Increase In Increased Intracranial Pressure Research Articles

Changes in mesenteric blood flow during intracranial hypertension due to acute elevations in intra-abdominal pressure

Elevated intra-abdominal pressure (IAP) has been associated with increased intracranial pressure (ICP) and diminished splanchnic blood flow. We investigated superior mesenteric artery flow and ICP following an increase in IAP. A flowmeter was placed on the superior mesenteric artery in five pigs and ICP was measured with an intraparenchymal bolt. IAP was elevated to 10 and 20 mmHg with nitrogen pneumoperitoneum. Changes in ICP, central venous pressure, mean arterial blood pressure and superior mesenteric artery blood flow were recorded at each level of IAP. Analysis of variants and paired t-test analyses were performed. ICP was increased and superior mesenteric artery flow decreased following IAP elevation. These changes were statistically significant when IAP was raised to 20 mmHg (ICP: p = 0.02; superior mesenteric artery flow: p = 0.006); central venous pressure was also increased. There was no significant change in mean arterial blood pressure and cerebral perfusion pressure. We have demonstrated a simultaneous effect of IAP on ICP (increase) and superior mesenteric artery blood flow (decrease). Further studies are warranted to evaluate the complete mechanism of these findings. In addition to direct transmission of pressures from the abdominal cavity, indirect effects of intra-abdominal hypertension may play a role in these documented changes.

Migraine with pleocytosis: a case of atypical progression

AIMS. Migraine with cerebrospinal fluid pleocytosis is a clinical pattern consisting in intermittent headaches accompanied by episodes of transient neurological deficit and lymphocytic pleocytosis, which last for varying lengths of time and have a spontaneous resolution. We describe the case of migraine with pleocytosis (MP) with atypical progression that responded well to corticoids. CASE REPORT A 27-year-old male with no familial or personal history of migraine who began with bouts of intense headaches that were preceded by neurological deficit (dysphasia and hemiparesis of the right-hand side) lasting varying amounts of time (including hours). The serial study of cerebrospinal fluid (CSF) revealed a notable degree of lymphocytosis (400/mm3) with increased intracranial pressure (ICP) (> 30 mmHg). The other explorations that were performed (microbiological study of CSF and blood, humoral and cellular immunity, MR angiography and thyroid hormones, among others) were all normal. The neurological exploration carried out in the following days revealed a mild paresis of the right lateral rectus muscle, which was attributed to the intracranial hypertension and which clearly disabled the patient. As a consequence of the recurrence of the seizures and the long-lasting increase in ICP, therapy was begun with 1 mg/kg/day of prednisone, at a descending rate; clinical remission and normalisation of the CSF was achieved within a period of two months. Discussion. We describe this case of MP because of how atypical the progression was (paresis of the right abducent nerve secondary to the increase in ICP) and the possibility of associating corticoids in cases in which the benignity of the entity is in doubt.

Intracranial hypertension in acute liver failure: pathophysiological basis of rational management.

Increased intracranial pressure (ICP) in patients with acute liver failure (ALF) remains a major cause of morbidity and mortality. Conventional methods of ammonia reduction such as the use of lactulose do not improve outcome, and metabolic substrates such as L-ornithine L aspartate may offer more promise. Mannitol remains the mainstay of therapy. An important role for cerebral hyperemia in the pathogenesis of increased ICP has led to a reevaluation of established therapies such as hyperventilation, N-acetylcysteine, thiopentone sodium, and propofol. Recent studies have focused on the role of systemic inflammatory response in the pathogenesis of increased ICP and support the use of antibiotics prophylactically. Moderate hypothermia reduces ICP in patients with uncontrolled intracranial hypertension and prevents increases in ICP during orthotopic liver transplantation (OLT). Advances in understanding the pathophysiological basis of intracranial hypertension in ALF have outstripped appropriate testing of the newly generated ideas in appropriate clinical trials, and more effort should be mounted at a national level to organize the appropriate multicenter studies required.

