Cerebrospinal fluid pressure monitoring after repair of cerebrospinal fluid leaks.

OBJECTIVE: To measure intracranial pressures (ICPs) via lumbar drains after surgical repair of cerebrospinal fluid (CSF) leaks. METHODS: We conducted a retrospective review of ICP measurements through lumbar drains during the immediate postoperative period after CSF leak repair. RESULTS: Eight patients with spontaneous CSF leaks underwent surgery and postoperative CSF pressures were measured via lumbar drains. ICP was elevated in 7/8 patients (mean, 32.5 cm H(2)O). Diuretics reduced ICP (mean, 10 cm H(2)O). Three traumatic CSF leaks patients served as controls (mean, ICP 14 cm H(2)O). CONCLUSION: Measurement of ICP through lumbar drains provides important information regarding the pathophysiology of CSF leaks that has an impact on subsequent medical and surgical treatment. Although the precise cause and mechanism of spontaneous CSF leaks are not fully understood, this study indicates that elevated ICP plays a role and that further medical or surgical treatment to correct the intracranial hypertension may be warranted.     

Ultrasonography of the optic nerve in neurocritically ill patients

The rapid diagnosis of intracranial hypertension is urgently needed for therapeutic reasons in various clinical settings. This can rarely be achieved without invasive procedures such as intracranial pressure (ICP) monitoring or neuroimaging. The optic nerve is surrounded by cerebrospinal fluid (CSF) and dura mater, which forms the optic nerve sheath (ONS). Because of the connection with the intracranial subarachnoid space, ONS diameter (ONSD) is influenced by CSF pressure variations. Bedside ultrasonographic measurement of ONSD has been proposed as a non-invasive and reliable means to detect raised ICP in neurocritically ill patients. In several studies, it proves to have a good correlation with the direct measurement of ICP and a low interobserver variability. However, no general consensus exists over the upper normal ONSD limit. We performed a review of the literature on the use of the ultrasonography of the optic nerve in the evaluation of patients with suspected intracranial hypertension. The aim of this review is to describe the technique and to assess the validity of this diagnostic method.     

Primary empty sella syndrome in a series of 142 patients

OBJECT: The primary empty sella syndrome (ESS) represents a heterogeneous clinical picture characterized by endocrine disturbances and signs of intracranial hypertension. An increase in intracranial pressure (ICP) is proposed to be one of the involved pathogenetic factors. METHODS: The series included 142 patients who were observed during a period of 20 years. All patients underwent an ICP and cerebrospinal fluid (CSF) dynamics evaluation through the use of a lumbar constant-rate infusion test. Impairment of ICP and CSF dynamics was observed in 109 patients (76.8%). In 35 of the 36 patients affected by severe intracranial hypertension without rhinorrhea, improvement in adverse neurological symptoms was achieved after implanting a CSF shunt. Visual function, already seriously compromised before surgery, remained severely altered in one patient. In the group of 34 patients affected by rhinorrhea, CSF leakage was controlled using different surgical treatments: CSF shunt placement in 16 cases, surgical repair of the sellar floor in three, and both procedures in the remaining 13. Two patients refused any surgical treatment. CONCLUSIONS: The role of increased ICP in the pathogenesis and perpetuation of primary ESS has been confirmed. Adverse neurological signs and a CSF leak are correlated with an actual increase in ICP and are relieved after CSF shunt insertion. Cerebrospinal fluid rhinorrhea is more common than generally thought. Its resolution can be achieved using a careful diagnostic protocol and sometimes may require different surgical procedures.     

Management of head injury. Treatment of abnormal intracranial pressure.

