How has acute syndesmotic injury management evolved over the last decade? Results from a national survey.

The management of acute distal tibiofibular syndesmotic injuries has evolved over time and therefore, the aim of this study was to evaluate the use of different methods and the changes regarding management of distal tibiofibular syndesmotic injury among Dutch trauma- and orthopedic surgeons. A digital survey based on a previous survey conducted in 2012 was sent to (orthopedic) trauma surgeons from all different hospitals in the Netherlands. Sixty out of the 68 invited hospitals completed at least one survey (88.2 %). For Weber B or low Weber C fractures, there was a preference for the use of a single syndesmotic screw (SS)(73.6 %), while two screws were mainly used in Maisonneuve fractures (89.3 %). Furthermore, there was a clear preference for 3.5-mm screws, engaging three cortices, 2 to 4-cm above the tibiotalar joint. There is a significant decrease in routine removal of SSs (23.2 % compared to 87.0 % in 2012, p < 0.01). The percentage of hospitals in this survey that used the suture button (SB) was relatively low: 8.3 % for low fibular fractures and 5.0 % in high fibular fractures. In conclusion, the most striking difference compared to 2012 is the large decline in routine removal of the SS, which is in line with current literature. The SS is mainly implanted engaging three cortices, placed 2-4 cm above the tibiotalar joint and 3.5 mm in size and for the treatment of Maisonneuve fractures, two screws are preferred over a single SS. LEVEL OF EVIDENCE: Level III.

Minifragment plating of the fibula in unstable ankle fractures.

INTRODUCTION: Only 6.4-17% of the load is transmitted through the fibula when weight-bearing. Plate fixation of distal fibular fractures using minifragments (≤ 2.8 mm) could lead to similar reduction with less implant removal (IR) rates, compared to small-fragment plates (3.5 mm). We hypothesized that the use of minifragment plates is at least similar in unscheduled secondary surgery. MATERIALS AND METHODS: In this retrospective cohort study, all patients with surgically treated distal fibular fractures between October 2015 and March 2021 were included. Patients treated with plate fixation using minifragments and patients treated with small-fragment plates were compared regarding the following outcomes: secondary dislocation, malreduction, implant malposition, nonunion, surgical site infections (SSI) and IR. RESULTS: Sixty-five patients (54.2%) received a minifragment implant (≤ 2.8 mm) and 55 patients (45.8%) received a small-fragment implant (3.5 mm). There were no patients needing secondary surgery in the minifragment group compared to 9 patients following fixation using small-fragment implants (3 with secondary dislocation, 5 with malreduction and 1 with malposition, p = 0.001). SSI rates were 3.1% for minifragment and 9.1% for small-fragment implants (p = 0.161). Implant removal was performed significantly less often following use of minifragment implants (17.8% and 53.2%, p < 0.001). CONCLUSIONS: In this cohort, minifragment plate fixation for distal fibular fractures is an adequate fixation method offering stable fixation with significant lower need for implant removal and comparable complications to small-fragment plates, although an adequately powered randomized controlled study is needed for implementation in a clinical setting. LEVEL OF EVIDENCE: Therapeutic, III.

Cost-effectiveness of on-demand removal of syndesmotic screws.

PURPOSE: Syndesmotic screw removal following acute syndesmotic injury is a commonly performed procedure. However, recent studies suggest that the removal does not result in improved patient reported outcome, while the procedure has proved not to be without complications. The aim of this study was to present a health-economic evaluation of on-demand removal (ODR) compared to routine removal (RR) of the syndesmotic screw. METHODS: Data were collected from the RODEO trial, a randomized controlled non-inferiority trial comparing functional outcome of ODR with RR. Economic evaluation resulted in total costs, costs (in Euro) per quality adjusted life year (QALY) and costs per point improvement on the Olerud Molander Ankle Score (OMAS). This included both direct and indirect costs. RESULTS: Total costs for ODR were significantly lower with a mean difference of 3160 euro compared to RR (p < 0.001). The difference in QALY was not significant. The difference in OMAS at 12 months was 1.79 with an incremental cost-effectiveness ratio (ICER) of €-1763 (p = 0.512). The ICER was well below the willingness to pay. Although unit costs might vary between hospitals and countries, these results provide relevant data of cost-effectiveness. CONCLUSION: The clinical effectiveness of both ODR and RR can be considered equal. The costs are lower for patients treated with ODR, which leads to the conclusion that ODR is cost-effective.

