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METHODS: 28 adults (16 males and 12 females) aged 30 ± 10 y [peak oxygen uptake (V̇O2peak): 59 ± 11 ml·kg-1·min-1] completed three experimental trials in a randomized, crossover, and double-blinded manner. Participants ingested either 0.3 (KE-LO) or 0.6 (KE-HI) g·kg-1 body mass of KE or a flavour-matched placebo (PLAC) ~30 min prior to exercise. Exercise involved a 3-minute warm-up, three 5-minute stages at fixed incremental workloads corresponding to 75%, 100%, and 125% of individual ventilatory threshold, followed by a ramp protocol to volitional exhaustion to determine peak power output (PPO). RESULTS: Venous blood [ß-hydroxybutyrate], the major circulating ketone body, was higher after KE ingestion compared to PLAC (KE-HI: 3.0 ± 1.1 ≥ KE-LO: 2.3 ± 0.6 ≥ PLAC: 0.2 ± 0.1 mM; all p ≤ 0.001. There were no differences between conditions in the primary outcome exercise economy, nor gross efficiency or delta efficiency, when analyzed over the entire submaximal exercise period or by stage. Heart rate and ventilation were higher in KE-HI and KE-LO compared to PLAC when assessed over the entire submaximal exercise period and by stage (all p ≤ 0.05). PPO after the ramp was lower in KE-HI compared to both KE-LO and PLAC (329 ± 60 vs 339 ± 62 and 341 ± 61 W respectively; both p < 0.05) despite no difference in V̇O2peak. CONCLUSIONS: KE ingestion did not change indices of exercise efficiency but increased markers of cardiorespiratory stress during submaximal incremental cycling and reduced PPO.

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Sprint interval training (SIT) increases peak oxygen uptake (V̇O2peak) but the mechanistic basis is unclear. We have reported that 12 wk of SIT increased V̇O2peak and peak cardiac output (Q̇peak) and the changes in these variables were correlated. An exploratory analysis suggested that Q̇peak increased in males but not females. The present study incorporated best practices to examine the potential influence of biological sex on the Q̇peak response to SIT. Male and female participants (n = 10 each; 21 ± 4 y) performed 33 ± 2 sessions of SIT over 12 wk. Each 10-min session involved 3 × 20-s 'all-out' sprints on an ergometer. V̇O2peak increased after SIT (3.16 ± 1.0 vs. 2.89 ± 1.0 L/min, η2p = 0.53, p < 0.001) with no sex × time interaction (p = 0.61). Q̇peak was unchanged after training (15.2 ± 3.3 vs. 15.1 ± 3.0 L/min, p = 0.85), in contrast to our previous study. The peak estimated arteriovenous oxygen difference increased after training (204 ± 30 vs. 187 ± 36 ml/L, p = 0.006). There was no effect of training or sex on measures of endothelial function. We conclude that 12 wk of SIT increases V̇O2peak but the mechanistic basis remains unclear. The capacity of inert gas rebreathing to assess changes in Q̇peak may be limited and invasive studies that use more direct measures are needed.

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Vigorous intermittent exercise can improve indices of glycemia in the 24 h postexercise period in apparently healthy individuals. We examined the effect of a single session of bodyweight exercise (BWE) on glycemic responses using continuous glucose monitoring (CGM) under controlled dietary conditions. Healthy inactive adults (n = 27; 8 males, 19 females; age: 23 ± 3 years) completed 2 virtually supervised trials spaced ~ 1 week apart in a randomized, crossover manner. The trials involved an 11-min BWE protocol that consisted of 5 × 1-min bouts performed at a self-selected pace interspersed with 1-min active recovery periods or a non-exercise sitting control period (CON). Mean heart rate during the BWE protocol was 147 ± 14 beats per min (75% of age-predicted maximum). Mean 24 h glucose after BWE and CON was not different (5.0 ± 0.4 vs 5.0 ± 0.5 mM respectively; p = 0.39). There were also no differences between conditions for measures of glycemic variability or the postprandial glucose responses after ingestion of a 75 g glucose drink or lunch, dinner, and breakfast meals. This study demonstrates the feasibility of conducting a remotely supervised BWE intervention using CGM under free-living conditions. Future studies should investigate the effect of repeated sessions of BWE training or responses in people with impaired glycemic control.