Intracranial hypertension is recognized as a fundamental pathophysiologic process in brain injury. Although the exact pressure level defining intracranial hypertension remains to be firmly established, the majority of evidence available currently suggests that ICP should generally be treated when it exceeds 20 mm Hg. We suggest that lesions in the temporal lobe be treated at 15 mm Hg owing to the special relationship of this region to the brain stem. Along with the individual intracranial pressure reading, however, the course of the pressure over time and the status of the intracranial compliance as reflected in the ICP waveform must be considered when evaluating the intracranial dynamics. There is mounting evidence that patients with intracranial hypertension may comprise a heterogeneous group and that subgroups differ in their optimal treatment strategies. Although we cannot as yet identify such groups, factors such as age, CT diagnosis, responsiveness to hyperventilation, pressure-volume index, and ICP waveform are emerging as important differentiating factors. In particular, young patients with absent perimesencephalic cisterns and a tight brain on CT scan who manifest intracranial hypertension may comprise a group more suitable for treatment with hyperventilation and hypnotics than with osmotic agents. Although this is yet to be firmly established, currently it should be considered when such a patient responds poorly early in the course of conventional therapy for raised ICP. Treatment of intracranial hypertension remains rooted in the conventional therapeutic maneuvers. Maintenance of the basic homeostatic state of the patient is to be supplemented with head elevation, sedation, pharmacologic paralysis, hyperventilation, CSF drainage, and osmotic therapy as indicated. Outside of the special considerations discussed earlier, barbiturates should only be considered in patients with refractory intracranial hypertension without preexisting cardiovascular contraindications. Although several other agents have shown promise, currently the most exciting agent appears to be etomidate, which may prove quite useful. As ICP is better defined and understood, many significant and experimentally approachable questions are recognized. The basic mechanisms of raised ICP are slowly becoming elucidated. Clinical clues with which to subdivide patients with intracranial hypertension are being defined. New agents with efficacy in lowering raised ICP are appearing, and determination of their mechanisms of action may provide insight into the underlying disorder.     

Changes in the cerebrospinal fluid pulse wave spectrum associated with raised intracranial pressure

The frequency spectrum of the cerebrospinal fluid (CSF) pulse and the amplitude transfer function between arterial and CSF pressures were measured from the cisterna magna of anesthetized, artificially ventilated cats when the intracranial pressure (ICP) was raised by saline infusion. The spectrum of CSF pulsation was composed of a fundamental and three higher harmonic waves. The amplitude and the amplitude transfer function of each spectral component revealed significant positive correlation with ICP and negative correlation with cerebral perfusion pressure (CPP). Both the amplitude and the transfer function of the fundamental CSF pulse wave showed an exponential correlation with ICP and CPP. A distortion factor of the CSF pulse wave, a measure of its difference from a simple sine wave, was calculated from the spectral components. This showed that distortion of the CSF pulse wave was rapidly and progressively reduced as the ICP rose to 50 mm Hg and then was reduced less thereafter.     

Hirndruck und Hirnödem

In primary and secondary brain diseases, increasing volumes of the three compartments of brain tissue, cerebrospinal fluid, or blood lead to a critical increase in intracranial pressure (ICP). A rising ICP is associated with typical clinical symptoms; however, during analgosedation it can only be detected by invasive ICP monitoring. Other neuromonitoring procedures are not as effective as ICP monitoring; they reflect the ICP changes and their complications by other metabolic and oxygenation parameters. The most relevant parameter for brain perfusion is cerebral perfusion pressure (CPP), which is calculated as the difference between the middle arterial pressure (MAP) and the ICP. A mixed body of evidence exists for the different ICP-reducing treatment measures, such as hyperventilation, hyperosmolar substances, hypothermia, glucocorticosteroids, CSF drainage, and decompressive surgery.     

The role of CSF ventricular drainage in controlling intracranial hypertension in patients with brain lesions. Comparison of three methods. Preliminary results.

Results obtained with three different CSF ventricular drainage methods (intermittent with no outflow resistance, continuous against a positive pressure, continuous with pre-arranged positive pressure), were evaluated in fifty nine cases of traumatic cerebral lesions and spontaneous intracerebral hematomas with intracranial hypertension. Continuous CSF withdrawal gives better clinical results and is more effective in controlling intracranial pressure than intermittent drainage (50% vs 13% successes respectively). Results obtained with continuous drainage against a steady positive pressure and with a pre-arranged pressure ("tidal drainage") are almost similar. However an outflow resistance 3-5 mmHg higher than diastolic level of ICP represents a rational approach to the problem.     

