Transient Increase In Intracranial Pressure Research Articles

EEG Correlates of Spikes in Intracranial Pressure Caused by Transient Ventriculoperitoneal Shunt Malfunction.

A 30-year-old man with recurrent headaches and seizure-like activity and a 26-year-old woman with worsening headaches were admitted to the hospital. Both had ventriculoperitoneal shunts and history of several shunt revisions for congenital hydrocephalus. The ventricle size visualized on computed tomography scans was unremarkable, and shunt series were negative in both cases. Both patients began to present with brief periods of unresponsiveness, and video electroencephalography at that time showed periods of diffuse delta slowing. Lumbar punctures revealed increased opening pressures. Despite normal imaging and shunt series, both patients ultimately had increased intracranial pressure caused by shunt malfunction. This series demonstrates the difficulty of diagnosing potential transient increases in intracranial pressure based on standard-of-care diagnostics/examination and the potentially critical role for EEG in the identification of shunt malfunction.

The MEK Inhibitor Trametinib Improves Outcomes following Subarachnoid Haemorrhage in Female Rats.

Aneurysmal subarachnoid haemorrhage (SAH) is a haemorrhagic stroke that causes approximately 5% of all stroke incidents. We have been working on a treatment strategy that targets changes in cerebrovascular contractile receptors, by blocking the MEK/ERK1/2 signalling pathway. Recently, a positive effect of trametinib was found in male rats, but investigations of both sexes in pre-clinical studies are an important necessity. In the current study, a SAH was induced in female rats, by autologous blood-injection into the pre-chiasmatic cistern. This produces a dramatic, transient increase in intracranial pressure (ICP) and an acute and prolonged decrease in cerebral blood flow. Rats were then treated with either vehicle or three doses of 0.5 mg/kg trametinib (specific MEK/ERK1/2 inhibitor) intraperitoneally at 3, 9, and 24 h after the SAH. The outcome was assessed by a panel of tests, including intracranial pressure (ICP), sensorimotor tests, a neurological outcome score, and myography. We observed a significant difference in arterial contractility and a reduction in subacute increases in ICP when the rats were treated with trametinib. The sensory motor and neurological outcomes in trametinib-treated rats were significantly improved, suggesting that the improved outcome in females is similar to that of males treated with trametinib.

Ultra-Short Duration Hypothermia Prevents Intracranial Pressure Elevation Following Ischaemic Stroke in Rats.

There is a transient increase in intracranial pressure (ICP) 18–24 h after ischaemic stroke in rats, which is prevented by short-duration hypothermia using rapid cooling methods. Clinical trials of long-duration hypothermia have been limited by feasibility and associated complications, which may be avoided by short-duration cooling. Animal studies have cooled faster than is achievable in patients. We aimed to determine whether gradual cooling at a rate of 2°C/h to 33°C or 1°C/h to 34.5°C, with a 30 min duration at target temperatures, prevented ICP elevation and reduced infarct volume in rats. Transient middle cerebral artery occlusion was performed, followed by gradual cooling to target temperature. Hypothermia to 33°C prevented significant ICP elevation (hypothermia ΔICP = 1.56 ± 2.26 mmHg vs normothermia ΔICP = 8.93 ± 4.82 mmHg; p = 0.02) and reduced infarct volume (hypothermia = 46.4 ± 12.3 mm3 vs normothermia = 85.0 ± 17.5 mm3; p = 0.01). Hypothermia to 34.5°C did not significantly prevent ICP elevation or reduce infarct volume. We showed that gradual cooling to 33°C, at cooling rates achievable in patients, had the same ICP preventative effect as traditional rapid cooling methods. This suggests that this paradigm could be translated to prevent delayed ICP rise in stroke patients.

