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Biomedical subjects

S G Soriano

Publications and source records attributed to S G Soriano.

At least 19 recordsLinked to original sources

Gentle dorsal root retraction and dissection can cause areflexia: implications for intraoperative monitoring during "selective" partial dorsal rhizotomy.

During partial dorsal rhizotomy (PDR), intraoperative dorsal rootlet stimulation often evokes nonreflex, rather than reflex, motor responses that are due to costimulation of adjacent ventral roots. Intraoperative areflexia typically predicts that motor responses evoked by dorsal rootlet stimulation are nonreflexive. The cause of areflexia during PDR is in part due to anesthesia, but other mechanisms are likely to play a role as well. In this study of three consecutive patients undergoing lumbosacral neurosurgery, soleus H-reflexes evoked by tibial nerve stimulation at the popliteal fossa were found to suddenly decline in amplitude following retraction and gentle dissection of the S-1 dorsal root. In one areflexic patient, dorsal rootlet stimulation proximal to the main site of dissection evoked soleus H-reflexes, although they could not be evoked by tibial nerve stimulation. We conclude that the gentle retraction and dissection of dorsal rootlets that occurs during PDR can induce conduction block of reflex afferents. High-intensity dorsal rootlet stimulation distal to the site of conduction block may then evoke not reflex responses, but rather nonreflex motor responses, due to the costimulation of adjacent ventral roots.

Cerebral Palsy↗

Pharmacokinetics and pharmacodynamics of vecuronium in children receiving phenytoin or carbamazepine for chronic anticonvulsant therapy.

The pharmacokinetics and time course of action of vecuronium in normal children and children receiving anticonvulsant drugs for prolonged periods were characterized. A bolus dose of vecuronium 0.15 mg kg(-1) was administered i.v. to 10 non-epileptic children and to 10 children on phenytoin and 10 children on carbamazepine, who were matched for age and weight. Plasma concentrations of vecuronium, 3-OH desacetylvecuronium (the primary metabolite of vecuronium) and alpha1-acid glycoprotein (AAG) were determined. Pharmacokinetic variables were derived from plasma samples collected before and after administration of vecuronium. Neuromuscular transmission was monitored by evoked compound electromyography. Recovery of the first twitch of the train-of-four (T1/T0) and the recovery index (RI), the time for 25-75% recovery of T1/T0, were determined. The elimination half-life of vecuronium was significantly reduced in both anticonvulsant groups compared with control [control 48.2 (SD 40.3), phenytoin 23.5 (13.1), carbamazepine 18.4 (16.6) min, P<0.05]. Vecuronium clearance was increased in both anticonvulsant groups [control 9.0 (3.6), phenytoin 15.1 (8.9), carbamazepine 18.8 (13.1) ml kg(-1) min(-1), 0.05<P<0.1]. Children on chronic anticonvulsant therapy had a significantly shorter RI than control [control 21.8 (11), phenytoin 12.5 (8.3), carbamazepine 10.6 (5.9) min, P<0.05]. Concentrations of vecuronium at different degrees of recovery of T1, volumes of distribution and AAG concentrations were not different between groups. Our data confirm anticonvulsant-induced resistance to vecuronium in children and support a pharmacokinetic component contributing to the resistance.

Adolescent↗

Hemostatic changes in pediatric neurosurgical patients as evaluated by thrombelastograph.

