Loss of resistance to saline -- does the dripping bother you?
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Biomedical subjects
Publications and source records attributed to B Finucane.
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PURPOSE: To report the detection of subarachnoid and intravascular catheter placement using nerve stimulation through an epidural catheter. CLINICAL FEATURES: Electrical stimulation (1-10 mA) was applied through the catheter. A positive motor response (truncal or limb movement) indicated that the catheter was in the epidural space. Absence of a motor response indicated that it was not. A low milliamperage (<1 mA) with bilateral response indicated subarachnoid placement. Intravascular catheter placement was indicated by a positive response to the test, which remains at or returns to the baseline levels (i.e. prior to any local anesthetic injection), despite the administration of local anesthetics. In the first patient, the test confirmed subarachnoid catheter placement during attempts at continuous spinal anaesthesia even though CSF could not be aspirated. Bilateral motor response in the legs was observed at 0.2 mA. In the second patient, inadvertent subarachnoid placement was detected during attempted lumbar epidural block by observing bilateral motor response in the legs at 0.3 mA. In the third patient, intravascular placement was suspected and confirmed by failure to obliterate the motor response despite repeated local anesthetic injection. CONCLUSION: The new test provides objective information in managing epidural catheters when their position is uncertain.
A standardized assessment of autistic symptomatology was completed for 29 children and young adults with a supernumerary isodicentric chromosome 15 (formerly known as inverted duplication 15). Although there was variability in severity, 20 individuals with an isodicentric chromosome 15 [idic(15)] had a high probability of being autistic. Eight of the 9 remaining children were under age 5 years and were more sociable than the rest of the cohort. Group characteristics such as gender and seizure presence could not explain the observed difference between older and younger individuals in our study. The natural history of isodicentric 15 syndrome remains to be shown through longitudinal work and may include an age-related risk for developing autism.
PURPOSE: To examine the reliability of low current electrical epidural stimulation to confirm epidural catheter placement. METHODS: Forty patients with epidural catheters (19G Arrow Flextip plus) already in place for post-operative pain management were studied. An adapter (Arrow-Johans ECG Adapter) was attached to the connector of the epidural catheter. The epidural catheter and adapter were filled with normal saline. The cathode lead of the nerve stimulator was attached to the metal hub of the adapter. Catheter placement was judged to be correct or incorrect, depending upon the presence or absence of truncal or limb movement to 1 Hz stimulation (1-10 mA). A standard test dose (3 ml lidocaine 1.5% with 1:200,000 epinephrine) was then injected. The efficacy of the epidural morphine was assessed independently. RESULTS: The sensitivity and specificity of the test was 100% and 91.6% compared with the standard test dose. The positive and negative predictive value was 96% and 100%. In predicting the clinical effect of epidural morphine, the sensitivity and specificity was 96.1% and 76.9%. The positive and negative predictive value was 89% and 90%. The correlation of unilateral or bilateral motor response from the test and sensory response from the lidocaine test with sensitivity and specificity was 91.6% and 53.0%. The predictive value for unilateral response was 61% and for bilateral was 88%. CONCLUSION: This study establishes this test as a simple, objective and reliable technique for confirmation of epidural catheter placement.
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PURPOSE: To compare ropivacaine 0.5% with bupivacaine 0.5% for epidural anaesthesia for Caesarean section. METHODS: Healthy pregnant women, scheduled for elective Caesarean section were enrolled into this randomized, double-blind, parallel-group study. Epidural block was obtained with 20-30 ml of ropivacaine (group R) or bupivacaine (group B) and surgery started when anaesthesia was reached T6. Maternal heart rate and blood pressure and fetal heart rate were assessed before the test dose and at five minute intervals until the end of surgery. At the same intervals, sensory and motor block characteristics were determined. Apgar scores and Neurologic and Adaptive Capacity Scores (NACS) were determined after delivery. Adverse events were recorded. RESULTS: Sixty-five patients were enrolled and data from 61 were available for analysis; 30 ropivacaine and 31 bupivacaine. Time from the end of the last injection to the start of surgery was 46 +/- 13 min (mean +/- SD) in gp R and 53 +/- 25 min in gp B (P:NS). The median duration of analgesia varied between 1.7 and 4.2 hr in gp R and between 1.8 and 4.4 hr in gp B (P:NS). In patients who developed Bromage 4 block, it persisted longer in those in gp B (2.5 hr) than in gp R (0.9 hr) (P < 0.05). The quality of analgesia was satisfactory in 27/29 patients (93%) in gp R and 27/31 patients (87%) in gp B (P:NS), although supplemental i.v. opioid was required in ten and seven patients, respectively. The most common adverse events in the mother were hypotension (63% gp R and 61% in gp B) (NS) and nausea (30% and 58%, in group R and B, respectively) (P = 0.05). Apgar scores were 7 after five minutes in all neonates. CONCLUSION: Ropivacaine 0.5% and bupivacaine 0.5% provided effective epidural anaesthesia for Caesarean section although supplementation with i.v. opioid was commonly required.
