 +/- 0.04 to 1.3 +/- 0.07 ml (+/- standard error of the mean) (p less than 0.001) and increased further to 3.6 +/- 0.17 ml (p less than 0.001) after opening the dura. The resistance to absorption of CSF (Ro), determined by bolus injection, decreased after craniectomy from 91.3 +/- 7.5 to 56.3 +/- 6.2 mm Hg/ml/min (p less than 0.001) and decreased further to 8.9 +/- 0.66 mm Hg/ml/min (p less than 0.001) after opening the dura. Although resistance determined by constant infusion was similar, results were dependent on the rate of infusion. Despite these changes of resistance and PVI, steady-state ICP and sagittal sinus venous pressure were similar in all three conditions of the skull and dura. These studies indicate that changes of the container of the brain affect pressure-volume relationships within the neural axis. However, the changes of resistance to absorption of CSF are in a direction that preserves a steady-state hydrodynamic equilibrium.     

Pression hydrostatique et pathologie neurochirurgicale

Hydrostatic pressure is a force applied by a liquid on the surface of an immersed body. Inside the circulatory system it depends on the weight of the blood column between the heart and a given level. In neurosurgical patients, the hydrostatic pressure plays an important role in cerebral perfusion, transcapillary fluid movements and venous air embolism. The mean arterial pressure (P̄a), the CSF pressure (CSFP) and the pressure in the jugular vein (JVP) are the hydrostatic determiners of the cerebral perfusion pressure (CPP). The hydrostatic pressure gradient associated with head raising decreases P̄a, cerebral venous pressure and JVP, decreases or increases intracranial pressure (ICP) and decreases CPP. The consequences of the resulting hypoperfusion depend on the status of autoregulation. When the skull is open, the pressure under the cerebral retractors determines the transmural pressure and cerebral perfusion. The transcapillary fluid movements depend on a permeability coefficient, a hydrostatic pressure gradient and an osmotic pressure gradient. In case of a rupture of blood brain barrier (BBB), the increase of P̄a and the decrease of ICP (craniotomies) favour the development of vasogenic oedema. When the P̄a stands higher than the upper limit of autoregulation, the hydrostatic capillary pressure increases. It results in a vasodilation, an increase of cerebral blood flow and oedema, the lesion of BBB being initiated by an increase of the amount and the activity of the pinocytotic vesicles in endothelial cells. The syndrome of BBB rupture at a normal CPP is the consequence of an increase in hydrostatic pressure in the dilated capillary territory and can make more difficult the surgical treatment of arterio-venous malformations. Finally, the occurrence of venous air embolism depends on a negative pressure gradient between the head and the right heart, favouring the penetration of air through a venous opening. This gradient is maximal in the conventional sitting position, however air embolism has been described in other neurosurgical postures. The compression of the jugular veins increases the cerebral venous pressure above the atmospheric pressure and has therefore been advocated for decreasing the risk of venous air embolism.     

Experimental feline hydrocephalus. The role of biomechanical changes in ventricular enlargement in cats

In a craniectomy-durectomy model of kaolin-induced feline hydrocephalus, the pressure-volume index (PVI) technique of bolus manipulations of cerebrospinal fluid (CSF) was used to study the biomechanical changes associated with hydrocephalus. Steady-state intracranial pressure (ICP), PVI, and the resistance to the absorption of CSF were determined acutely and 3 to 5 weeks later in hydrocephalic cats and time-matched control cats. Steady-state ICP was 11.0 +/- 2.1 mm Hg (+/- standard deviation) in the hydrocephalic cats, compared to 10.8 +/- 2.2 mm Hg in the chronic control group (p greater than 0.1). The ICP in both the chronic hydrocephalic and chronic control groups was significantly higher (p less than 0.001) than after acute durectomy (mean ICP 8.5 +/- 1.2 mm Hg). Immediately after dural opening, the mean PVI was 3.6 +/- 0.2 ml (+/- standard error of the mean); over time, it decreased to 1.3 +/- 0.1 ml in the chronic control group (p less than 0.001), but remained elevated in the hydrocephalic group at 3.5 +/- 0.4 ml (p less than 0.001). Resistance to CSF absorption was 9.1 +/- 1.4 mm Hg/ml/min immediately after dural opening and increased to 28.8 +/- 4.5 mm Hg/ml/min (p less than 0.001) in the hydrocephalic cats; it increased even further in the chronic measurements in control cats, to 82.3 +/- 9.2 mm Hg/ml/min (p less than 0.001). Ventricular size was moderate to severely enlarged in all hydrocephalic cats, and normal in the control group. These results indicate that the biomechanical profile of the altered brain container model of kaolin-induced feline hydrocephalus resembles that described in hydrocephalic infants. As shown in the control subjects, an absorptive defect alone is not sufficient to cause progressive ventricular enlargement. Increased volume-buffering capacity coupled with a moderate increase of CSF absorption resistance facilitates volume storage in the ventricles.     

Is cerebral perfusion pressure a major determinant of cerebral blood flow during head elevation in comatose patients with severe intracranial lesions?

OBJECT: Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury. METHODS: The effect of 0 degrees, 15 degrees, 30 degrees, and 45 degrees head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro - Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45 degrees, from 46.3+/-4.8 to 28.7+/-2.3 ml x min(-1) x 100 g(-1) (mean +/- standard error, p<0.01), and the PsaMonro - Pj from 80+/-3 to 73+/-3 mm Hg (p< 0.01). The CPP remained stable between 0 degrees and 30 degrees of head elevation, at 62+/-3 mm Hg, and decreased from 62+/-3 to 57+/-4 mm Hg between 30 degrees and 45 degrees (p<0.05). A simulation showed that the 38% decrease in CBF between 0 degrees and 45 degrees resulted from PsaMonro - Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%. CONCLUSIONS: During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45 degrees of head elevation.