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Acute ketone monoester (KE) supplementation can alter exercise responses, but the performance effect is unclear. The limited and equivocal data to date are likely related to factors including the KE dose, test conditions, and caliber of athletes studied. We tested the hypothesis that mean power output during a 20-min cycling time trial (TT) would be different after KE ingestion compared to a placebo (PL). A sample size of 22 was estimated to provide 80% power to detect an effect size dz of 0.63 at an alpha level of .05 with a two-tailed paired t test. This determination considered 2.0% as the minimal important difference in performance. Twenty-three trained cyclists (N = 23; peak oxygen uptake: 65 ± 12 ml·kg-1 min-1; M ± SD), who were regularly cycling >5 hr/week, completed a familiarization trial followed by two experimental trials. Participants self-selected and replicated their diet and exercise for ∼24 hr before each trial. Participants ingested either 0.35 g/kg body mass of (R)-3-hydroxybutyl (R)-3-hydroxybutyrate KE or a flavor-matched PL 30 min before exercise in a randomized, triple-blind, crossover manner. Exercise involved a 15-min warm-up followed by the 20-min TT on a cycle ergometer. The only feedback provided was time elapsed. Preexercise venous [ß-hydroxybutyrate] was higher after KE versus PL (2.0 ± 0.6 vs. 0.2 ± 0.1 mM, p < .0001). Mean TT power output was 2.4% (0.6% to 4.1%; mean [95% confidence interval]) lower after KE versus PL (255 ± 54 vs. 261 ± 54 W, p < .01; dz = 0.60). The mechanistic basis for the impaired TT performance after KE ingestion under the present study conditions remains to be determined.

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PURPOSE: This study aimed to examine the effect of KE ingestion on exercise cardiac output ( Q˙ ) and the influence of blood acidosis. We hypothesized that KE versus placebo ingestion would increase Q ˙, and coingestion of the pH buffer bicarbonate would mitigate this effect. METHODS: In a randomized, double-blind, crossover manner, 15 endurance-trained adults (peak oxygen uptake (V̇O 2peak ), 60 ± 9 mL·kg -1 ·min -1 ) ingested either 0.2 g·kg -1 sodium bicarbonate or a salt placebo 60 min before exercise, and 0.6 g·kg -1 KE or a ketone-free placebo 30 min before exercise. Supplementation yielded three experimental conditions: basal ketone bodies and neutral pH (CON), hyperketonemia and blood acidosis (KE), and hyperketonemia and neutral pH (KE + BIC). Exercise involved 30 min of cycling at ventilatory threshold intensity, followed by determinations of V̇O 2peak and peak Q ˙. RESULTS: Blood [ß-hydroxybutyrate], a ketone body, was higher in KE (3.5 ± 0.1 mM) and KE + BIC (4.4 ± 0.2) versus CON (0.1 ± 0.0, P < 0.0001). Blood pH was lower in KE versus CON (7.30 ± 0.01 vs 7.34 ± 0.01, P < 0.001) and KE + BIC (7.35 ± 0.01, P < 0.001). Q ˙ during submaximal exercise was not different between conditions (CON: 18.2 ± 3.6, KE: 17.7 ± 3.7, KE + BIC: 18.1 ± 3.5 L·min -1 ; P = 0.4). HR was higher in KE (153 ± 9 bpm) and KE + BIC (154 ± 9) versus CON (150 ± 9, P < 0.02). V̇O 2peak ( P = 0.2) and peak Q ˙ ( P = 0.3) were not different between conditions, but peak workload was lower in KE (359 ± 61 W) and KE + BIC (363 ± 63) versus CON (375 ± 64, P < 0.02). CONCLUSIONS: KE ingestion did not increase Q ˙ during submaximal exercise despite a modest elevation of HR. This response occurred independent of blood acidosis and was associated with a lower workload at V̇O 2peak .