Does Propofol Improve Postischemic Myocardial Dysfunction by Reducing the Postischemic Adhesion of Polymorphonuclear Neutrophils?

Background: Fluid replacement after hemorrhage usually results in hemodilution, and hemodilution leads to increased cerebral blood flow, which is known to be beneficial to the outcome of ischemic brain damage. However, the effect of hemodilution may be different in patients with head injuries and increased intracranial pressure (ICP). The aim of this study was to evaluate the effects of normovolemic hemodilution on cerebral blood flow (CBF), brain tissue oxygen tension (), and the severity of cryogenic brain injury, and to determine the acceptable limit of hemodilution during cryogenic brain injury. Methods: Thirty New Zealand white rabbits were anesthetized with -isoflurane. Cryogenic brain injury (1 cm in diameter) was produced by applying liquid nitrogen on the surface of the right parietal bone for 90 seconds. Sixty minutes after cryogenic brain injury, acute normovolemic hemodilution was induced with 10% pentastarch for 30 minutes. In group I (n = 7), hemodilution was not induced. In groups II (n = 7), III (n = 8), and IV (n = 8), the hemoglobin concentrations were adjusted to 9-10, 6-7 and 3-4 g/dl, respectively. Mean arterial pressure, central venous pressure and ICP were measured, and local CBF and of the right parietal subcortex were continuously monitored. The rabbits were euthanized 150 minutes after brain injury, and the brains were removed and sectioned coronally through the center of the lesion. The extent of brain injury in the coronal plane was measured by light microscopic examination. The posterior part of the brain was divided into two halves and the water fraction of each part was measured by the dry-weight method. Data obtained were compared by the Kruskal-Wallis test or by repeated measures ANOVA. The difference was considered significant when P ＜ 0.05. Results: No differences were observed in mean arterial pressure, central venous pressure or rectal temperature. However, significant differences were found in ICP, CBF and among the groups. ICP was significantly higher in group IV than in groups I and II. The CBF values of groups III and IV were higher than those of group I. The values of of group IV were lower than those of groups I and II. Normovolemic hemodilution, of up to 6-7 g/dl of hemoglobin, led to an abrupt increase in CBF and a subsequent increase in ICP. Hemodilution, of up to 3-4 g/dl of hemoglobin, decreased brain tissue oxygen tension significantly. No differences in the brain water fractions and the extent of cryogenic injury were found among the groups. Conclusions: It is concluded that the acceptable limit of acute normovolemic hemodilution in cryogenic brain injury is 9-10 g/dl of hemoglobin, as ICP and CBF do not increase and does not deteriorate.

Controlled drainage of lumbar cerebrospinal fluid for the management of increased intracranial pressure in patients with subarachnoid hemorrhage

Intercranial hypertension represents a significant complication in patients with severe subarachnoid hemorrhage (SAH) from aneurysm rupture. In the acute state of SAH, increased intracranial pressure (ICP) is usually due to the direct effect of the initial hemorrhage. Over the following days, ICP may rise as a result of cerebral ischemia from developing vasospasm. Management protocols for intercranial hypertension include hyperventilation, use of mannitol ventricular cerebrospinal fluid (CSF) drainage, sedation, hypertonic saline, barbiturate coma, and decompressive surgery. In addition to these measures, we have introduced lumbar CSF drainage for the control of malignant hypertension over the last 3 years. A total of 21 patients included. All had SAH from ruptured aneurysm and underwent early surgery. Postoperative increase of ICP was treated according to a standard protocol. When all other measures had failed, lumbar CSF drainage was initiated under continuous ICP monitoring. In all patients, this resulted in an immediate decrease of ICP and an increase of cerebral perfusion pressure (CPP). Lumbar drainage was continued for a mean of 4.8 days, and without exception, resulted in lasting control of elevated ICP. In two patients with absent basal cisterns before treatment, transient herniation of the brain resulted from lumbar drainage. We conclude that controlled lumbar CSF drainage represents an effective method to control refractory intercranial hypertension in carefully selected patients.