Relationships between intracranial pressure, ventricular size, and resistance to CSF outflow

In 230 patients with normal-pressure hydrocephalus, high-pressure hydrocephalus, or benign intracranial hypertension, measurements of the intracranial pressure (ICP), ventricular size, and cerebrospinal fluid (CSF) outflow resistance (Ro) have revealed a linear relationship between ICP and Ro. It is shown that on average the CSF formation rate tends to decrease with increasing ICP. It is also shown that the size of the ventricles increases as the ICP levels off toward normal values. The clinical implication of this is that a small or normal ventricular size in acute or subacute phases does not preclude defective CSF resorption.     

Intracranial pressure effects on auditory evoked responses in the rabbit: preliminary report

Acute elevated intracranial pressure (ICP) effects on the auditory evoked response (AER) were studied in the rabbit. Simultaneous CSF infusions to increase ICP and contralateral ICP pressure recordings were done through bilateral ventriculostomies. During rarefaction auditory stimulation, a minicomputer obtained a time-locked AER from ongoing electroencephalographic activity at base line ICP mean pressure and at three levels of increased ICP (250, 500, and 700 mm CSF) above base line. The results showed a statistically significant increased latency of the N3-P3 portion of the AER as well as of the P1-P3 central conduction time. The amplitude of AERs appeared unchanged. The effect is reversible and presumably is a neuropraxic type pressure effect on brain stem auditory pathways. Its clinical relevance is discussed.     

Spectrin breakdown products in the cerebrospinal fluid in severe head injury – preliminary observations

Summary Background. Calcium-induced proteolytic processes are considered key players in the progressive pathobiology of traumatic brain injury (TBI). Activation of calpain and caspases after TBI leads to the cleavage of cytoskeletal proteins such as non-erythroid alpha II-spectrin. Recent reports demonstrate that the levels of spectrin and spectrin breakdown products (SBDPs) are elevated in vitro after mechanical injury, in the cerebrospinal fluid (CSF) and brain tissue following experimental TBI, and in human brain tissue after TBI.Methods. This study was initiated to detect spectrin and SBDP accumulation in the ventricular CSF of 12 severe TBI-patients with raised intracranial pressure (ICP). Nine patients with non-traumatically elevated ICP and 5 undergoing diagnostic lumbar puncture (LP) served as controls. Intact spectrin and calpain and caspase specific SBDPs in CSF collected once a day over a several day period were assessed via Western blot analysis. Parameters of severity and outcome such as ICP, Glasgow Coma Scale and Glasgow Outcome Scale were also monitored in order to reveal a potential correlation between these CSF markers and clinical parameters.Results. In control patients undergone LP no immunoreactivity was detected. Non-erythroid alpha-II-spectrin and SBDP occurred more frequently and their level was significantly higher in the CSF of TBI patients than in other pathological conditions associated with raised ICP. Those TBI patients followed for several days post-injury revealed a consistent temporal pattern for protein accumulation with the highest level achieved on the 2^nd –3^rd days after TBI.Conclusion. Elevation of calpain and caspase specific SBDPs is a significant finding in TBI patients indicating that intact brain spectrin- and SBDP-levels are closely associated with the specific neurochemical processes evoked by TBI. The results strongly support the potential utility of these surrogate markers in the clinical monitoring of patients with severe TBI and provide further evidence of the role of calcium-induced, calpain- and caspase-mediated structural proteolysis in TBI.     

Low pressure hydrocephalus and ventriculomegaly: hysteresis,non-linear dynamics,and the benefits of CSF diversion