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PURPOSE: This study aimed to compare Q˙peak elicited by a constant load protocol ( Q˙CL ) and an incremental step protocol ( Q˙step ). METHODS: A noninferiority randomized crossover trial was used to compare Q˙peak between protocols using a noninferiority margin of 0.5 L·min -1 . Participants ( n = 34 (19 female, 15 male); 25 ± 5 yr) performed two baseline V̇O 2peak tests to determine peak heart rate (HR peak ) and peak work rate ( Wpeak ). Participants then performed the Q˙CL and Q˙step protocols each on two separate occasions with the order of the four visits randomized. Q˙peak was measured using IGR (Innocor; COSMED, Rome, Italy). The Q˙CL protocol involved a V̇O 2peak test followed 10 min later by cycling at 90% Wpeak , with IGR initiated after 2 min. Q˙step involved an incremental step test with IGR initiated when the participant's HR reached 5 bpm below their HR peak . The first Q˙CL and Q˙step tests were compared for noninferiority, and the second series of tests was used to measure repeatability (typical error (TE)). RESULTS: The Q˙CL protocol was noninferior to Q˙step ( Q˙CL = 17.1 ± 3.2, Q˙step = 16.8 ± 3.1 L·min -1 ; 95% confidence intervals, -0.16 to 0.72 L·min -1 ). The baseline V̇O 2peak (3.13 ± 0.83 L·min -1 ) was achieved during Q˙CL (3.12 ± 0.72, P = 0.87) and Q˙step (3.12 ± 0.80, P = 0.82). The TE values for Q˙peak were 6.6% and 8.3% for Q˙CL and Q˙step , respectively. CONCLUSIONS: The Q˙CL protocol was noninferior to Q˙step and may be more convenient because of the reduced time commitment to perform the measurement.

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OBJECTIVE: This article aimed to evaluate pregnancy outcomes when a plan to perform fetal blood sampling (FBS) or delivery was based solely on the first abnormal middle cerebral artery peak velocity (MCA-PV) measurement compared with making a plan after a confirmatory test on a subsequent day. STUDY DESIGN: We performed a descriptive study of pregnancy outcomes including all patients in a single healthcare system with maternal red cell alloimmunization undergoing ultrasound between 2005 and 2017 who had at least one MCA-PV>1.5 multiples of the median (MoM). We excluded patients with any sign of hydrops prior to the index visit or abnormal MCA-PV at>35 weeks. The first exam with a MCA-PV>1.5 MoM was deemed the index visit. RESULTS: Fifty patients were identified. Twenty-one patients underwent intervention (FBS or delivery) based on the first abnormal MCA-PV. Of those, 9 had moderate or severe anemia (positive predictive value [PPV]: 43%), while 12 had mild or no anemia. The other 29 patients underwent a confirmatory MCA test between 2 and 8 days later. Of these, 13 patients had an abnormal confirmatory test and 11 of these underwent FBS and 7 had moderate or severe anemia (PPV: 54%). Sixteen patients undergoing confirmatory MCA Doppler had a normal test on repeat and did not undergo FBS. Of those, none developed moderate or severe anemia. CONCLUSION: A substantial number of patients (55%) had normal MCA-PV testing on repeat, allowing avoidance of invasive testing. Deferring FBS until the abnormal MCA-PV was confirmed was not associated with undetected moderate or severe anemia. KEY POINTS: · False-positive results from MCA-PV Doppler prediction of fetal anemia are common.. · Repeat noninvasive testing is normal in many patients with suspected fetal anemia.. · Invasive fetal testing can often be safely avoided by performing a confirmatory Doppler exam ination..