Variation in caregiver perceptions of teamwork climate in labor and delivery units.

OBJECTIVE: To test the psychometric soundness of a teamwork climate survey in labor and delivery, examine differences in perceptions of teamwork, and provide benchmarking data. DESIGN: Cross-sectional survey of labor and delivery caregivers in 44 hospitals in diverse regions of the US, using the Safety Attitudes Questionnaire teamwork climate scale. RESULTS: The response rate was 72% (3382 of 4700). The teamwork climate scale had good internal reliability (overall alpha = 0.78). Teamwork climate scale factor structure was confirmed using multilevel confirmatory factor analyses (CFI = 0.95, TLI = 0.92, RMSEA = 0.12, SRMR(within) = 0.04, SRMR(between) = 0.09). Aggregation of individual-level responses to the L&D unit-level was supported by ICC (1) = 0.06 (P < 0.001), ICC (2) = 0.83 and mean r (wg(j)) = 0.83. ANOVA demonstrated differences between caregivers F (7, 3013) = 10.30, P < 0.001 and labor and delivery units, F (43, 1022) = 3.49, P < 0.001. Convergent validity of the scale scores was measured by correlations with external teamwork-related items: collaborative decision making (r = 0.780, P < 0.001), use of briefings (r = 0.496, P < 0.001) and perceived adequacy of staffing levels (r = 0.593, P < 0.001). CONCLUSION: We demonstrate a psychometrically sound teamwork climate scale, correlate it to external teamwork-related items, and provide labor and delivery teamwork benchmarks. Further teamwork climate research should explore the links to clinical and operational outcomes.

Extracellular glutamate levels and neuropathology in cerebral white matter following repeated umbilical cord occlusion in the near term fetal sheep.

Umbilical cord occlusion causes fetal hypoxemia which can result in brain injury including damage to cerebral white matter. Excessive glutamate release may be involved in the damage process. This study examined the relation between extracellular glutamate levels in the cerebral white matter of the ovine fetus during and after intermittent umbilical cord occlusion and the degree of resultant fetal brain injury. Fetal sheep underwent surgery for chronic catheterisation and implantation of an intra-cerebral microdialysis probe at 130 days of gestation (term approximately 147 days). Four days after surgery (day 1), seven fetuses were subjected to 5x2 min umbilical cord occlusions, and on the following day (day 2) they were subjected to either 4 or 5x4 min umbilical cord occlusions; seven fetuses served as controls. Microdialysis samples were collected before, during and after the umbilical cord occlusions to determine extracellular glutamate levels in the cerebral white matter. Fetal blood gas status was measured and the fetal electrocorticogram was recorded continuously. During the periods of umbilical cord occlusions on both days 1 and 2, fetal arterial oxygen saturation, arterial partial pressure of oxygen and arterial pH decreased (P<0.05) while arterial partial pressure of carbon dioxide increased (P<0.05). All fetuses showed episodes of isoelectric electrocortical activity during umbilical cord occlusions on both days 1 and 2. In fetuses with patent microdialysis probes there were marked increases of glutamate efflux in the cerebral white matter following umbilical cord occlusion. Fetal brains were removed at autopsy on day 5 and subjected to histological assessment. Brain damage was observed in all fetuses exposed to cord occlusion, particularly in the periventricular white matter, with the most extensive damage occurring in the fetuses with the greatest increases in glutamate levels. We conclude that, in the unanesthetised fetus in utero, glutamatergic processes are associated with umbilical cord occlusion-induced brain damage in the cerebral white matter.

Effect of hypoxia on glutamate efflux and synaptic transmission in the guinea pig hippocampus.