PURPOSE: To evaluate a rapid and time-saving precurarization technique using rocuronium to prevent succinylcholine-induced myalgia. METHOD: In a prospective, double blind randomized study, 42 ASA 1-2 patients were assigned to one of three pretreatment groups: 0.01 ml.kg-1 normal saline, 0.1 mg.kg-1 atracurium, and 0.1 mg.kg-1 rocuronium. Anaesthesia commenced with 1.5 micrograms.kg-1 fentanyl and 0.5 mg.kg-1 lidocaine at time zero. Pretreatment was administered 60 sec later, followed by 2.5 mg.kg-1 propofol. At 90 sec, 1.5 mg.kg-1 succinylcholine was injected and 30 sec later, the trachea was intubated and the ease of intubation was graded. The patient was observed for the presence and severity of fasciculations. Myalgias were recorded on postoperative days 1, 2 and 7. RESULTS: The incidence of fasciculations in the rocuronium group (21.4%) was lower (P < 0.001) than atracurium (78.5%) or placebo (92.8%) groups. On postoperative day 1, the incidence of postoperative myalgia in the rocuronium group (14.2%) was less than the placebo group (78.2%; P < 0.002) and atracurium group (85.7%; P < 0.001). The incidence of myalgia in the rocuronium group (7.1%) was lower than in the placebo group (78.5%; P < 0.001) but not different from the atracurium group (42.8%; P = 0.077) on postoperative day 2. On postoperative day 7, there was no difference among the three groups. Fasciculations were related to postoperative myalgia. There was no difference in intubating conditions among the three groups. CONCLUSION: Rocuronium pretreatment given just before induction of anaesthesia with propofol reduces fasciculations and succinylcholine-induced myalgia.
Smith-Magenis syndrome (SMS) comprises a complex physical and behavioral phenotype that is associated with an interstitial deletion of chromosome 17p11.2. The deletions observed in patients can range from <2 to >9 megabases of DNA and may include more than 100 genes. In order to determine the critical deletion interval responsible for the syndrome phenotype, we have examined several patients with varying deletions involving 17p11.2 by somatic cell hybrid analyses. We have binned 112 markers along 17p11.2, including 27 markers within the critical interval for SMS, which is bound proximally by D17S29 and distally by cCI17-638. In addition, we present two patients who carry deletions involving 17p11.2 but do not exhibit the typical features of SMS. Patients such as these will allow genotype:phenotype correlations to be made and the gene(s) responsible for the SMS phenotype to be determined.
We conducted two multicenter studies on adaptive trajectories and profiles in males with fragile X syndrome. Study 1 longitudinally assessed 29 males ages 1-20 years using age-equivalent scores from the Vineland Adaptive Behavior Scales. Fragile X boys ages 1-10 years showed significant gains in adaptive skills from first to second testing; males ages 11-20 years were stable in their adaptive development. Study 2 cross-sectionally examined 132 males ages 1-20 years. Significant age-related gains were found in boys ages 1-10, particularly in preschool children. Subjects ages 11-20 showed increased variability and nonsignificant relations between age and adaptive skills. Preliminary findings from 26 young adults with fragile X syndrome ages 21-40 years showed stable age-equivalent adaptive scores during these years. Relative strengths in daily living skills and weaknesses in communication were only evident among older subjects. Significant relations were found between adaptive behavior standard scores and IQ; these two scores also showed age-related declines that likely parallel one another. Findings are related to adaptive features in other genetic syndromes, and to directions for future adaptive behavior research.