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INTRODUCTION: Sprint interval training (SIT), characterized by brief bouts of 'supramaximal' exercise interspersed with recovery periods, increases peak oxygen uptake ([Formula: see text]) despite a low total exercise volume. Per the Fick principle, increased [Formula: see text] is attributable to increased peak cardiac output ([Formula: see text]) and/or peak arterio-venous oxygen difference (a-vO2diff). There are limited and equivocal data regarding the physiological basis for SIT-induced increases in [Formula: see text], with most studies lasting ≤ 6 weeks. PURPOSE: To determine the effect of 12 weeks of SIT on [Formula: see text], measured using inert gas rebreathing, and the relationship between changes in [Formula: see text] and [Formula: see text]. METHODS: 15 healthy untrained adults [6 males, 9 females; 21 ± 2 y (mean ± SD)] performed 28 ± 3 training sessions. Each session involved a 2-min warm-up at 50 W, 3 × 20-s 'all-out' cycling bouts (581 ± 221 W) interspersed with 2-min of recovery, and a 3-min cool-down at 50 W. RESULTS: Measurements performed before and after training showed that 12 weeks of SIT increased [Formula: see text] (17.0 ± 3.7 vs 18.1 ± 4.6 L/min, p = 0.01, partial η2 = 0.28) and [Formula: see text] (2.63 ± 0.78 vs 3.18 ± 1.1 L/min, p < 0.01, partial η2 = 0.58). The changes in these two variables were correlated (r2 = 0.46, p < 0.01). Calculated peak a-vO2diff also increased after training (154 ± 22 vs 174 ± 23 ml O2/L; p < 0.01) and was correlated with the change in [Formula: see text] (r2 = 0.33, p = 0.03). Exploratory analyses revealed an interaction (p < 0.01) such that [Formula: see text] increased in male (+ 10%, p < 0.01) but not female participants (+ 0.6%, p = 0.96), suggesting potential sex-specific differences. CONCLUSION: Twelve weeks of SIT increased [Formula: see text] by 6% in previously untrained participants and the change was correlated with the larger 21% increase in [Formula: see text].

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There is growing interest in the effect of exogenous ketone body supplementation on exercise responses and performance. The limited studies to date have yielded equivocal data, likely due in part to differences in dosing strategy, increase in blood ketones, and participant training status. Using a randomized, double-blind, counterbalanced design, we examined the effect of ingesting a ketone monoester (KE) supplement (600 mg/kg body mass) or flavour-matched placebo in endurance-trained adults (n = 10 males, n = 9 females; V̇O2peak = 57 ± 8 mL/kg/min). Participants performed a 30-min cycling bout at ventilatory threshold intensity (71 ± 3% V̇O2peak), followed 15 min later by a 3 kJ/kg body mass time-trial. KE versus placebo ingestion increased plasma ß-hydroxybutyrate concentration before exercise (3.9 ± 1.0 vs 0.2 ± 0.3 mM, p < 0.0001, dz = 3.4), ventilation (77 ± 17 vs 71 ± 15 L/min, p < 0.0001, dz = 1.3) and heart rate (155 ± 11 vs 150 ± 11 beats/min, p < 0.001, dz = 1.2) during exercise, and rating of perceived exertion at the end of exercise (15.4 ± 1.6 vs 14.5 ± 1.2, p < 0.01, dz = 0.85). Plasma ß-hydroxybutyrate concentration remained higher after KE vs placebo ingestion before the time-trial (3.5 ± 1.0 vs 0.3 ± 0.2 mM, p < 0.0001, dz = 3.1), but performance was not different (KE: 16:25 ± 2:50 vs placebo: 16:06 ± 2:40 min:s, p = 0.20; dz = 0.31). We conclude that acute ingestion of a relatively large KE bolus dose increased markers of cardiorespiratory stress during submaximal exercise in endurance-trained participants. Novelty: Limited studies have yielded equivocal data regarding exercise responses after acute ketone body supplementation. Using a randomized, double-blind, placebo-controlled, counterbalanced design, we found that ingestion of a large bolus dose of a commercial ketone monoester supplement increased markers of cardiorespiratory stress during cycling at ventilatory threshold intensity in endurance-trained adults.