Detection of intracochlear and intracranial pressure changes with otoacoustic emissions: a gerbil model

Increased intracranial pressure (ICP) is known to affect the phases and levels of lower-frequency distortion-product otoacoustic emissions (DPOAE) in a characteristic manner suggestive of an increase in the stiffness of the stapes system, likely in relation to an attendant increased intracochlear pressure (ICoP). DPOAEs may thus provide an easy non-invasive means of gaining access to the otherwise elusive ICoP. However, the mechanisms by which DPOAEs actually relate to ICoP are unclear and may involve changes in the stiffness of the annular ligament, stapedius muscle and even some indirect contributions of other parts of the middle ear such as the tensor tympani. A systematic study of the role of each middle-ear element on ICoP-to-DPOAE relationships as a function of frequency was undertaken in gerbils under direct control of ICP via an intracranial catheter (from 0 to 500 daPa). After the bulla was widely opened, the tendons of the stapedius and tensor tympani muscles were severed in turn. A standard electroacoustic analog model of the middle ear was used for predicting the forward and reverse middle-ear transfer-functions changes under different experimental manipulations and their consequences on DPOAEs. The observed DPOAE changes chiefly consisted in a phase-lead peaking around 2.15 kHz in closed-bulla, and 1.2 kHz in open-bulla conditions. It was proportional to ICP increase provided ICP exceeded a threshold of about 50 daPa. The profiles of DPOAE shifts matched those derived from the premise that ICoP mainly induced a change in the stiffness of the stapes system. The possible involvement of the stapedius muscle was ruled out by the absence of any effect of cutting its tendon so that the intrinsically non-linear stiffness of the annular ligament must have been the main factor. A relatively minor contribution from the tensor tympani was observed, possibly in relation to the detection of ICoP-induced displacement of the ossicular chain by neuromuscular spindles.

Intracranial effects of endotracheal suctioning in the acute phase of head injury.

In patients with head injury, endotracheal suctioning (ETS) is a potentially dangerous procedure, because it can increase intracranial pressure (ICP). The purpose of this prospective nonrandomized study was to evaluate the impact of ETS on intracranial dynamics in the acute phase of head injury. Seventeen patients with severe head injury (Glasgow Coma Score < or = 8, range 4-8), sedated and mechanically ventilated, were studied during the first week after trauma. Single-pass ETS maneuver (with a 16-French catheter, negative pressure of 100 mm Hg, and duration of less than 30 seconds) was performed 60 seconds after the FiO2 was increased to 100%. After ETS, FiO2 was maintained at 100% for another 30 seconds. Before and after ETS, arterial blood gases and jugular oxygen saturation (S(j)O2), ICP, and mean arterial pressure (MAP) were measured and cerebral perfusion pressure (CPP) was calculated. A total of 131 ETS episodes, which consisted of repeated assessment of each patient, were analyzed. Six patients in 20 cases coughed and/or moved during ETS because of inadequate sedation. After ETS, ICP increased from 20 +/- 12 to 22 +/- 13 mm Hg in well-sedated patients and from 15 +/- 9 to 28 +/- 9 mm Hg in patients who coughed and/or moved (mean change, 2 +/- 6 versus 13 +/- 6 mm Hg, P <.0001). CPP and S(j)O2 increased in well-sedated patients (from 78 +/- 16 to 83 +/- 19 mm Hg, and from 71 +/- 10 to 73 +/- 13%, respectively) and decreased in patients who reacted to ETS (from 79 +/- 14 to 72 +/- 14 mm Hg and from 69 +/- 7 to 66 +/- 9%, respectively), and the differences were significant (mean change, CPP: 5 +/- 14 versus -7 +/- 15 mm Hg, P =.003; (S(j)O2) 2 +/- 5 vs. -3 +/- 5%, P <.0001). In well-sedated patients, endotracheal suctioning caused an increase in ICP, CPP, and S j O 2 without evidence of ischemia. In contrast, in patients who coughed or moved in response to suctioning, there was a slight and significant decrease in CPP and S(j)O2. In the case of patients with head injuries who coughed or moved during endotracheal suctioning, we strongly suggest deepening the level of sedation before completing the procedure to reduce the risk of adverse effects.