UNLABELLED: Thromboembolic events are a known complication in neurosurgical patients. There is evidence to suggest that a hypercoagulable state may develop perioperatively. Thrombelastograph (TEG) coagulation analysis is a reliable method of evaluating hypercoagulability. We evaluated coagulation by using TEG data in pediatric neurosurgical patients undergoing craniotomy to determine whether a hypercoagulable state develops intraoperatively or postoperatively. Thirty children undergoing craniotomy for removal of a tumor or seizure focus were studied. Blood was analyzed with TEG) data by using native and celite techniques, at three time points for each patient: preoperatively after induction of anesthesia; intraoperatively during closure of the dura; and on the first postoperative day. Compared with preoperative indices, closing and postoperative celite TEG values were indicative of hypercoagulability with shortened coagulation time values (P < 0.001), prolonged alpha angle divergence values (P < 0.001), and above-normal TEG coagulation indices (P < or = 0.002). Reaction time values were shortened, and maximal amplitude of clot strength values were prolonged but did not reach statistical significance. Hypercoagulation develops early after resection of brain tissue in pediatric neurosurgical patients as assessed by using TEG data. Further studies are needed to determine the clinical significance of this hypercoagulable state. IMPLICATIONS: Hypercoagulability in postoperative neurosurgical patients has been demonstrated in the adult population, but few studies have dealt with the pediatric population. We found that children undergoing craniotomy for focal resection, lobectomy, and hemispherectomy are hypercoagulable as detected by thrombelastograph coagulation analysis. Further studies are needed to determine whether this is clinically significant.

Adolescent↗

The effect of propofol on intraoperative electrocorticography and cortical stimulation during awake craniotomies in children.

Propofol has been proposed as a sedative agent during awake craniotomies. However, there are reports of propofol suppressing spontaneous epileptiform electrocorticography (ECoG) activity during seizure surgery, while others describe propofol-induced epileptiform activity. The purpose of this study was to determine if propofol interferes with ECoG and direct cortical stimulation during awake craniotomies in children. Children scheduled for awake craniotomies for resection of epileptic foci or tumours were studied. An intravenous bolus of 1-2 mg.kg-1 followed by infusion of 100-200 microgram.kg-1.min-1 of propofol was administered to induce unconsciousness. Fentanyl (0.5 microgram.kg-1) was administered incrementally to provide analgesia. After the cortex was exposed, the propofol infusion was stopped and the patient permitted to awaken. Cortical electrodes were applied. ECoG was recorded continuously on a Grass polygraph. Motor, sensory, language, and memory testing were done throughout the procedure. The cortex was stimulated with a hand-held electrode using sequential increases in voltage to map the relevant speech and motor areas. We studied 12 children (aged 11-15 years) with intractable seizures. The raw ECoG did not reveal any prolonged beta-waves associated with propofol effect. Electroencephalogram spikes due to spontaneous activity or cortical stimulation were easily detected. Cognitive, memory and speech testing was also successful. We conclude that propofol did not interfere with intraoperative ECoG during awake craniotomies. Using this technique, we were able to fully assess motor, sensory, cognitive, speech and memory function and simultaneously avoid routine airway manipulation.

Adolescent↗

Onset and duration of action of rocuronium in children receiving chronic anticonvulsant therapy.

The onset and time course of action of rocuronium in normal children and children receiving anticonvulsant drugs for prolonged periods was characterized. A single bolus dose of 0.6 mg.kg-1 rocuronium was administered i.v. to seven nonepileptic patients on no medication, and eight patients on chronic anticonvulsant therapy consisting of either phenytoin, carbamazepine, or both who were age and weight matched. Neuromuscular transmission was monitored by the evoked compound electromyography of the thenar muscles using train of four stimulation every 20 s. Recovery times of the first twitch to 10%, 25%, 50%, 75% and 100% of baseline values and recovery index were obtained. The onset times were 1.05+/-0.5 and 1.41+/-0.5 min for the control and anticonvulsant groups respectively and were not significantly different. Children receiving chronic anticonvulsant therapy had significantly shorter recovery index than the control group (control 10.4+/-5.1 min, anticonvulsant 4.8+/-1.7 min, P<0.05). Furthermore, the duration of recovery to 10%, 50%, 75% and 100% of baseline T1 values was less in the anticonvulsant drug group. Our data confirm resistance to rocuronium in children on chronic anticonvulsant drugs.

Analysis of Variance↗

P- and E-selectin-deficient mice are susceptible to cerebral ischemia-reperfusion injury.

We examined brain sections from P- and E-selectin-deficient mice (-/-) and their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) tissue injury. There was no difference in the subsequent infarct volume after 3 h of ischemia and 21 h of reperfusion. These data indicate that selectin-independent mechanisms mediate tissue injury after a prolonged period of transient focal ischemia.