Simultaneous assessment of synaptic activity and glutamate efflux in guinea pig hippocampal brain slices was made before, during and after a 10-min period of hypoxia. Spontaneous glutamate efflux was assessed by determining glutamate concentration in the superfusion medium at discrete times using high performance liquid chromatography (HPLC). Synaptic activity was assessed using extracellular recording of the evoked population spike in the CA1 region following stimulation of the Schaffer collateral pathway. Hypoxia decreased (P < 0.05) the amplitude of the population spike by 3 min and abolished it by 5 min. This was accompanied by an increase (P < 0.05) in glutamate concentration in the superfusate at 10 min. Following re oxygenation, the population spike returned to baseline amplitude by 5 min and was greater (P < 0.05) than baseline at 10 and 20 min of recovery. Glutamate concentration returned to baseline levels by 1 min of recovery. This experimental preparation can be used to explore the temporal relationship between glutamate efflux and synaptic activity during hypoxia. The results of this study indicate that, in the hippocampal CA1 region, post-synaptic elements are more sensitive than their presynaptic counterparts to hypoxia.

Chronic hypoxemia causes extracellular glutamate concentration to increase in the cerebral cortex of the near-term fetal sheep.

Fetal hypoxia is an important cause of neurologic morbidity and mortality. Hypoxia-induced increase in extracellular glutamate concentration can lead to excitotoxic neuronal death in adults. The objective of this study was to test whether chronic fetal hypoxemia increases extracellular glutamate concentration in the unanesthetized intact cerebral cortex of the near-term fetal sheep. Microdialysis probes were implanted into the parasagittal parietal cortex and periventricular white matter of near-term fetal sheep. At 124 +/- 1 days of gestation, extracellular glutamate concentration was determined before and during 24 h of fetal hypoxemia. Chronic hypoxemia was produced by tightening a vascular occluder placed around the maternal common iliac artery. Larger decreases in fetal arterial oxygen content were associated with larger increases in extracellular glutamate concentration in the parietal cortex (Kendall's tau = 0.81, N = 7, p = 0.005). No such relationship was detected in the periventricular white matter. Chronic hypoxemia increases extracellular glutamate concentration in the intact cerebral cortex of the unanesthetized near-term fetal sheep.

Nitrate and nitrite anion concentration in the intact cerebral cortex of preterm and nearterm fetal sheep: indirect index of in vivo nitric oxide formation.

Pregnant sheep with a microdialysis probe implanted in the fetal cerebral cortex were used to determine if nitrate and nitrite anions (nitrate/nitrite) could be quantitated in the microdialysate as an indirect index of in vivo nitric oxide formation. Pregnant ewes (term, about 147 days) were surgically instrumented at gestational day (GD) 90 (n = 3; preterm) and GD 121 (n = 3; nearterm). Three days later, following an overnight probe equilibration period, five dialysate samples were collected continuously on ice at 1-h intervals (infusion rate of 1 (microl/min). The nitrate/nitrite concentration was determined by reducing a 10-microl aliquot of each dialysate fraction with hot acidic vanadium followed by chemiluminescence quantitation of the nitric oxide product. The lower limit of quantitative sensitivity of the method is 25 picomoles. Nitrate/nitrite concentration was 16.6+/-7.3 microM for the preterm fetus and 19.7+/-1.9 microM for the nearterm fetus. The data demonstrate that nitrate/nitrite, as an index of in vivo nitric oxide formation, can be quantitated in microdialysate samples collected from the intact fetal sheep cerebral cortex.

Effect of exposure in vitro to ethanol and hypoxia on gamma-aminobutyric acid efflux in the hippocampus of the fetal and adult guinea-pig.

The objective of this study was to determine the effects of acute direct exposure to ethanol, hypoxia or ethanol plus hypoxia on K+-stimulated gamma-aminobutyric acid (GABA) efflux (neuronal release minus uptake) in the hippocampus of the near-term fetal and adult guinea-pig. Transverse hippocampal slices were studied in a static-interface system. Exposure in vitro to ethanol or hypoxia involved 10-min incubation with 50 mM ethanol or 10-min incubation in a 95% N2/5% CO2 environment. GABA was quantitated by HPLC. Ethanol did not alter K+-stimulated GABA efflux; hypoxia augmented K+-stimulated GABA efflux three-fold in the near-term fetus and seven-fold in the adult; concurrent exposure to ethanol did not alter the effect of hypoxia. The data demonstrate that, for acute direct exposure to hypoxia and/or ethanol, only hypoxia increases K+-stimulated GABA efflux, the magnitude of which is dependent on the extent of development of the GABA system.