Transient Increases in Intracranial Pressure After Soccer Heading

Objective To evaluate whether intracranial pressure (ICP) continued to stay elevated in trained athletes 24 hours after soccer heading. Methods Eight male subjects (21.7±1.7 years) were recruited from the UCSD soccer team to participate in the study. Baseline ICP and cardiovascular variables were recorded, and measurements were repeated after subjects underwent the heading trial. Acoustical evoked tympanic membrane displacement was used to estimate ICP, where decreasing volume displacement (-Vm) is associated with an increase in ICP. Mean arterial pressure (MAP) and heart rate (HR) were measured through the volume-clamp method. The heading trial consisted of 6 repeated headers of a soccer ball kicked from 32 meters away into a regulation goal. Follow up measurements of ICP, MAP, and HR were recorded 24 hours after heading trial. Measurements were taken in three randomized positions: 15° head-up tilt (HUT), 0° supine, -15° head-down tilt (HDT). Results At 15° HUT, baseline mean Vm was 37.81±133.21 nL, -20.82±158.27 nL immediately after heading trial (P=0.0482, paired t test), and 27.20±140.61 nL at 24 hours post soccer heading (P=0.1738, paired t test), corresponding to a significant increase in ICP immediately after the heading trial that then returns to baseline levels after 24 hours. At 0° supine, baseline mean Vm was -46.19±178.50 nL, -84.27±183.55 nL after heading trial (P=0.0321, paired t test) and -62.90±135.44 nL at 24 hours post soccer heading (P=0.5048, paired t test), corresponding to the same trend observed in the 15° HUT position. At -15° HDT, mean Vm was -148.48±196.07 nL at baseline, -187.02±186.19 nL after heading trial (P=0.1176, paired t test), and -151.10±174.86 nL at 24 hours post soccer heading (P=0.9329), corresponding to no significant increase in ICP at either time point. MAP and HR did not significantly change at any point after soccer heading. Discussions ICP significantly increased after soccer heading at 15° HUT and 0° supine but returned to baseline levels after 24 hours. ICP at -15° HDT, MAP, and HR did not significantly change immediately after soccer heading or 24 hours after soccer heading. While these results demonstrate a mild increase in ICP that subsides after 24 hours, athletes may experience these transient increases in ICP continuously for extended periods of time during their entire athletic careers. These cycles of increased ICP may result in a state of intermittent but persistently altered cerebral blood flow, which may suggest a health risk of participating in head contact sports such as soccer.

Diagnosis and management of spontaneous cerebrospinal fluid fistula and encephaloceles.

To describe the current state in the diagnosis and management of spontaneous cerebrospinal fluid (sCSF) fistula and encephaloceles. The increased incidence of obesity has resulted in more cases of sCSF fistula and encephaloceles. Obesity results in increased intracranial pressure and a greater chance of developing a sCSF fistula or encephalocele. Obstructive sleep apnea can also result in transient increase in intracranial pressure and has been shown to be common in patients with sCSF fistula. Treatment of CSF fistula is usually necessary because of the increased risk of meningitis. The use of hydroxyapatite bone cements to repair the temporal bone defects has been described with a high success rate of closing the fistula and a low complication rate. Concurrent superior semicircular canal dehiscent can be seen in up to 15% of cases and should be suspected during the surgical approach to avoid potential sensorineural hearing loss and chronic imbalance. sCSF fistula and encephaloceles are an uncommon cause of hearing loss, middle ear effusion, and otorrhea, but should be recognized and repaired because of the risk of meningitis.

Comparison of Effects of Manual and Mechanical Airway Clearance Techniques on Intracranial Pressure in Patients With Severe Traumatic Brain Injury on a Ventilator: Randomized, Crossover Trial.

Physical therapist intervention can play a significant role in the prevention of mechanical and infectious complications in patients with traumatic brain injury (TBI) who are mechanically ventilated. The objective of this study was to observe and compare the effects of manual and mechanical airway clearance techniques on intracranial pressure (ICP) and hemodynamics in patients with severe TBI. The design was a prospective, randomized, crossover trial. The setting was a neurointensive care unit at a level 1 trauma center. Forty-six adult patients aged 18 to 75 years, of either sex, with severe TBI, receiving mechanical ventilatory support with continuous ICP monitoring, and undergoing regular airway clearance techniques participated in this study. Two techniques were performed by a single trained physical therapist. Treatment A was a manual chest percussion technique and treatment B used a mechanical chest wall vibrator. Each treatment was applied for 10 minutes alternately, separated by an interval of 4 hours. ICP was measured from the start of intervention to 10 minutes postintervention. Secondary measurements included cerebral perfusion pressure, heart rate, mean arterial pressure (each from the start of the intervention until 10 minutes postintervention at 1-minute intervals), and arterial blood gas parameters (from just before the start of the intervention and 10 minutes postintervention). The increases in mean (95% CI) intracranial pressure of 2.4 (1.4-3.4) and 1.0 (0.2-1.8) mmHg, during and after the intervention with treatment A, respectively, were statistically significantly higher than for treatment B, irrespective of sequence. In contrast, a mean heart rate rise of 6.4 (3.3-9.5) beats/min and mean arterial pressure rise of 5.3 (2.0-8.6) mmHg were significantly higher only during the intervention phase of treatment A compared with treatment B. Peak mean values of ICP, heart rate, and arterial pressure were also significantly higher during treatment A. However, mean values of cerebral perfusion pressure or its degree of change were statistically comparable in both treatment groups. Patients with high baseline ICP values (>20 mmHg) were excluded, and, because of the crossover design, the effect of individual technique on final (long-term) neurological or respiratory outcomes could not be studied. Manual chest percussion technique in patients with severe TBI was associated with statistically significant transient increases in ICP and hemodynamics, compared with the mechanical method. However, such transient increases in ICP by either technique were not clinically relevant in patients with moderate-to-severe TBI without intracranial hypertension on a mechanical ventilator.