Endoscopic endocrine neck surgery with carbon dioxide insufflation: the effect on intracranial pressure

Abstract Background The endoscopic approach to the thyroid and parathyroid glands requires insufflation with carbon dioxide at 10–15 mmHg. This may decrease the cerebral venous return and increase intracranial pressure (ICP). The aim of this study was to evaluate the effect of carbon dioxide neck insufflation on ICP and haemodynamic variables. Methods Twelve 25-kg pigs underwent endoscopic thyroid dissection using carbon dioxide insufflation at 0 mmHg (sham), 10 mmHg (G10), 15 mmHg (G15) and 20 mmHg (G20). Three pigs were used in each group. ICP, mean arterial pressure, central venous blood pressure (CVP), cardiac output and blood gas were measured at baseline, 30, 60 and 120 min. Results There were no differences in mean ICP between the sham group and G10. However, ICP significantly increased in G15 and G20. The partial pressure of carbon dioxide was similar in G10 and G15 (mean(s.d.) 49·8(2·4) and 49·8(5·2) mmHg respectively at 120 min), while it was dramatically increased in G20 (63·1(6·9) mmHg at 120 min). Haemodynamic parameters were stable in all groups except for G20 in which CVP significantly increased with respect to baseline (8·5(2·1) versus 1·3(1·5) mmHg; P &amp;lt; 0·01). Jugular vein collapse occurred during endoscopic dissection at all insufflation pressures, but pigs operated at 10 mmHg were able to maintain an intermittent blood flow. Conclusion A severe increase in ICP occurs with insufflation pressures higher than 15 mmHg, possibly owing to decreased cervical venous blood flow. Carbon dioxide insufflation up to 10 mmHg does not alter ICP, and is recommended for clinical application in endoscopic endocrine neck surgery.

Consultation with the specialist: increased intracranial pressure.

1. Gitte Y. Larsen, MD* 2. Brahm Goldstein, MD† 1. 2. *Assistant Professor of Pediatrics, Division of Pediatric Critical Care, Doernbecher Children’s Hospital, Oregon Health Sciences University, Portland, OR. 3. 4. †Editorial Board. Increased intracranial pressure (ICP) may result from multiple etiologies, including cerebral edema associated with head trauma, hypoxic-ischemic events, infection, metabolic derangement, hydrocephalus, and space-occupying lesions. If unrecognized and untreated, increased ICP results in significant morbidity and mortality by causing irreversible neurologic injury. The intracranial cavity contains three components: blood, brain, and cerebrospinal fluid (CSF). CSF accounts for 10% of the total volume, blood for 10%, and brain for approximately 80%. CSF provides 70% of the intracranial buffering capacity. As the brain swells following an insult, CSF is displaced initially into the arachnoid space, cerebral blood flow (CBF) is altered, and ICP rises. The autoregulation of CBF is relatively constant at 50 to 150 mm Hg mean arterial pressure in adults. However, CBF is highly responsive to various metabolic factors, including Paco2, Pao2, and pH. For example, CBF rises linearly with increases in Paco2 of 20 to 70 torr and increases when the Pao2 falls below 50 torr. The ability to autoregulate blood flow often is altered or lost following a variety of insults, including head trauma. This may result in inappropriately high blood flows and an even higher ICP. As the compliance of the brain decreases, a relatively small change in volume will result in a large change in ICP. Infants were believed to be relatively protected against increases in ICP compared with older children, but little protection is afforded by an infant’s cranial and cerebral anatomy. Despite the presence of open sutures and larger subarachnoid spaces and cisterns, which serve to decompress expanding brain tissue, the smaller neural axis results in a less compliant pressure-volume relationship. Pathophysiology following brain injury occurs in two phases: primary and secondary. Primary brain injury refers to the initial insult, whether it be ischemic, anoxic/hypoxic, or shear injury …

Intracranial pressure and venous cannulation for cardiopulmonary bypass.