Bolus maternal cocaine administration does not produce a large increase in fetal sheep cerebral cortical glutamate concentration.

Human cocaine use during pregnancy may result in postnatal neurologic dysfunction and abnormal behavior. L-Glutamate, the major excitatory neurotransmitter in the brain, plays an important role in cerebral cortical development. An optimal level of glutamate is required for normal neuronal development. We tested whether acute cocaine exposure produces large increases in glutamate release in the intact cerebral cortex of the near-term fetal sheep. Cocaine 3.0 mg kg(-1) IV bolus produced the expected increase in maternal and fetal mean arterial pressure, increase in fetal heart rate, decrease in uterine blood flow, and decrease in fetal arterial blood pO2 (N = 5). The percentage increases in extracellular glutamate concentration in the fetal cerebral cortex measured by in utero microdialysis were 7%, 15%, 17%, 17%, and 43% in each fetus (upper 95% confidence bound for the median = 43%). We conclude that if cocaine increases glutamate concentration in the developing cerebral cortex, the increase in magnitude is small relative to the changes produced by other interventions such as ethanol or umbilical cord occlusion. Mechanisms other than increases in cerebral cortical glutamate concentration probably contribute to the neurologic injury associated with prenatal cocaine exposure.

Ethanol increases uterine blood flow and fetal arterial blood oxygen tension in the near-term pregnant ewe.

Fetal hypoxia is a hypothesized mechanism of ethanol teratogenesis. The objective of this study was to test this hypothesis by determining the effects of maternal ethanol infusion on uterine blood flow (UBF) and fetal oxygen status. UBF was measured with an electromagnetic flow probe placed around the left maternal uterine artery of the surgically recovered instrumented near-term pregnant sheep at 124 +/- 3 days of gestation (term = 147 days). Experimental treatment involved maternal infusion of 2 g (n = 3) or 4 g (n = 5) ethanol/kg maternal body weight, or 0.9% saline (n = 4) over a 5-h period. Arterial blood samples were collected at regular intervals to monitor maternal ethanol concentration and fetal PO2. Maternal ethanol infusion produced a dose-dependent increase (p = 0.0009) in UBF. Ethanol infusion also increased (p = 0.03) fetal arterial PO2. Overall, these findings indicate that fetal hypoxia is not a mechanism of ethanol teratogenesis.

Management of a parturient with an uncorrected atrioventricular canal defect.

A 24-year-old woman at 37 weeks gestation, with an uncorrected atrioventricular canal defect and incipient congestive heart failure is presented. This rare defect is part of the larger group of endocardial cushion defects. The peripartum anesthetic management of this condition has not been described. Our patient had a large atrial septal defect, a common regurgitant atrioventricular valve, a large left-to-right shunt and a small ventricular septal defect. Her pregnancy was maintained until she developed symptoms of congestive heart failure. We discuss her peripartum management, monitoring and anesthetic choices.

Anesthetic management of labor in a patient with congenitally corrected transposition of the great arteries.

Laboring patients with congenitally corrected transposition of the great arteries present an interesting challenge to anesthesiologists because of the physiological changes that take place during pregnancy and the stress induced by labor. This paper describes the detailed management of a symptomatic parturient with congenitally corrected transposition of the great arteries. The patient was managed with epidural analgesia instituted early in labor with a continuous low-concentration infusion of local anesthetic and opioid but without an initial bolus. She underwent uneventful forceps-assisted vaginal delivery.

Yohimbine-precipitated clonidine withdrawal: an experimental model of the antihypertensive drug withdrawal syndrome.