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BACKGROUND: Most low-risk obstetric patients do not have crossmatched blood available to treat unexpected postpartum hemorrhage. An emergency-release blood transfusion (ERBT) program is critical for hospitals with obstetrical services. We performed a retrospective analysis of obstetrical ERBTs administered in our multihospital system. DESIGN AND METHODS: We collected data from the past 8 years at all Intermountain Healthcare hospitals on every ERBT after postpartum hemorrhage; logging circumstances, number and type of transfused products, and outcomes. RESULTS: Eighty-nine women received ERBT following 224,035 live births, for an incidence of 3.97 transfused women/10,000 births. The most common causally-associated conditions were: uterine atony (40%), placental abruption/placenta previa (16%), retained placenta (11%), and uterine rupture (5%). The mean number of total units transfused was 7.9 (range 1-76). The mean number of red blood cells (RBCs) transfused was 4.8, the median 4, and SD was ±4.4. Massive transfusion protocols (MTPs) for trauma recommend using a ratio of 1:1:1 or 2:1:1 of RBC:FFP:Platelets, however the ratios varied widely for postpartum hemorrhage. Only 1.5% received a 1:1:1 ratio and 7.5% received a 2:1:1 ratio. Nineteen percent (17/89) of women underwent hysterectomy, 7% (6/89) had uterine artery embolization, 36% (32/89) had an intensive care unit admission, and 1% (1/89) died. CONCLUSION: Emergency transfusion for postpartum hemorrhage occurred after 1/2500 births. Most women received less FFP and platelets than recommended for traumatic hemorrhage. A potentially better practice for postpartum hemorrhage would be a balanced ratio of blood products, transfusion of low-titer, group O, cold-stored, whole blood, or inclusion in a MTP.

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This chapter describes several circumstances in which the interpretation of the intrapartum fetal heart rate pattern falls outside the usual frame of reference. This includes a more extensive discussion of causes of tachycardia and bradycardia. Ways in which a fetal dysrhythmia may manifest itself in the context of heart rate monitoring are described. Finally, the chapter reviews technological innovations designed to clarify the fetal status when compromise is suspected from the fetal heart rate pattern.

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OBJECTIVE: A short cervix is an important risk factor for spontaneous preterm birth. There is substantial evidence that antenatal exposure to corticosteroids significantly benefits infants that are born when delivery occurs between 24 and 34 weeks' gestation and after 48 hours but within 7 days of their administration. Our study was to evaluate whether asymptomatic women who are given a course of antenatal corticosteroids (ACS) at the time a short cervix is identified deliver within the window of proven steroid benefit. STUDY DESIGN: This was a retrospective chart review of patients who had a cervical length of < 2.5 cm between 23 and 34 weeks and who did not have cervical dilation or significant symptoms of preterm labor. RESULTS: Of 367 asymptomatic patients with a short cervix, only two (0.5%) delivered within 7 days of the time a short cervix was identified. With a policy of giving ACS at the time an ultrasound shows a short cervix, 184 patients would have to be treated for each one who realizes a steroid benefit by delivering within 7 days. CONCLUSION: We conclude that unless future studies show that neonates benefit from ACS given more than 7 days before delivery, giving ACS to asymptomatic women solely because the cervix is short is not advised.

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Use of marginal liver grafts, especially those from donors after circulatory death (DCD), has been considered as a solution to organ shortage. Inferior outcomes have been attributed to donor warm ischaemic damage in these DCD organs. Here we sought to profile the metabolic mechanisms underpinning donor warm ischaemia. Non-targeted Fourier transform ion cyclotron resonance (FT-ICR) mass spectrometry metabolomics was applied to biopsies of liver grafts from donors after brain death (DBD; n = 27) and DCD (n = 10), both during static cold storage (T1) as well as post-reperfusion (T2). Furthermore 6 biopsies from DBD donors prior to the organ donation (T0) were also profiled. Considering DBD and DCD together, significant metabolic differences were discovered between T1 and T2 (688 peaks) that were primarily related to amino acid metabolism, meanwhile T0 biopsies grouped together with T2, denoting the distinctively different metabolic activity of the perfused state. Major metabolic differences were discovered between DCD and DBD during cold-phase (T1) primarily related to glucose, tryptophan and kynurenine metabolism, and in the post-reperfusion phase (T2) related to amino acid and glutathione metabolism. We propose tryptophan/kynurenine and S-adenosylmethionine as possible biomarkers for the previously established higher graft failure of DCD livers, and conclude that the associated pathways should be targeted in more exhaustive and quantitative investigations.