Animals↗

Mice deficient in Mac-1 (CD11b/CD18) are less susceptible to cerebral ischemia/reperfusion injury.

BACKGROUND AND PURPOSE: Macrophage-1 antigen (Mac-1) (CD11b/CD18), a leukocyte beta2 integrin, facilitates neutrophil adhesion, transendothelial migration, phagocytosis, and respiratory burst, all of which may mediate reperfusion-induced injury to ischemic brain tissue in conditions such as stroke. To determine the role of Mac-1 during ischemia and reperfusion in the brain, we analyzed the effect of transient focal cerebral ischemia in mice genetically engineered with a specific deficiency in Mac-1. METHODS: Transient focal ischemia/reperfusion was induced by occluding the left middle cerebral artery for 3 hours followed by a 21-hour reperfusion period in Mac-1-deficient (n=12) and wild-type (n=11) mice. Regional cerebral blood flow was determined with a laser-Doppler flowmeter. Brain sections were stained with 2% 2,3,5-triphenyltetrazolium chloride to determine the infarct volume. Neutrophil accumulation was determined by staining the brain sections with dichloroacetate esterase to identify neutrophils. RESULTS: Compared with the wild-type cohort, Mac-1-deficient mice had a 26% reduction in infarction volume (P<0.05). This was associated with a 50%, but statistically insignificant, reduction in the number of extravasated neutrophils in the infarcted areas of the brains in the mutant mice. There were no differences in regional cerebral blood flow between the 2 groups. CONCLUSIONS: Mac-1 deficiency reduces neutrophil infiltration and cerebral cell death after transient focal cerebral ischemia. This finding may be related to a reduction in neutrophil extravasation in Mac-1-deficient mice.

Animals↗

ICAM-1 dependent pathway is not involved in the development of neuronal apoptosis after transient focal cerebral ischemia.

We examined brain sections from ICAM-1 deficient mice (-/-) and their nontransgenic littermates (+/+) after focal cerebral ischemia and reperfusion (I/R) for the presence of apoptosis. Despite the reduction in necrosis, the -/- mice had apoptotic cells in the ischemic hemisphere as shown by terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick end-labeling (TUNEL) staining and DNA laddering. ICAM-1 deficiency minimizes necrosis but not apoptosis after temporary MCAO in mice, thereby leaving the potential for delayed neuronal cell death despite ICAM-1 inactivation.

Animals↗

Tissue plasminogen activator (tPA) increases neuronal damage after focal cerebral ischemia in wild-type and tPA-deficient mice.

Intravenous tissue plasminogen activator (tPA) is used to treat acute stroke because of its thrombolytic activity and its ability to restore circulation to the brain. However, this protease also promotes neurodegeneration after intracerebral injection of excitotoxins such as glutamate, and neuronal damage after a cerebral infarct is thought to be mediated by excitotoxins. To investigate the effects of tPA on cerebral viability during ischemia/reperfusion, we occluded the middle cerebral artery in wild-type and tPA-deficient mice with an intravascular filament. This procedure allowed us to examine the role of tPA in ischemia, independent of its effect as a thrombolytic agent. tPA-deficient mice exhibited approximately 50% smaller cerebral infarcts than wild-type mice. Intravenous injection of tPA into tPA-/- or wild-type mice produced larger infarcts, indicating that tPA can increase stroke-induced injury. Since tPA promotes desirable (thrombolytic) as well as undesirable (neurotoxic) outcomes during stroke, future therapies should be aimed at countering the excitotoxic damage of tPA to afford even better neuroprotection after an acute cerebral infarct.

Animals↗

Rebound swelling of astroglial cells exposed to hypertonic mannitol.