Low pressure hydrocephalus (LPH) is a rare clinical condition. We report our experience with 10 patients treated at the Johns Hopkins Hospital. We reviewed the records of 10 patients (five men, five women; mean age 43 years) treated between 1996 and 2000. All underwent intracranial pressure (ICP) monitoring and subatmospheric cerebrospinal fluid (CSF) drainage with an intraventricular or lumbar catheter. All patients developed ventriculomegaly: five following aneurysmal subarachnoid haemorrhage; one after meningitis; one after intraventricular haemorrhage. Three patients presented with chronic aqueductal stenosis. Ventriculomegaly was clinically detected on average 12 days after presentation. Mean ICP was 4.8 mmHg (range 0-10). All patients improved only in the setting of negative pressure CSF drainage, and were subsequently treated with low pressure ventriculo- or lumboperitoneal shunts. At 1 year, eight patients (80%) showed good recovery to minimal disability; seven patients (70%) had resolving ventriculomegaly. The mechanism of low pressure hydrocephalus remains unclear. In our cohort, different aetiologies were responsible for the change in compliance/elastance of the brain parenchyma and subsequent development of ventriculomegaly. We propose that while ventriculomegaly (and therefore neuronal dysfunction) can be initiated in the setting of high ICP, the maintenance of ventriculomegaly at normal or low ICP is a physiological example of hysteresis. This behaviour, which has been characterized by the chaos theory of non-linear dynamics as a Hopf bifurcation, explains how a system can exhibit two different states (ventricular size) at a single parameter value (ICP). Most importantly, it helps to explain how lowering ICP in the setting of LPH can resolve ventriculomegaly and its neurologic sequelae.     

Brain oedema,intracranial pressure and cerebral blood flow

Brain oedema leads to pathological changes in intracranial pressure (ICP) and cerebral blood flow in a wide range of clinical scenarios, because the brain produces oedema in response to many diseases. Clinical management often focuses on minimizing elevations of ICP and maintaining adequate cerebral blood flow. A working knowledge of physiological principles linking brain oedema, ICP and blood flow is essential for clinicians facing these clinical problems. These principles are explained here, and also some insights are provided concerning the mechanisms of disease on the cellular level. This is then applied to the clinical problem of traumatic brain injury illustrating physiological principles in clinical practice.     

Intracranial venous sinus hypertension: cause or consequence of hydrocephalus in infants?

From a previous study of achondroplasia as well as from the observation of patients with hydrocephalus associated with craniostenosis, the authors have concluded that an increased superior sagittal sinus venous pressure (SSVP) could be the cause of the enlarged ventricles. However, other workers have demonstrated that an increased SSVP could be the consequence of increased intracranial pressure (ICP). Therefore, the authors undertook a study to determine if there was a physiological test that could distinguish between rare instances of increased SSVP caused by structural and irreversible narrowing of the sinus and those caused by increased ICP. In 20 hydrocephalic infants and children, pressure was simultaneously measured in the lateral ventricle, the superior sagittal sinus, and the jugular vein. Stable baseline pressures were recorded, as well as the variations observed after the withdrawal of an amount of cerebrospinal fluid (CSF) sufficient to lower ICP to zero. Similar recordings were taken after reinjection of an equal quantity of CSF. In all of the patients, SSVP was increased, but not as much as the ICP. In the cases of hydrocephalus without any associated cranial malformation, and therefore without any likely anatomical interruption of the sinus, CSF withdrawal induced a simultaneous decrease of ICP and SSVP. However, whereas ICP could be lowered to zero, SSVP never fell below the jugular venous pressure, which remained stable (around 5 mm Hg) throughout the recording session. Results were different when sinography demonstrated an anatomical interruption of the sinus, as in cases of hydrocephalus associated with achondroplasia or craniostenosis. In these cases, although ICP was normally lowered by CSF withdrawal, SSVP remained nearly unchanged, usually greater than the jugular venous pressure. The present study demonstrated that SSVP recording during ICP variations induced by CSF withdrawal permits differentiation between a reversible collapse of the sigmoid sinus due to increased ICP and a fixed obstructive lesion of the sinuses. Based upon this test and the results of sinography, the authors inserted a venous bypass between the lateral sinus and a jugular vein in three patients.     

The impact of raised intracranial pressure on cerebral venous hemodynamics: a prospective venous transcranial Doppler ultrasonography study.