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OBJECTIVES: The sensitivity of sonography to predict accreta has been reported as higher than 90%. However, most studies are from single expert investigators. Our objective was to analyze interobserver variability of sonography for prediction of placenta accreta. METHODS: Patients with previa with and without accreta were ascertained, and images with placental views were collected, deidentified, and placed in random sequence. Three radiologists and 3 maternal-fetal medicine specialists interpreted each study for the presence of accreta and specific findings reported to be associated with its diagnosis. Investigator-specific sensitivity, specificity, and accuracy were calculated. κ statistics were used to assess variability between individuals and types of investigators. RESULTS: A total of 229 sonographic studies from 55 patients with accreta and 56 control patients were examined. Accuracy ranged from 55.9% to 76.4%. Of imaging studies yielding diagnoses, sensitivity ranged from 53.4% to 74.4%, and specificity ranged from 70.8% to 94.8%. Overall interobserver agreement was moderate (mean κ ± SD = 0.47 ± 0.12). κ values between pairs of investigators ranged from 0.32 (fair agreement) to 0.73 (substantial agreement). Average individual agreement ranged from fair (κ = 0.35) to moderate (κ = 0.53). CONCLUSIONS: Blinded from clinical data, sonography has significant interobserver variability for the diagnosis of placenta accreta.

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Metabolomics in systems biology research unravels intracellular metabolic changes by high throughput methods, but such studies focusing on liver transplantation (LT) are limited. Microdialysate samples of liver grafts from donors after circulatory death (DCD; n=13) and brain death (DBD; n=27) during cold storage and post-reperfusion phase were analyzed through coulometric electrochemical array detection (CEAD) for identification of key metabolomics changes. Metabolite peak differences between the graft types at cold phase, post-reperfusion trends, and in failed allografts, were identified against reference chromatograms. In the cold phase, xanthine, uric acid, and kynurenine were overexpressed in DCD by 3-fold, and 3-nitrotyrosine (3-NT) and 4-hydroxy-3-methoxymandelic acid (HMMA) in DBD by 2-fold (p<0.05). In both grafts, homovanillic acid and methionine increased by 20%-30% with each 100 min increase in cold ischemia time (p<0.05). Uric acid expression was significantly different in DCD post-reperfusion. Failed allografts had overexpression of reduced glutathione and kynurenine (cold phase) and xanthine (post-reperfusion) (p<0.05). This differential expression of metabolites between graft types is a novel finding, meanwhile identification of overexpression of kynurenine in DCD grafts and in failed allografts is unique. Further studies should examine kynurenine as a potential biomarker predicting graft function, its causation, and actions on subsequent clinical outcomes.

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BACKGROUND: Congenital diaphragmatic hernia (CDH) is a frequently lethal birth defect and, despite advances, extracorporeal life support (ie, extracorporeal membrane oxygenation [ECMO]) is commonly required for severely affected patients. Published data suggest that CDH survival after 2 weeks on ECMO is poor. Many centers limit duration of ECMO support. STUDY DESIGN: We conducted a single-institution retrospective review of 19 years of CDH patients treated with ECMO, designed to evaluate which factors affect survival and duration of ECMO and define how long patients should be supported. RESULTS: Of two hundred and forty consecutive CDH patients without lethal associated anomalies, 96 were treated with ECMO and 72 (75%) survived. Eighty required a single run of ECMO and 65 survived (81%), 16 required a second ECMO run and 7 survived (44%). Of patients still on ECMO at 2 weeks, 56% survived, at 3 weeks 46% survived, and at 4 weeks, 43% of patients still on ECMO survived to discharge. After 5 weeks of ECMO, survival had dropped to 15%, and after 40 days of ECMO support there were no survivors. Apgar score at 1 minute, Apgar score at 5 minutes, and Congenital Diaphragmatic Hernia Study Group predicted survival all correlated with survival on ECMO, need for second ECMO, and duration of ECMO. Lung-to-head ratio also correlated with duration of ECMO. All survivors were discharged breathing spontaneously with no support other than nasal cannula oxygen if needed. CONCLUSIONS: In patients with severe CDH, improvement in pulmonary function sufficient to wean from ECMO can take 4 weeks or longer, and might require a second ECMO run. Pulmonary outcomes in these CDH patients can still be excellent, and the assignment of arbitrary ECMO treatment durations <4 weeks should be avoided.