BACKGROUND: Mannitol is widely used in anesthesia and critical care medicine. Although its clinical effects were originally attributed to osmotic dehydration of brain cells, other mechanisms have also been proposed. Osmotic dehydration of astroglial cells is opposed by powerful volume-regulating mechanisms that involve inward transport of electrolytes. These mechanisms have been studied previously by exposing cells to hypertonic saline gradients. Because of its potential clinical relevance, the volume response of astroglial cells exposed to hypertonic mannitol was investigated. METHODS: Rat C6 glioma cells were cultured to confluence, and their volume behavior was observed by laser light scattering. After equilibration at physiologic temperature and pH, cells were abruptly exposed to hypertonic mannitol solutions. In separate experiments, C6 cells were exposed to hypertonic solutions containing radiolabeled mannitol, and its cellular uptake was determined. RESULTS: Hypertonic mannitol exposure produced initial cell shrinkage followed by rapid volume recovery and rebound swelling. The rebound swelling was similar in magnitude to the initial maximal shrinkage. For +40 mOsm and +70 mOsm mannitol challenges, mean volume recovery was 184+/-31% and 227+/-62%, respectively (where full recovery to baseline volume = 100%). Rebound swelling was substantially inhibited by furosemide. When exposed to mannitol in varying concentrations, uptake was linear, ranging from 82+/-7 nmol/mg to 406+/-26 nmol/mg protein. After 5 min, estimated intracellular concentrations of mannitol were similar to extracellular concentrations. CONCLUSIONS: Unlike hypertonic saline, hypertonic mannitol exposure produces rebound cell swelling. Cellular penetration of mannitol appears to account for much of this phenomenon. The clinical implications of these observations remain to be determined.

Animals↗

The critical importance of stimulus intensity in intraoperative monitoring for partial dorsal rhizotomy.

During partial lumbosacral dorsal rhizotomy (PDR), intraoperative dorsal rootlet stimulation (drs) evokes motor responses, presumed to be reflexes, which are used to select rootlets for section. However, dr stimuli may also costimulate ventral root (vr) and evoke an M rather than a reflex response, the two being distinguishable only by comparison of response latencies after drs at two separate sites. In 15 consecutive spastic cerebral palsy patients undergoing PDR, we asked whether reflex and M responses were distinguishable on the basis of stimulus intensity (SI). For soleus H reflexes evoked by percutaneous tibial nerve stimulation, the SI for reflex afferents was usually subthreshold for exciting motor fibers. Similarly, for nerve roots, reflexes were evoked by drs at SIs generally less than that for M responses evoked by vr stimulation (vrs). In contrast, M responses evoked by drs required SIs that were on average 20 times greater. Finally, costimulation of contralateral vr after ipsilateral vrs occurred at SIs shown to evoke M responses after drs. We conclude that: (1) reflex and M responses evoked by drs are distinguishable on the basis of the required SI; and (2) drs employing SIs greater than required for vrs evokes M rather than reflex responses due to costimulation of ipsilateral and contralateral vr.

Cerebral Palsy↗

Intercellular adhesion molecule-1-deficient mice are less susceptible to cerebral ischemia-reperfusion injury.

Neutrophil emigration is mediated by adhesion proteins that are highly expressed on the endothelial surface during inflammatory processes in the brain. Intercellular adhesion molecule-1 (ICAM-1) is an inducible adhesion molecule that binds to leukocyte integrins and facilitates neutrophil adhesion and transendothelial migration. To study the role of ICAM-1 during ischemia and reperfusion in the brain, we analyzed the effect of transient focal cerebral ischemia in ICAM-1-deficient mice generated by gene targeting in embryonic stem cells. Transient focal ischemia was induced by occluding the left middle cerebral artery for 3 hours followed by a 21- or 45-hour reperfusion period. When compared with their wild-type littermates, ICAM-1-deficient mice were less susceptible to cerebral injury as demonstrated by a 5.6- or 7.8-fold reduction in infarction volume, respectively. These data support the premise that neutrophil adhesion in ischemic areas may be deleterious and that ICAM-1 deficiency reduces neurological damage after transient focal cerebral ischemia.

Animals↗

Cerebral blood flow velocity after mannitol infusion in children.