Early analysis of operative management of Chiari I malformation in pediatric cystic fibrosis patients.

Chiari I malformation, defined as herniation of the cerebellar tonsils at least 5mm below the foramen magnum, can result from congenital or acquired pathology. While the mechanism is not well understood, an association between Chiari I and cystic fibrosis has been described in the literature. The lifelong respiratory status management necessitated by cystic fibrosis creates a greater risk of Chiari symptomatology as well as post-operative CSF-related complications in the setting of duraplasty secondary to recurrent transient increases in intracranial pressure. We will review the literature, describe our experience with these patients, and propose bony decompression as an approach to treatment. A retrospective review of pediatric patients treated at our institution with both cystic fibrosis and Chiari I was performed. Since our first case in 2016, our department has evaluated four patients carrying that dual diagnosis. All four underwent posterior fossa decompression surgery. Two patients had incidental pathology. Two symptomatic patients exhibited headaches and/or coordination difficulty. Half of the patients had associated syringomyelia. All patients were offered posterior fossa decompression utilizing intraoperative ultrasound. All four patients underwent posterior fossa decompression without duraplasty. Average operative time was 128min. There were no complications post-operatively. Average hospital stay was 3.8days. Average surgical length of stay was 2.3days. Morbidity and mortality were 0%. The longest follow-up to date is 20months. The two asymptomatic patients remained so post-operatively. The child with headaches and imbalance had complete resolution of his symptoms after surgery, as did the toddler with headaches. Both patients with syringomyelia demonstrated significant decrease in the size of their syrinxes on imaging performed at least 3months post-operatively. Based on the literature and our experience, we recommend considering posterior fossa decompression without duraplasty as treatment for pediatric cystic fibrosis patients with Chiari I malformation. This approach can be effective for symptomatic and prophylactic cases in this particular patient demographic because their comorbidities predispose them to Chiari pathology and symptomatology as well as certain post-operative complications.

A prospective international observational prevalence study on prone positioning of ARDS patients: the APRONET (ARDS Prone Position Network) study.

While prone positioning (PP) has been shown to improve patient survival in moderate to severe acute respiratory distress syndrome (ARDS) patients, the rate of application of PP in clinical practice still appears low. This study aimed to determine the prevalence of use of PP in ARDS patients (primary endpoint), the physiological effects of PP, and the reasons for not using it (secondary endpoints). The APRONET study was a prospective international 1-day prevalence study performed four times in April, July, and October 2016 and January 2017. On each study day, investigators in each ICU had to screen every patient. For patients with ARDS, use of PP, gas exchange, ventilator settings and plateau pressure (Pplat) were recorded before and at the end of the PP session. Complications of PP and reasons for not using PP were also documented. Values are presented as median (1st-3rd quartiles). Over the study period, 6723 patients were screened in 141 ICUs from 20 countries (77% of the ICUs were European), of whom 735 had ARDS and were analyzed. Overall 101 ARDS patients had at least one session of PP (13.7%), with no differences among the 4 study days. The rate of PP use was 5.9% (11/187), 10.3% (41/399) and 32.9% (49/149) in mild, moderate and severe ARDS, respectively (P=0.0001). The duration of the first PP session was 18 (16-23) hours. Measured with the patient in the supine position before and at the end of the first PP session, PaO2/FIO2 increased from 101 (76-136) to 171 (118-220) mmHg (P=0.0001) driving pressure decreased from 14 [11-17] to 13 [10-16] cmH2O (P = 0.001), and Pplat decreased from 26 [23-29] to 25 [23-28] cmH2O (P = 0.04). The most prevalent reason for not using PP (64.3%) was that hypoxemia was not considered sufficiently severe. Complications were reported in 12 patients (11.9%) in whom PP was used (pressure sores in five, hypoxemia in two, endotracheal tube-related in two ocular in two, and a transient increase in intracranial pressure in one). In conclusion, this prospective international prevalence study found that PP was used in 32.9% of patients with severe ARDS, and was associated with low complication rates, significant increase in oxygenation and a significant decrease in driving pressure.