The onset of cardiopulmonary bypass (CPB) is a period of changing hemodynamics, and during this transition, the position of the aortic and venous cannulas is assessed. Increased arterial line pressures may indicate a malposition of the aortic cannula, whereas reduced venous return to the reservoir of the CPB circuit suggests suboptimal position of a venous cannula. Classically described signs of compromised venous drainage, such as engorgement of the head and neck, are rare, and incomplete obstruction of the superior vena cavae may be difficult to detect clinically but can significantly alter cerebral physiology. Impedance to superior vena caval (SVC) flow may increase intracranial pressure (ICP) and decrease cerebral perfusion pressure (CPP) (CPP 5 mean arterial pressure [MAP] 2 [ICP] (1). In the experimental setting, we have incidentally, but repeatedly, observed this effect. The same physiologic phenomenon is of relevance in the operating suite and may bear on practice. The purpose of this article is to briefly describe the influence of venous cannula position on ICP during CPB.

Intracranial Pressure and Venous Cannulation for Cardiopulmonary Bypass

Intracranial Pressure and Venous Cannulation for Cardiopulmonary Bypass

Hypothermia related changes in electrocortical activity at stepwise increase of intracranial pressure in piglets

Recent experimental studies have demonstrated that mild hypothermia can be effective in the control of intracranial hypertension. However, investigations to analyze the effects of hypothermia on changes in brain oxygen metabolism and electrocortical activity caused by increased intracranial pressure (ICP) are lacking. We examined the effects of mild hypothermia on electrocorticogram (ECoG) in combination with measurement of regional cerebral blood flow (CBF) and estimation of brain oxygen metabolism during stepwise increase of ICP. For this purpose thirteen female piglets (14 days old, 4-5 kg b.w.) were anaesthetized and mechanically ventilated. An epidural balloon was gradually inflated in order to increase ICP to 25 mmHg, 35 mmHg and 45 mmHg every 30 minutes at adjusted mean arterial blood pressures (MAP). This procedure resulted in gradual cerebral perfusion pressure (CPP) reduction of about 70%, 50%, and 30% of baseline [baseline CPP: normothermia (NT) 80+/-3 mmHg; hypothermia (HT) 84+/-3 mmHg]. Control animals were maintained in a normothermic state (38.6+/-0.2 degrees C). HT animals were surface cooled and maintained at 31.9+/-0.1 degrees C. ECoG, regional CBF, cerebral oxygen delivery (cDO2) and the cerebral metabolic rate of oxygen (CMRO2) were estimated during the normothermic period, after hypothermic stabilization, and after the gradual CPP reductions. The baseline ECoG showed the typical delta-dominated frequency pattern for isoflurane anaesthesia. At the hypothermic level, a frequency shift was seen from delta activity towards the higher frequencies (theta- and alpha activity) and the total spectral power was significantly reduced (56+/-17% from baseline, p < 0.05). the cortical CBF decreased markedly to 67+/-10% (p < 0.05), whereas the medulla oblongata blood flow increased slightly. During controlled increase of ICP by regional mass expansion from epidural balloon inflation, we found at mild and moderate stages of ICP increase (25 and 35 mmHg) only minimal changes in the ECoG in hypothermic animals compared to the hypothermic baseline, whereas the ECoG in normothermic animals showed a marked decrease in frequency, amplitude and total spectral power. We conclude that mild hypothermia produces an arousal-like ECoG activity with marked frequency shift to alpha activity and a change from high to low voltage activity. Furthermore, the hypothermic brain showed a preserved neuronal function at moderate stages of ICP. Obviously, hypothermia improves the functional tolerance of the brain to impaired oxygen supply.