PURPOSE: There is conflicting evidence as to whether the effect of mannitol on brain bulk arises from haemodynamic, rheologic, or osmotic mechanisms. If mannitol alters cerebral haemodynamics by inducing vasoconstriction, this change should be reflected in cerebral blood flow velocity (CBFV) in the middle cerebral artery (MCA). The purpose of this study was to evaluate the effect of mannitol on CBFV in children. METHODS: Children scheduled for intracranial surgery were enrolled. After a loading dose of 10 micrograms.kg-1 of fentanyl, general anaesthesia was maintained with fentanyl (3 micrograms.kg-1.hr-1), 66% nitrous oxide, and isoflurane (0.2-0.5% inspired). Mean and systolic CBFV (Vm and Vs) and pulsatility index (PI) were recorded with a transcranial Doppler (TCD) directed at the M1 segment of the MCA. Mannitol was administered, 1 gm.kg-1 iv over 15 min. The osmolality (Osm), haematocrit (Hct), mean arterial pressure (MAP), heart rate (HR), and TCD variables were recorded before and 15, 30, 45, and 60 min after the mannitol infusion. RESULTS: Mannitol infusion resulted in an increase in Osm and decrease in Hct (P < 0.05). Heart rate, MAP and arterial carbon dioxide tensions did not change (P > 0.05) during the measuring period. The Vm did not vary from baseline. The Vs and PI both increased briefly (P < 0.01 at 15 min and P < 0.05 at 30 min) after the mannitol, suggesting an increase in resistance distal to the MCA. CONCLUSION: The time course of CBFV changes produced by mannitol corresponds with previous animal data concerning cerebrovascular tone. Our results suggest that mannitol briefly increases cerebrovascular resistance and thereby diminishes cerebral blood volume.

Adolescent↗

Effects of ondansetron on emesis in the first 24 hours after craniotomy in children.

Children undergoing neurosurgical resection are at high risk for postoperative nausea and vomiting. Ondansetron, a selective serotonergic (5-HT3) antagonist, is effective in reducing postoperative vomiting in several high-risk populations. In a prospective, randomized study, we compared the prophylactic use of intravenous ondansetron, 0.15 mg/kg, versus placebo for the prevention of emesis in 60 children, aged 2-18 yr, undergoing craniotomies for resective procedures. Patients with preoperative emesis were excluded from the study. All patients were tracheally extubated at the conclusion of surgery, and each episode of emesis during the first 24 postoperative hours was recorded. For the entire 24-h interval, the incidence of emesis in children who received ondansetron (57%) was not significantly different from that in those who received placebo (66%); however, in the first 8 h, the incidence was 25% (ondansetron) vs 44% (placebo) (P = not significant). In those receiving placebo, there was no difference in emesis between patients undergoing operations above versus below the tentorium. Although our sample size was too small to completely exclude any beneficial effect, ondansetron appears ineffective in preventing postoperative emesis in this patient population.

Adolescent↗

Sevoflurane depresses myocardial contractility less than halothane during induction of anesthesia in children.

BACKGROUND: Cardiovascular stability is an important prerequisite for any new volatile anesthetic. We compared echocardiographically derived indices of myocardial contractility during inhalation induction with sevoflurane and halothane in children. METHODS: Twenty children were randomized to receive either halothane or sevoflurane for inhalation induction of anesthesia. No preoperative medications were given. Myocardial contractility was evaluated at baseline and at sevoflurane and halothane end-tidal concentrations of 1.0 minimum alveolar concentration (MAC) and 1.5 MAC. RESULTS: There were no differences between groups in patient age, sex, physical status, weight, or height. Equilibration times and MAC multiples of sevoflurane and halothane were comparable. Vital signs remained stable throughout the study. Left ventricular end-systolic meridional wall stress increased with halothane but remained unchanged with sevoflurane. Systemic vascular resistance decreased from baseline to 1 MAC and 1.5 MAC with sevoflurane. Halothane depressed contractility as assessed by the stress-velocity index and stress-shortening index, whereas contractility remained within normal limits with sevoflurane. Total minute stress and normalized total mechanical energy expenditure, measures of myocardial oxygen consumption, did not change with either agent. CONCLUSIONS: Myocardial contractility was decreased less during inhalation induction of anesthesia with sevoflurane compared with halothane in children. Although the induction of anesthesia with sevoflurane or halothane was equally well tolerated, the preservation of myocardial contractility with sevoflurane makes it an attractive alternative for inducing anesthesia in children.