OBJECT: The effect of increased intracranial pressure (ICP) on cerebral venous blood flow has been the subject of very few clinical and experimental studies. The authors assessed the usefulness of venous transcranial Doppler (TCD) ultrasonography as a noninvasive monitoring tool for predicting raised ICP. METHODS: Serial venous TCD studies of the basal vein of Rosenthal and the straight sinus (SS) were prospectively performed in 30 control volunteers and 25 patients with raised ICP. Correlations with ICP data were calculated using a multivariate regression model. Venous blood flow velocities (BFVs) in the basal vein of Rosenthal showed, within a certain range, a linear relationship between mean ICP and maximal venous BFV (r = 0.645; p<0.002). Moreover, a linear relationship was found for maximal venous BFVs in the SS and mean ICP (r = 0.928; p<0.0003). CONCLUSIONS: Venous TCD studies may provide an additional noninvasive monitoring tool for raised ICP and give further insights into the cerebral venous hemodynamics present during raised 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.     

Multiparametric monitoring of brain under elevated intracranial pressure in a rat model

Intracranial hypertension may develop in most patients exposed to traumatic head injury. In many cases, patients enduring elevated intracranial pressure (ICP) will incur morbidity or mortality. Several methods are used in animal models to investigate the influence of ICP elevation on physiological parameters. In this study, we developed a cisterna magna model by adding a mechanism for warming the mock cerebrospinal fluid (CSF) entering the cisterna space to a temperature of 37 degrees C and combined this method for ICP elevation with the multiparametric monitoring system (Multiprobe Assembly [MPA]). Using the MPA, we monitored, for the first time, mitochondrial NADH redox state as well as ionic homeostasis under elevated ICP in a rat model. In addition, we monitored cerebral blood flow (CBF) by laser Doppler flowmetry, ECoG (bipolar electrodes), and surface temperature. Blood pressure was measured in the cannulated femoral artery. The ICP (monitored by Camino probe) was elevated to 50-60 mm Hg for 13-15 min, followed by 2 h of recovery. The results show that CBF was decreased by 90%, while NADH was elevated by 80% as compared to the normoxic levels. Complete depolarization occurred as evidence by the decrease in extracellular Ca2+ and a significant increase in K+. All parameters recovered 10 min after reopening the cannula to the cisterna magna to air pressure. We conclude that ICP elevation through the cisterna magna infusion method, used simultaneously with multiparametric monitoring, supplies reliable information on the brain tissue metabolic state with intracranial hypertension in a rat model.     

Recirculatory spinal subarachnoid perfusions in dogs: a method for determining CSF dynamics under non-steady state conditions

Open-ended ventriculocisternal perfusion techniques for determining cerebrospinal fluid production and absorption rates are severely restricted by the absolute requirement that steady state conditions be present. A new closed recirculatory spinal perfusion technique is described. Because steady state equilibrium is not necessary, numerous determinations at multiple intracranial pressures or under varied experimental conditions are possible within relatively brief perfusion periods. Cerebrospinal fluid (CSF) and nondiffusible albumin tracer are rapidly recirculated through the spinal subarachnoid space in a cephalad direction. The concentration of fluorescein-tagged albumin is continuously monitored as the CSF is circulated through a fluorometric flow cell. Measured continuously, intracranial pressure (ICP) is regulated by changing the volume of the external perfusion circuit with a syringe pump connected in series to the recirculatory spinal perfusion. CSF formation and absorption rates are calculated from measurements of albumin concentration, concentration changes with time, ICP, syringe pump infusion rate, and the external perfusion circuit volume. In dogs, data can be collected after only 45 minutes for mixing; perfusions at four or five intracranial pressures in addition to normal resting pressure can be completed within 2 to 3 hours. The data from 15 perfusions in 14 dogs are presented. The method provides normal resting pressure values of CSF production and absorption consistent with those values in the literature determined by traditional ventriculocisternal perfusion techniques. Determinations at multiple intracranial pressures suggest a proportional relationship between absorption and ICP. No consistent acute change in CSF formation with pressures to 50 mm Hg can be inferred from these data.     