Sepsis: cause of late deterioration of intracranial pressure in patients with severe traumatic brain injury?

Increased intracranial pressure (ICP) in patients with severe traumatic brain injury without findings of CT scan deterioration is frequently observed late during the course of treatment. The aim of this study was to evaluate the possible relationship between the late increase of ICP in head injured patients and the development of sepsis during their course on ICU.

Maintaining normal intracranial pressure in a rabbit model during treatment of severe diabetic ketoacidemia.

Increased intracranial pressure (ICP) resulting in death or neurologic morbidity continues to complicate traditional management of diabetic ketoacidemia (DKA) in pediatric patients. When ICP or cerebrospinal fluid pressures have been measured, correction of hyperglycemia in animals and treatment of DKA in humans have consistently resulted in pathologic increases in ICP. We hypothesized that elevations in ICP can be minimized if changes in effective osmolality (Eosm) are controlled during treatment of DKA. During a six-hour study period, three groups of rabbits were studied: a normal control group of nondiabetic animals (Cnor, n = 10), a control group of animals with DKA (CDKA, n = 8), and an experimental group of animals with DKA (EDKA, n = 8). There was no significant difference between the two groups with DKA regarding pretreatment degree of dehydration, blood pressure, hyperglycemia, acidemia or ICP. During the treatment period, Cnor received maintenance fluids only. CDKA received insulin and an assumed volume of deficit (150 ml/kg) along with maintenance fluids and urinary output replacement with 0.45% NaCl. EDKA received insulin and one-half the volume of deficit calculated by the weight lost with 0.9% NaCl plus maintenance fluids. There was no significant difference between CDKA and EDKA regarding the rate at which DKA was corrected. While CDKA demonstrated a progressive and statistically significant increase in ICP, EDKA exhibited no such increase in ICP compared to normal, nondiabetic controls (Cnor) during treatment. Changes in Eosm during treatment in CDKA compared to Cnor and in CDKA compared to EDKA were significantly greater (p < .01), however, changes in EOSM in EDKA compared to Cnor were not significant. These data support the clinical observation that decreasing EOSM during treatment of DKA is associated with increased ICP and suggest that DKA can be treated effectively with i.v. fluids and insulin without increasing ICP.

The Diagnostic Value of Optic Disc Evaluation in Acute Elevated Intracranial Pressure

Ophthalmologists often are asked to evaluate the optic disc for evidence of acute increased intracranial pressure (ICP). The authors studied the incidence of papilledema in a population of patients with a documented acute increase in ICP. Included in this study were 37 patients with acute elevated ICP due to a spontaneous hemorrhage or craniocerebral trauma. In all patients, the ICP was monitored continuously. Fundus examination was performed twice daily on at least 7 consecutive days. According to the level and duration of the ICP, the patients were divided into three groups. Group 1 included 13 patients who had a slightly elevated ICP (range, 20-30 mmHg) on at least 3 consecutive days. In this group, 3 of 13 patients demonstrated venous congestion on the fifth or sixth day. No swelling of the optic disc was seen in this group. Group 2 included seven patients with an elevated ICP, with values ranging from 30 to 70 mmHg lasting for at least 3 consecutive days. In this group, one patient had a blurred disc margin on the sixth day. Group 3 included 17 patients with shortlasting ICP values, ranging from 30 to 60 mmHg for less than 72 hour. Neither papilledema nor abnormalities of fundus vessels were seen in this group. Papilledema in acute elevation of ICP is an uncommon event. Its absence does not preclude the presence of ICP elevation.

Sumatriptan-induced cerebral vasoconstriction as treatment of experimental intracranial hypertension.