In this study, a model of the clonidine withdrawal syndrome in normotensive rats was used to investigate the mechanisms and sites of the cardiovascular responses associated with this withdrawal. Clonidine (400 micrograms.kg-1.day-1), an alpha 2-adrenergic receptor agonist, was administered to rats via indwelling osmotic minipumps for 7 days. Withdrawal was precipitated by an intravenous injection of the alpha 2-adrenergic receptor antagonist yohimbine under alpha-chloralose anaesthesia, and the blood pressure and heart rate responses were recorded. Yohimbine (0.25, 0.50, and 1.0 mg/kg i.v.) in clonidine-treated rats provoked an immediate rise in blood pressure and heart rate. Similar injections in saline-treated rats produced slight hypotension and modestly increased the heart rate. Intracerebroventricular (i.c.v.) yohimbine injection (30 or 120 micrograms/kg in 10 microL volume) failed to elicit signs of withdrawal in clonidine-treated animals, but a subsequent intravenous injection of yohimbine (0.5 mg/kg) provoked brisk signs of withdrawal. hexamethonium (2 mg/kg) pretreatment did not abolish the increase in the heart rate, but it delayed the blood pressure increase. Pretreatment with atropine sulfate (1 mg/kg) did not block the yohimbine-induced increase in heart rate or blood pressure. This study demonstrates that yohimbine can effectively produce cardiovascular signs of withdrawal in rats chronically exposed to clonidine. The lack of i.c.v. yohimbine suggests that the antagonist-precipitated withdrawal may not have a central origin.(ABSTRACT TRUNCATED AT 250 WORDS)

Obstetrical analgesia in a parturient with antithrombin III deficiency.

Antithrombin III (AT III) deficiency is a rare inherited disorder which predisposes patients to thrombotic complications. Anticoagulation is necessary to prevent recurrent thrombosis and high doses of heparin are often required. Anticoagulation complicates analgesia in parturients with the condition. We describe such a patient, in pre-term labour, who was successfully managed during labour with intravenous nalbuphine and inhaled nitrous oxide (N2O).

Epidural analgesia in parturients with previous spinal irradiation.

PURPOSE: To present two successful cases of labour analgesia in patients who had been treated with radiation to the lumbar spine for neuroblastomas and to discuss the considerations when planning the anaesthetic management of these patients. CLINICAL FEATURES: We recently encountered two primigravidas requesting labour analgesia, both of whom were noted to have very thin backs with prominent spinous processes and obvious scoliosis. In both patients, the epidural space was easily identified and very shallow. Successful labour analgesia was achieved in both patients, one with a combined spinal epidural technique and the other with an epidural catheter. CONCLUSION: Craniospinal irradiation is known to have long-term effects on exposed nervous tissue, bone, and blood vessels. While a larger experience is necessary to demonstrate safety of regional anaesthesia in parturients following previous spinal irradiation, we provide reports of two successful cases.

Anesthesia for Cesarean section in a patient with paraplegia resulting from tumour metastases to spinal cord.

PURPOSE: Spinal cord injured patients present multiple unique challenges to the anesthesiologist. These include choice of muscle relaxant and management of autonomic hyperreflexia. We report the anesthetic management for Cesarean delivery in a patient who was paraplegic due to spinal canal metastases. Preeclampsia and fever complicated this case. CLINICAL FEATURES: The patient presented at 29 wk gestation with progressive paraplegia at the T10 level due to metastatic osteosarcoma. She had a decompressive laminectomy without improvement in her paralysis. She subsequently developed preeclampsia at 31 wk gestation, and underwent Cesarean delivery for breech presentation under general anesthesia. Anatomical concerns left us unsure of the efficacy or safety of neuraxial anesthesia. CONCLUSIONS: Preeclampsia and autonomic hyperreflexia are generally indications for regional anesthesia for Cesarean section. Tumour in her spinal canal and laboratory abnormalities including thrombocytopenia and a potential urosepsis dissuaded us from this option. Additionally, rapid sequence induction and intubation were not preferred due to paraplegia, leading us to secure the airway fibreoptically.

Flumazenil does not affect the increase in rat hippocampal extracellular glutamate concentration produced during thioacetamide-induced hepatic encephalopathy.