Nitrous oxide withdrawal reduces intracranial pressure in the presence of pneumocephalus

Nitrous oxide anesthesia has been implicated as contributing to the development of delayed tension pneumocephalus following surgery performed in the sitting position. The authors tested the hypothesis that withdrawal of nitrous oxide anesthesia administered during formation of an intracranial gas cavity would lead to a decrease in intracranial pressure (ICP) as N2O diffuses from the cavity back into the blood. Ten halothane-anesthetized rabbits were prepared for measurement of supracortical ICP and arterial blood pressure (BP) and for intracranial volume alterations via a cisterna magna infusion catheter. Hyperventilation (Paco2 = 28-30 mmHg) and mannitol were used to shrink the brain to accommodate intracranial infusion of either air or lactated Ringer's (LR) solution, which was used to elevate ICP to between 10-15 mmHg from a baseline ICP of 2.1 +/- 2.5 mmHg over a period of 8 to 10 min. Following stabilization at an elevated ICP, inhalation of nitrous oxide (75%) was either initiated or withdrawn (if already present during the induced ICP increase) and the subsequent changes in mean ICP and BP were recorded. Following ICP elevation with LR to 10 +/- 1 mmHg, initiation of 75% N2O administration resulted in no change in ICP and modest increases (P less than 0.05) in BP and cerebral perfusion pressure (CPP = BP - ICP) after 4 min. However, when ICP was raised (to 12 +/- 3.5 mmHg) with intracranial air infusion, subsequent initiation of 75% N2O inhalation caused an abrupt ICP increase to 22.3 +/- 9 mmHg (from control P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

CSF dynamics in patients with subarachnoid and/or intraventricular hemorrhage

The purpose of this study was to examine the extent to which reduction of cerebrospinal fluid (CSF) absorption contributes to raised intracranial pressure (ICP) in patients with acute subarachnoid hemorrhage (SAH). Seventeen patients suffering from SAH and/or intraventricular hemorrhage were studied; all were admitted in Grades II to V according to Hunt and Hess. Eleven patients had a proven aneurysm. The ICP, monitored via an intraventricular catheter, was above 15 mm Hg (2 kPa) during part of the monitoring period in all patients. B-waves at 1/min were noted in all patients. Resistance to outflow of CSF was determined by the following techniques: 1) bolus injection; 2) constant-rate steady-state infusion; or 3) controlled withdrawal ("inverse infusion"). Resistance to outflow of CSF was increased in all patients, ranging from 11.5 to 85 mm Hg/ml/min. The ICP was linearly correlated with outflow resistance. Four (50%) of the eight survivors required a shunt. Neither the presence of hydrocephalus on admission, nor the level of ICP, nor the magnitude of resistance to outflow of CSF was clearly related to the requirement of a permanent CSF diversion.     

Detection and monitoring of intracranial pressure dysregulation in liver failure by ultrasound

BACKGROUND: Development of elevated intracranial pressure (ICP) in hepatic failure indicates poor prognosis. Its detection by invasive methods poses methodological problems. We applied ultrasound studies of the optic nerves to noninvasively estimated ICP status. METHODS: A total of 22 pediatric patients with hepatic failure were examined by serial B scan ultrasound and followed up clinically. Outcome was scored as survival or death due to multiorgan failure (MOF) or raised ICP. In 18 patients, transplantations were performed. RESULTS: Four patients died before transplantation was possible (raised ICP: n=3, MOF: n=1). After OLT there were 10 survivors and 8 patients died (MOF: n=3, raised ICP: n=5). In 10 patients we found optic nerve sheath diameter (ONSD) above normal limits. Eight patients died, mostly because of raised ICP (n=7). Only 2 of the 10 survivors experienced a transient ONSD increase, steadily normalized after transplantation. Preoperatively, normal ONSD was detected in four of seven patients. The outcome of these four cases was clearly superior (three survivors and one MOF) compared with abnormal pre-OLT ultrasound findings (raised ICP: n=3). CONCLUSION: Patients with poor prognosis related to raised ICP in pediatric liver failure can be identified by ultrasound measurement of ONSD without the disadvantages of invasive procedures. Although the exact intracranial pressure level cannot be deduced from single examinations, ONSD trends can reflect the evolution of ICP in hepatic encephalopathy.