Increased intracranial pressure (ICP) is a major cause of mortality in severe head injuries and pharmacologically induced cerebral vasoconstriction has been suggested as a possible treatment. In the present study a porcine model of increased ICP was utilized to study the changes in cerebral haemodynamics and energy metabolism induced by a selective 5-hydroxytryptamine1 agonist (sumatriptan). ICP was raised by inflation of two balloons covering both parieto-occipital regions extradurally. The animals were randomized into four groups receiving sumatriptan. 0.01 mg.kg-1 (A), 0.03 mg.kg-1 (B), 0.1 mg.kg-1 (C), and 0.5 mg.kg-1 (D) intravenously over 10 min. Measurements of cerebral blood flow (CBF), arterio-venous oxygen content difference (CavO2), and jugular venous pH (vpH) were performed 5, 20, 40, 60, and 75 min after start of the infusion. ICP, mean arterial pressure, and EEG were recorded continuously. Direct effects of sumatriptan were also compared in cortical arteries and veins in vitro. Significant decreases in ICP were obtained in groups A, B, and C while group D exhibited a progressive increase in ICP. Significant reductions in CBF, increase in CavO2, and slowing of EEG were observed in groups B, C, and D. Sumatriptan caused moderate constriction of the arteries and a more pronounced dilatation of veins in vitro. The results indicate that a low dose of sumatriptan has the potential to reduce a raised ICP. High doses of sumatriptan cause a further increase of ICP possibly by dilatation of intracerebral veins.

Incidence of increased intracranial pressure after early surgical treatment of syndromic craniosynostosis.

The late development of intracranial hypertension after an aesthetically successful cranial vault expansion has been noted anecdotally in children with syndromic synostosis. If untreated, this process can lead to neurological and visual deterioration; however, the frequency of this problem is uncertain. In an attempt to detect this process before the onset of irreversible impairment, the authors have since 1991 incorporated routine ophthalmological evaluations into the multidisciplinary follow-up protocol for all patients with complex craniosynostosis. These examinations were performed at initial evaluation and at 6-month intervals thereafter. The present report focuses on the results in 22 consecutive infants with syndromic synostosis who underwent initial surgery between 1991 and 1994. All but 4 children underwent initial cranial reconstruction at 6-18 months of age. Four patients had papilledema preoperatively which in each instance resolved postoperatively. During the follow-up period, 8 children manifested evidence of late intracranial hypertension at a median of 16.5 months after initial operation(s): 4 developed asymptomatic papilledema, 1 had progressive proptosis, and 3 had other subtle clinical signs of increased intracranial pressure (ICP). Further evaluation disclosed a Chiari 1 malformation in 2 children; 4 had a 'beaten copper' appearance on skull radiographs, and 4 underwent lumbar puncture, which in each case demonstrated an opening pressure above 20 cm H2O. Only 3 children exhibited symptoms from the ICP elevation. Six children with a head size < or = the 25th percentile underwent a repeat cranial expansion; after the cranial vault expansion, one child who initially had slit-like ventricles developed ventriculomegaly and, because of persistent papilledema, underwent insertion of ventriculoperitoneal (VP) shunt. Two other patients with a head circumference above the 50th percentile and the development of moderate ventriculomegaly underwent VP shunt insertion alone. All children have had complete resolution of papilledema as well as other symptoms and signs of increased ICP without evidence of optic atrophy or neurological sequelae. This study indicates that the incidence of delayed, asymptomatic increases in ICP among children with complex craniosynostosis is higher than previously estimated. The pathophysiologic bases for this process are discussed. Because the detection of this problem at a presymptomatic stage should optimize the likelihood of a good functional outcome, we strongly recommend close ophthalmological and clinical follow-up as a part of the comprehensive care of all young children with complex craniosynostosis, even after a cosmetically successful cranial expansion.

Hypertonic saline dextran prime reduces increased intracranial pressure during cardiopulmonary bypass in pigs.