Evidence of Changes in Brain Tissue Stiffness After Ischemic Stroke Derived From Ultrasound‐Based Elastography

Ischemia, edema, elevated intracranial pressure, and reduced blood flow can occur in the brain as a result of ischemic stroke, including contralateral to the stroke via a process known as diaschisis. In this study, ultrasound elastography, an imaging process sensitive to the stiffness of tissue, including its relative fluid content, was used to study changes in the stiffness of individual cerebral hemispheres after transient ischemic injury. Elastographic images of mouse brains were collected 24 and 72 hours after middle cerebral artery occlusion. The shear moduli of both ipsilateral and contralateral brain hemispheres for these mice were measured and compared to corresponding values of control animals. At 24 hours (but not 72 hours) after induction of ischemic stroke, there was a significant decrease in the shear modulus in the ipsilateral hemisphere (P < .01) and a significant increase in the shear modulus in the contralateral hemisphere compared to that of control animals (P < .01). Significant differences were also evident between ipsilateral and contralateral shear modulus values at 24 and 72 hours after infarction (P < .01 for both). The differences between intrahemispheric averages of shear moduli of the brains of animals with stroke at 24 and 72 hours after stroke induction likely reflect the initial formation of edema and reduction of cerebral blood flow known to develop ipsilateral to ischemic infarction, the known transient increase in intracranial pressure, as well as the known initial reduction of blood flow and subsequent development of edema in the contralateral hemisphere (diaschisis). Thus, elastography offers a possible method to detect subtle changes in brain after ischemic stroke.

The Apnea Test: Rationale, Confounders, and Criticism

The apnea test is recommended for the diagnosis of brain death. There are several reasons this test should be reconsidered. Confounding factors for performing the test are vaguely and poorly specified. The following 2 confounders are usually present and not considered: potentially reversible high cervical spinal cord injury and central endocrine failure of adrenal and thyroid axes. There are case reports of breathing at a higher partial pressure of arterial carbon dioxide threshold and cases of recovery of breathing after brain death is diagnosed. The test is dangerous for an injured brain in the setting of high intracranial pressure. It can convert viable penumbral brain tissue to irreversibly nonfunctioning tissue via a transient increase in intracranial pressure and no-reflow phenomena. Hyperoxia during the apnea test can further suppress the function of medullary respiratory rhythm centers. Finally, the philosophical rationale for the need to show lack of spontaneous breathing in brain death is lacking.

Transient Axial Hypotonia and Alteration of Consciousness in an Infant With Chiari I Malformation

This is an 11-months-old girl, who presented to a pediatric neurologist with episodes of “becoming limp with eye deviation to the left and falling backwards while awake.” The first episode occurred 3 weeks before presentation as an isolated event, rapidly became frequent, occurring multiple times a day. The past medical history and development were normal except for mild gross motor delay, as the infant was not sitting unsupported at 10 months. The examination showed mild symmetric hypotonia with normal reflexes. Family history was unremarkable regarding neurological disorders. Magnetic resonance imaging (MRI) of the brain revealed Chiari I malformation with an abnormal T2 signal within the cervical cord, consistent with possible syringomyelia. Electroencephalogram (EEG) showed the presence of spikes in the left temporal region. During the EEG, a typical episode occurred, associated with diffuse delta activity. Because the nature of the events was unclear, and because of the potential need for surgical intervention, the infant was referred for further evaluation. Table 1 summarizes the diagnostic work-up in the hospital. Repeat MRI of the brain and spine, with and without gadolinium, confirmed Chiari I malformation, in which cerebellar tonsils extended approximately 1.5 cm below the foramen magnum. MRI of the cervical spine revealed focal expansion of the spinal cord at C2-C3 level with associated T2 signal changes (Fig 1). The degree of tonsillar ectopia with an abnormal T2 signal within the cervical spinal cord coupled with the developmental motor delay prompted a neurosurgical recommendation of decompressive craniotomy. Additionally, there was the clinical suspicion that the events of axial hypotonia may be caused by transient increases in intracranial pressure due to Chiari I malformation. Several target events were captured on video-EEG during the 7-day admission. Most of these events occurred while the infant was sitting. The infant would start responding poorly to the mother’s voice as well as ignoring the toys presented to her, then sway from side to side and become limp, followed by falling on her back with preserved bilateral finger and feet movements. The events lasted approximately 3 minutes, with a slow return to previous activities. There were no associated changes in respiration or cardiac patterns. Neurological examination showed that the infant was not responsive to verbal and visual stimulation, and there was proximal hypotonia