We have used bivariate flow karyotyping to quantify the deletions involving chromosome 17 in sixteen patients with Smith-Magenis syndrome (SMS). The fluorescence intensities of mitotic chromosomes stained with Hoechst 33258 and chromomycin were quantified in a dual-beam flow cytometer. For each patient, the position of the peak representing the deleted chromosome 17 was compared to those of the normal homologs of an unaffected parent. The patients could be classified into four groups based on the size of their deletions. The deletions ranged from approximately 9-10 Mb (approximately 10-11% of the chromosome) to below the detection limit of the technique (2 Mb). Different deletion sizes were detected among patients whose high-resolution banding results were similar. Some deletions detected by banding were not detected by flow analyses. Deletion estimates are largely consistent with the results of molecular analyses. Patients with larger deletions that extend into band 17p 12 have abnormal electrophysiologic studies of peripheral nerves. Deletion size does not appear to correlate with the degree of mental retardation, presence of behavioral abnormalities, craniofacial anomalies or common skeletal findings in SMS. By identifying patients with varying deletion sizes, these data will aid the construction of a long-range deletion-based map of 17p11.2 and identification of the genes involved in this syndrome.
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Fifth-eight people receiving residential or other services for idiopathic mental retardation were evaluated for evidence of metabolic disease. Five (8%) demonstrated persistent urinary organic acid abnormalities on at least three occasions, which pointed towards specific genetic metabolic defects. Instigation of specific treatment programs may have improved the quality of life for one of these participants. Appropriate genetic counseling was provided but could have been instigated much earlier had these investigations been performed as part of a routine workup for idiopathic mental retardation. This pilot study suggests a need for evaluation of other similar populations with idiopathic mental retardation.
The recent identification of an abnormally amplified trinucleotide (cytosine guanine guanine) repeat in the fragile X gene (FMR-1) of males with fragile X syndrome and their carrier mothers allows the study of the mutation in individuals at risk. In this report, data on 396 patients and 35 normal controls are reported. Included in this sample are patients with no known family history of fragile X syndrome or mental retardation for whom the risks of fragile X syndrome are unclear. All 39 cytogenetically positive affected males and six females had the full mutation, as represented by a restriction fragment size increase (delta) of 500 base pairs (bp) or more within the cytosine guanine guanine repeat-bearing fragment of the FMR-1 gene; and all 16 of the normal obligate carrier females bore the premutation, as demonstrated by a delta of 100 to 500 bp. Of 124 patients (62 males and 62 females) with a family history of fragile X syndrome, five (8%) of the males and 25 (40%) of the females had the premutation. Five (2.2%) of the 231 mentally impaired patients with no confirmed family history of fragile X syndrome were found to have the full mutation. Twelve (33%) of 36 mentally impaired males and one (20%) of five females with unknown family history were found to carry an amplified cytosine guanine guanine repeat. Using this technique, we also reevaluated risk assessments previously generated by linkage analysis and unambiguously determined the carrier status of individual family members.
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We present 2 unrelated children with a distinct pattern of anomalies, including mental retardation, hearing impairment, unusual facial appearance, and skeletal defects. Both children have severe behavior disturbance and hyperactivity. The characteristic facial findings include a broad mouth, broad nasal bridge, mildly anteverted nares with a fleshy nasal tip, and deep nasolabial folds. Skeletal findings include mild to moderate short stature, dysharmonic maturation of epiphyseal ossification centers in the hands, and mild scoliosis.
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The trajectory of cognitive development in males with fragile X syndrome was identified in a cross-sectional study of 56 males and in a smaller, longitudinal study of 10 fragile X males. Results from both studies indicated steady cognitive growth until late childhood and early adolescence (10 to 15 years of age), at which point mental age plateaued and IQ declined. Males with higher initial IQ scores manifested more IQ decline than those with initial lower levels of intelligence. The trajectories of IQ differ from those in other etiological groups and mixed groups of retarded individuals. Results have direct implications for intervention strategies with fragile X males. Parents and teachers should be informed about the possibility of an early plateau in mental age, the impact this may have on the child's academic performance, and that the plateau and IQ decline may not be apparent in the child's adaptive behaviors.