Anesthesia, Inhalation↗

Resection of a massive sacrococcygeal teratoma using hypothermic hypoperfusion: a novel use of extracorporeal membrane oxygenation.

A 33-week-gestation infant with a massive sacrococcygeal teratoma weighted 4,000 g, but the actual weight of the infant was approximately 1,500 g. With the potential for massive blood loss and impaired lung compliance during resection, some type of cardiopulmonary support was necessary. Resection was undertaken with the assistance of venoarterial extracorporeal membrane oxygenation (ECMO) and hypothermic hypoperfusion. Immediately after removal of the tumor, which weighted 2,420 g, the infant was decannulated from ECMO, and the carotid artery was primarily reconstructed end-to-end. The amount of intraoperative blood loss was 550 mL Postoperatively, the child weighted 1,580 g. Follow-up head ultrasound results were normal, and the patient has done well. This is the first reported case in which ECMO with hypothermic hypoperfusion was used for resection of a massive tumor. This experience shows that ECMO is both useful and safe as a means of temporary cardiopulmonary support for resection of massive tumors in infants.

Coccyx↗

Nitrous oxide depresses the H-reflex in children with cerebral palsy.

Hoffmann's reflex or H-reflex (HR) is an electrically elicited reflex that measures excitability of motoneurons and shares some physiologic properties with the deep tendon reflex. Children with tendon hyperreflexia due to cerebral palsy usually have higher amplitude HRs. Nitrous oxide (N2O) depresses the HR in patients with normal spinal reflexes, although the effect of N2O in conditions with hyperreflexia such as cerebral palsy is not known. We propose to determine the effect of N2O on the amplitude of the HR under general anesthesia in children with hyperreflexia due to cerebral palsy. We studied eight children undergoing selective dorsal rhizotomy (SDR) for the relief of spasticity. The maximum amplitudes of the HR (HRmax) and direct motor response (MRmax) were routinely evoked under the following anesthetic conditions: 1) sufentanil and 66% N2O/33% oxygen; and 2) sufentanil and 100% oxygen. The HRmax amplitude was significantly lower when N2O was part of the inspired gas mixture. The differences between the no N2O and the 66% N2O groups were significant. The MRmax did not change significantly. Abnormal spinal reflexes seen in spastic diplegia can be abolished by inhaled N2O. This finding also suggests that N2O-induced depression of spinal reflexes should be a consideration during physiologic monitoring of the spinal cord under general anesthesia.

Cerebral Palsy↗

Anesthesia for stereotactic radiosurgery in children.

The development of stereotactic radiosurgery has been a major advance in the treatment of intracranial lesions. By using a stereotactic head frame attached to the skull, large doses of radiation can be delivered precisely to the lesion while sparing surrounding tissues. Although adults can usually undergo this procedure with local anesthesia or conscious sedation alone, children frequently require general anesthesia. This report describes our experience with the anesthetic management of all children who have received this therapy at our institution since the inception of our stereotactic radiosurgery program in 1986 through June 1993. Sixty-eight radiosurgery procedures were performed in 65 patients. Anesthesia time averaged 9.2 h (range, 7-15). Twenty-two patients (ages 11-17; mean 14.3) received local anesthesia alone, two patients (ages 11 and 15) received local anesthesia plus i.v. sedation, and 44 patients (ages 2-14; mean, 7.3) received general anesthesia. Four potentially serious anesthesia-related events occurred; in one child (age 7) receiving general anesthesia, an endotracheal tube obstruction developed during radiosurgery requiring rapid reintubation while the child was still in the head frame; another (age 7) who was undergoing chemotherapy and had neutropenia and rhinitis had a lobar collapse while intubated, requiring mechanical ventilation and endotracheal tube suctioning for lung expansion. Another (age 5) with a recent upper respiratory tract infection had copious endotracheal secretions and sinusitis (ethmoid and maxillary) noted on initial computed tomography scanning and was given antibiotics and decongestants (following nasotracheal extubation), and another (age 15) receiving sedation without endotracheal intubation vomited an undigested meal midway through the procedure while her head was partially immobilized in the head frame.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