Children and adults who develop neurologic deficits after cardiac surgery may experience cerebral ischemia during cardiopulmonary bypass. Increased intracranial pressure (ICP) may contribute to cerebral ischemia during bypass. Hypertonic saline dextran (HSD), a hyperosmotic, hyperoncotic resuscitation solution, decreases ICP in trauma resuscitation. We hypothesized that HSD would decrease ICP, reduce brain water, and reduce intravascular fluid requirements during bypass. Twelve swine were divided into two bypass groups: Group 1 (ISO = isotonic) received as prime 1 L of lactated Ringer's solution and 500 mL of 6% hydroxyethyl starch. Group 2 (HSD = hypertonic saline/dextran) received as prime 1 L of lactated Ringer's solution, 500 mL of 6% hydroxyethyl starch, and 1 mL/kg of 24% hypertonic saline/25% dextran. Normothermic bypass was instituted at 100 mL.kg-1.min-1. ICP increased significantly during bypass with ISO prime but not with HSD. Brain water in the cerebrum did not differ between groups but was reduced in the cerebellum to 75.9% +/- 1.4%. We conclude that HSD prevented any significant increase in ICP during normothermic bypass, and substantially improved fluid balance during bypass. In cardiac surgery patients in whom maintaining decreased ICP and reducing isotonic fluid administration is important, HSD may be a useful addition to the bypass prime solution.

&lt;I&gt;The Effect of Increased Intracranial Pressure during the Appearance of Pressure Waves on the Brainstem&lt;/I&gt;

The effects of increased intracranial pressure (ICP) during the appearance of plateau waves or B-waves to the brainstem functions were investigated by evaluation of evoked potentials. The ICP and systemic blood pressure were continuously recorded in nine cases of intracranial hypertension. In the four cases demonstrating plateau waves in ICP recording, the latencies of the auditory brainstem evoked potentials (ABEP) measured during the appearance of plateau waves showed no significant differences compared to those measured during the interval phase between two plateau waves. In the five cases demonstrating B-waves in ICP recording, four cases showed significant (p less than 0.05) prolongation of the V wave of ABEP and three showed significant (p less than 0.05) prolongation of the P15 of somatosensory evoked potentials during the phase of increased ICP level with B-waves compared to those measured during the phase of decreased ICP level without B-waves, produced by external drainage of the cerebrospinal fluid or mannitol administration. The results indicated that during the appearance of plateau waves there were no significant changes of electrical activity in the brainstem, even though there was a significant reduction in cerebral perfusion pressure. It is suggested that in cases with the appearance of B-waves, an increase in ICP frequently affects the electrical activity in the brainstem.

RATE OF INDUCTION OF HYPOTENSION WITH TRIMETAPHAN MODIFIES THE INTRACRANIAL PRESSURE RESPONSE IN CATS

An infusion of 0.1% trimetaphan was administered to eight cats with artificially increased intracranial pressure (ICP) in order to decrease their mean arterial pressure (MAP) from 121 +/- 9.5 (SEM) to 58 +/- 4.6 mm Hg in less than 1 min. All cats developed an increase in intracranial pressure (ICP) (from 16 +/- 1.4 to 23 +/- 3.2 mm Hg) accompanied by a partial rebound in MAP. Eight additional cats received 0.1% trimetaphan to decrease their MAP from 128 +/- 13.4 to 52 +/- 8.1 mm Hg over more than 2 min. Four of these cats followed the same pattern, with ICP increases from 19 +/- 1.1 to 31 +/- 3.9 mm Hg, while in the other four ICP did not change. In nine of the 12 cats with an ICP increase, that increase was initiated before the partial MAP rebound. We conclude that trimetaphan causes clinically significant ICP increases in cats with increased ICP, that partial rebound in MAP frequently exacerbates these increases in ICP, and that rapid induction of hypotension tends to increase the frequency with which trimetaphan increases ICP.