Intracerebral haemorrhage — initial actions are critical

As newer time-dependent therapies become available for patients with cerebrovascular diseases, emergency physicians must become more comfortable in the diagnosis and management for these patients. This is true of both ischaemic and haemorrhagic stroke. As Marietta and colleagues point out in their excellent review on intracerebral haemorrhage (ICH) [1], airway consideration is always the priority, not only to protect the airway, but also to prevent secondary brain injury from hypoxia and hypercarbia. When intubating, many emergency physicians pre-treat with lidocaine and fentanyl, and some administer a defasciculating dose of vecuronium, all to prevent transient increases in intracranial pressure. While the supporting data for these interventions are weak, there are minimal associated risks. Marietta’s review focuses on the most common causes of ICH — hypertension, cerebral amyloid angiopathy and oral anticoagulant therapy; however, some causes such as aneurysms and arteriovenous malformations can present in an identical fashion, and require definitive therapy. Therefore, cerebrovascular imaging should be considered in selected ICH patients, particularly in young, normotensive ones who are surgical candidates [2]. The current review also discusses the STICH study [3]. This investigation has two important limitations. Firstly, it did not test the hypothesis that very early surgery helps; many patients in the surgical arm did not have their procedure in the first 12 h from onset of symptoms. Secondly, 26% of the patients randomised to conservative treatment later crossed over and had surgery for neurological deterioration. Because they were (by definition) surgical candidates, earlier surgery in this group may have changed the overall results. So, while the STICH study shows that surgical evacuation should not be routinely applied, early neurosurgical consultation is still an important emergency action. The other important recently published study of ICH is a randomised trial of recombinant factor VII [4]. This preliminary study tested various doses of factor VII vs. placebo within 4 h of symptom onset in nearly 400 patients with ICH. There are therapeutic benefits, but as one might anticipate, thromboembolic events (myocardial infarction and stroke) were more common in the treatment group than the placebo group (though not statistically significant − 7% vs. 2%, p=0.12). This drug is very expensive. Emergency physicians ought to be aware of this treatment because some experts have begun to use it off-label. Phase III study results will soon be available but as of January 2007 this treatment is not FDA-approved in the USA for this indication. Blood pressure control is another key issue for emergency physicians. Here, there is a paucity of quality data. While the AHA recommends not treating blood pressure of <180/105 mmHg, decisions must be individualised. It is the cerebral perfusion pressure and the underlying vascular lesion that clinicians must consider. Blind adherence to a specific target blood pressure in all patients may do more harm than good. The PROGRESS trial referred to in the closing paragraph of Marietta’s review refers to secondary stroke prevention using long-term antihypertensives [5]. This should not be misinterpreted as proof that acutely lowering blood pressure improves outcomes in ICH patients. Marietta’s superb review of this important and common problem is well worth reading. Applied intelligently, airway management, blood pressure control, use of pro-thrombotic agents and neurosurgical consultation in the emergency department can have a favourable significant impact on longterm outcomes of patients with ICH.

Regional Anesthesia for a Parturient with Venous Sinus Thrombosis and Placental Abruption Undergoing Fractional Heparin Therapy

THE increased incidence of thrombosis and hypercoagu-lability during pregnancy are well recognized and require anticoagulation for symptomatic sequelae. The following case illustrates our perioperative treatment of a patient with vaginal bleeding while undergoing treatment for a transverse sinus thrombosis.