Hepatic encephalopathy (HE) is a neuropsychiatric disorder that often occurs as a consequence of acute or chronic liver failure. Previous reports have suggested that alterations in amino acid neurotransmission, particularly glutamate, may play an important role in the pathogenesis of HE. The objectives of the present study were to test the hypothesis that extracellular glutamate concentration is increased during HE, and to determine if flumazenil, a benzodiazepine antagonist, alters the extracellular concentration of glutamate during HE. The experimental approach involved using microdialysis probes to measure rat hippocampal extracellular glutamate concentration. HE was brought about as a result of thioacetamide-induced liver failure. Thioacetamide produced behavioral and metabolic effects, such as somnolence, hyperventilation and hyperammonemia, consistent with stage three HE. Comparison with saline-treated rats demonstrated that HE was associated with a significant increase (p = 0.010) in extracellular hippocampal glutamate concentration. Administration of flumazenil caused a transient increase in arousal level, but did not affect the increase in glutamate concentration (p = 0.93). These results corroborate the theory that glutamate neurotransmission is altered during HE and suggest that the flumazenil arousal of HE rats is not mediated by a change in extracellular glutamate concentration.

Glutamate release from the ovine fetal brain during maternal hemorrhage. A study using chronic in utero cerebral microdialysis.

BACKGROUND: Glutamate has been implicated in the pathophysiology of neuronal injury associated with cerebral hypoxia-ischemia. A model using chronic in utero microdialysis was developed to sample the extracellular space of the fetal brain. Using this model, we tested the hypothesis that glutamate efflux from the parasagittal parietal cortex of near-term fetuses would increase during maternal hemorrhage. METHODS: Twelve near-term fetal sheep were instrumented with vascular catheters, and a microdialysis probe(s) was implanted into the parasagittal parietal cortex. After a 3-day recovery period, the animals were subjected to maternal hemorrhage until either the fetal pH was < 7.00 or the fetus died. The extracellular glutamate concentration in the collected dialysate was determined by high pressure liquid chromatography (HPLC). RESULTS: Maternal hemorrhage resulted in an 80-90% decrease in uterine blood flow, a decrease fetal po2, and a mixed metabolic and respiratory fetal acidosis. There were two groups of fetuses, survivors (n = 5) and nonsurvivors (n = 7). The nonsurvivor group showed a large increase (10-30-fold) in peak glutamate release (P = 0.0015). Survivors demonstrated a small (threefold) increase that was not statistically significant (P = 0.065), unless one animal with very low probe recovery was excluded (P = 0.0048). CONCLUSIONS: Extracellular glutamate release from the fetal brain can occur during maternal hemorrhage with fetal acidemia. The pathophysiologic role (if any) of glutamate release in the survivors remains to be elucidated. Our results are consistent with the hypothesis that in utero release of glutamate occurs during periods of fetal asphyxia. This experimental preparation of chronic fetal brain microdialysis can be used to monitor the brain extracellular concentration of any dialyzable substance in response to stress, including maternal hemorrhage.

Neuropathology of the near-term and midgestation ovine fetal brain after sustained in utero hypoxemia.

OBJECTIVE: The neuropathologic mechanisms of the ovine fetal brain in response to several hours of sustained hypoxemia with variable degrees of metabolic acidemia was investigated in both the preterm and near-term ovine fetus. STUDY DESIGN: Three groups of fetuses were studied in each of the near-term and midgestation groups: a hypoxic group, a control group, and an uninstrumented control group. Histopathologic studies were performed after a 40-hour recovery period after experimentation. RESULTS: Pathologic findings consisted of predominately white matter damage with some adjacent cortical necrosis but no selective neuronal injury. In the near-term group the hypoxia group fetuses demonstrated significantly higher white matter injury scores than did control group fetuses (p < 0.05). Periventricular white matter injury was the predominant pattern seen in the midgestation group. CONCLUSIONS: In spite of normalization of biophysical and biochemical parameters after hypoxemia both midgestation and near-term fetuses sustained pathologic changes. Presence or extent of injury did not correlate with the degree of hypoxemia or metabolic acidosis achieved.