A SPECTRUM OF EXERTIONAL HEADACHES

Headaches that have an explosive onset with exercise, including sexual activity, generally are benign in origin. A subarachnoid hemorrhage, a mass lesion in the brain, or an anomaly of the posterior fossa must be considered, however. The mechanisms that produce sexually induced or cough headaches of abrupt onset are unknown. It is known, however, that a rapid increase in intrathoracic pressure suddenly reduces right atrial pressure and presumably decreases venous sinus drainage from the brain. This situation results in a transient increase in intracranial pressure. Jaw pain that occurs with chewing often is considered to be TMJ dysfunction when arthritic in quality and if subluxations of the jaw can be shown on the physical examination. Giant cell arteritis and common or external carotid artery occlusive disease should be considered when the pain is ischemic in quality. An anginal equivalent is another possibility. Headaches that worsen with vigorous exercise are commonly migrainous. When their onset is apoplectic with exertion (particularly exertion against a closed glottis), the most likely diagnoses are increased intracranial pressure, a posterior fossa abnormality, or benign exertional headaches. Most cardiac induced headaches, but not all, are of a more gradual onset. If there are significant risk factors for coronary artery disease, an exercise stress test is appropriate. A therapeutic trial of nitroglycerin may help to establish a diagnosis if it improves the headache. Using antimigraine drugs as a diagnostic test is inappropriate because triptans and ergots are contraindicated in the presence of coronary artery disease, and a positive response is not diagnostic of migraine.

Subarachnoid blood infusion versus raised intracranial pressure: Effects on the amino acid pattern in the extracellular fluid of the rabbit hippocampus

In order to evaluate the role of a hemorrhage versus that of a transient increase in intracranial pressure in subarachnoid hemorrhage, the two components were induced separately in rabbits. Extracellular glutamate, sampled from the hippocampus with microdialysis, was used to evaluate the degree of CNS tissue damage. In four rabbits, autologous arterial blood was infused in the cisterna magna in a volume that would not affect the intracranial pressure. The other group of animals was infused with saline to elevate the intracranial pressure from 10 to > 100 mmHg. The increase of intracranial pressure per se did not induce significant changes in extracellular glutamate. However, 20-60 min after infusion of blood, a significant glutamate increase was recorded. Furthermore, aspartate, alanine, glycine and serine were also raised. The results indicate that blood in the subarachnoid space damages the brain primarily by inducing ischemia. Furthermore, the parameters employed gave no indication that an increase in intracranial pressure had a deleterious effect on CNS tissue. [Neurol Res 1999; 21: 404-408]

Preventing transient increases in intracranial pressure.

Preventing transient increases in intracranial pressure.

A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics.

A simple mathematical model of intracranial pressure (ICP) dynamics oriented to clinical practice is presented. It includes the hemodynamics of the arterial-arteriolar cerebrovascular bed, cerebrospinal fluid (CSF) production and reabsorption processes, the nonlinear pressure-volume relationship of the craniospinal compartment, and a Starling resistor mechanism for the cerebral veins. Moreover, arterioles are controlled by cerebral autoregulation mechanisms, which are simulated by means of a time constant and a sigmoidal static characteristic. The model is used to simulate interactions between ICP, cerebral blood volume, and autoregulation. Three different related phenomena are analyzed: the generation of plateau waves, the effect of acute arterial hypotension on ICP, and the role of cerebral hemodynamics during pressure-volume index (PVI) tests. Simulation results suggest the following: 1) ICP dynamics may become unstable in patients with elevated CSF outflow resistance and decreased intracranial compliance, provided cerebral autoregulation is efficient. Instability manifests itself with the occurrence of self-sustained plateau waves. 2) Moderate acute arterial hypotension may have completely different effects on ICP, depending on the value of model parameters. If physiological compensatory mechanisms (CSF circulation and intracranial storage capacity) are efficient, acute hypotension has only negligible effects on ICP and cerebral blood flow (CBF). If these compensatory mechanisms are poor, even modest hypotension may induce a large transient increase in ICP and a significant transient reduction in CBF, with risks of secondary brain damage. 3) The ICP response to a bolus injection (PVI test) is sharply affected, via cerebral blood volume changes, by cerebral hemodynamics and autoregulation. We suggest that PVI tests may be used to extract information not only on intracranial compliance and CSF circulation, but also on the status of mechanisms controlling CBF.

Changes in cerebral hemodynamics after a single dose of clonidine in severely head-injured patients.

alpha 2-Adrenergic agonists induce cerebral vasoconstriction, reduce intracranial pressure (ICP) in experimental animals and may be useful in the hemodynamic management of head-injured patients. We studied the effects of the alpha 2 agonist clonidine on the cerebral circulation in 12 head-injured patients (Glasgow Coma Scale score < 8). Middle cerebral artery flow velocity (MCAV), ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP), were continuously recorded before (T0), at the end (T1), and 30 min after (T2) a 10-min intravenous (i.v.) infusion of 2.5 micrograms/kg clonidine. The cerebral arteriovenous oxygen content difference (AVDO2) and Paco2 were sequentially obtained. ICP, Paco2, AVDO2, and MCAV did not change after clonidine administration. In contrast, MAP and CPP decreased (P < 0.05 and P < 0.05, respectively, at T1 and T2). Three subjects displayed a transient increase in ICP (> 10 mm Hg) at T1; this increase was concomitant with the decrease in MAP. Clonidine administered as an i.v. infusion may induce a critical but transient increase in ICP in some severely head-injured patients. This effect may result from cerebral autoregulatory vasodilation and increased cerebral blood volume as a response to the hypotensive effects of clonidine.

Changes in Cerebral Hemodynamics After a Single Dose of Clonidine in Severely Head-Injured Patients

alpha2-Adrenergic agonists induce cerebral vasoconstriction, reduce intracranial pressure (ICP) in experimental animals and may be useful in the hemodynamic management of head-injured patients. We studied the effects of the alpha2 agonist clonidine on the cerebral circulation in 12 head-injured patients (Glasgow Coma Scale score < 8). Middle cerebral artery flow velocity (MCAV), ICP, mean arterial pressure (MAP), and cerebral perfusion pressure (CPP), were continuously recorded before (T0), at the end (T1), and 30 min after (T2) a 10-min intravenous (IV) infusion of 2.5 micro g/kg clonidine. The cerebral arteriovenous oxygen content difference (AVDO2) and PaCO2 were sequentially obtained. ICP, PaCO2, AVDO2, and MCAV did not change after clonidine administration. In contrast, MAP and CPP decreased (P < 0.05 and P < 0.05, respectively, at T1 and T2). Three subjects displayed a transient increase in ICP (>10 mm Hg) at T1; this increase was concomitant with the decrease in MAP. Clonidine administered as an IV infusion may induce a critical but transient increase in ICP in some severely head-injured patients. This effect may result from cerebral autoregulatory vasodilation and increased cerebral blood volume as a response to the hypotensive effects of clonidine. (Anesth Analg 1997;84:127-32)

Effects of Sufentanil on Cerebral Hemodynamics and Intracranial Pressure in Patients with Brain Injury

The current study investigates the effects of sufentanil on cerebral blood flow velocity and intracranial pressure (ICP) in 30 patients with intracranial hypertension after severe brain trauma (Glasgow coma scale < 6). Mechanical ventilation (FIO2 0.25-0.4) was adjusted to maintain arterial carbon dioxide tensions of 28-30 mmHg. Continuous infusion of midazolam (200 micrograms/kg/h intravenous) and fentanyl (2 micrograms/kg/h intravenous) was used for sedation. Mean arterial blood pressure (MAP, mmHg) was adjusted using norepinephrine infusion (1-5 micrograms/min). Mean blood flow velocity (Vmean, cm/s) was measured in the middle cerebral artery using a 2-MHz transcranial Doppler sonography system. ICP (mmHg) was measured using an epidural probe. After baseline measurements, a bolus of 3 micrograms/kg sufentanil was injected, and all parameters were continuously recorded for 30 min. The patients were assigned retrospectively to the following groups according to their blood pressure responses to sufentanil: group 1, MAP decrease of less than 10 mmHg, and group 2, MAP decrease of more than 10 mmHg. Heart rate, arterial blood gases, and esophageal temperature did not change over time in all patients. In 18 patients, MAP did not decrease after sufentanil (group 1). In 12 patients, sufentanil decreased MAP > 10 mmHg from baseline despite norepinephrine infusion (group 2). ICP was constant in patients with maintained MAP (group 1) but was significantly increased in patients with decreased MAP. Vmean did not change with sufentanil injection regardless of changes in MAP. The current data show that sufentanil (3 micrograms/kg intravenous) has no significant effect on middle cerebral artery blood flow velocity and ICP in patients with brain injury, intracranial hypertension, and controlled MAP. However, transient increases in ICP without changes in middle cerebral artery blood flow velocity may occur concomitant with decreases in MAP. This suggests that increases in ICP seen with sufentanil may be due to autoregulatory decreases in cerebral vascular resistance secondary to systemic hypotension.