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OBJECTIVE: Ultrasound has been reported to be greater than 90% sensitive for the diagnosis of accreta. Prior studies may be subject to bias because of single expert observers, suspicion for accreta, and knowledge of risk factors. We aimed to assess the accuracy of ultrasound for the prediction of accreta. STUDY DESIGN: Patients with accreta at a single academic center were matched to patients with placenta previa, but no accreta, by year of delivery. Ultrasound studies with views of the placenta were collected, deidentified, blinded to clinical history, and placed in random sequence. Six investigators prospectively interpreted each study for the presence of accreta and findings reported to be associated with its diagnosis. Sensitivity, specificity, positive predictive, negative predictive value, and accuracy were calculated. Characteristics of accurate findings were compared using univariate and multivariate analyses. RESULTS: Six investigators examined 229 ultrasound studies from 55 patients with accreta and 56 controls for 1374 independent observations. 1205/1374 (87.7% overall, 90% controls, 84.9% cases) studies were given a diagnosis. There were 371 (27.0%) true positives; 81 (5.9%) false positives; 533 (38.8%) true negatives, 220 (16.0%) false negatives, and 169 (12.3%) with uncertain diagnosis. Sensitivity, specificity, positive predictive value, negative predictive value, and accuracy were 53.5%, 88.0%, 82.1%, 64.8%, and 64.8%, respectively. In multivariate analysis, true positives were more likely to have placental lacunae (odds ratio [OR], 1.5; 95% confidence interval [CI], 1.4-1.6), loss of retroplacental clear space (OR, 2.4; 95% CI, 1.1-4.9), or abnormalities on color Doppler (OR, 2.1; 95% CI, 1.8-2.4). CONCLUSION: Ultrasound for the prediction of placenta accreta may not be as sensitive as previously described.

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OBJECTIVE: Recent recommendations called for obstetricians to abandon the terms of "hyperstimulation" and "hypercontractility" in favor of the more rigidly defined term, "tachysystole" (TS). The aim of the current study is to describe incidence of and risk factors for TS, describe fetal heart rate (FHR) changes associated with TS, and investigate maternal and neonatal outcomes associated with TS. STUDY DESIGN: For this retrospective cohort study, we reviewed and analyzed the intrapartum FHR and tocometric characteristics of all patients with a singleton, nonanomalous fetus in term labor in a single hospital system over a 28-month period. Univariate association testing was done using χ(2) and t tests, comparing demographics, pregnancy characteristics, outcomes, and TS events. Multivariable association testing between risk factors and TS events were tested using generalized estimating equations, adjusting for multiple pregnancies during the study period for the same woman. RESULTS: There were a total of 50,335 deliveries from 48,529 women during the 28-month period. Of these, there were a total of 7567 TS events in 5363 deliveries among 5332 women. Use of oxytocin or misoprostol, an epidural, hypertension, and induction of labor were associated with an increased risk of TS. We found a doubling of TS events with any oxytocin, a dose-response correlation between oxytocin and TS, FHR changes occurring in a quarter of TS events and, finally, that presence of TS increases the chance of composite neonatal morbidity. CONCLUSION: TS is associated with specific risk factors and impacts FHR and neonatal morbidity.

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OBJECTIVES: Deviation of the intra-abdominal umbilical vein has been described as a marker of congenital diaphragmatic hernia (CDH) and has been shown to help identify liver herniation into the fetal chest. The purpose of this study was to quantify the degree of deviation in affected fetuses and to determine the accuracy of measurements for diagnosing liver herniation. METHODS: In patients undergoing prenatal sonography for CDH, the midhepatic portion of the umbilical vein was identified, and the distance between the lateral edge of the vein and the inner rib margin was measured. The same was done on the right, and the ratio of the left to right measurement was termed the "umbilical vein ratio." The accuracy of the umbilical vein ratio for predicting the presence and side of the hernia and for diagnosing liver herniation was determined. RESULTS: All but 1 of the cases with right-sided hernias had an umbilical vein ratio above the normal range, and all had liver herniation. Of those with a left-sided hernia, only 2 had a ratio within the normal range. Of those with a left-sided hernia, an umbilical vein ratio less than 0.4 was shown by receiver operating characteristic curve analysis to be the best predictor of liver herniation. This cutoff had sensitivity of 89% for predicting herniation, with a false-positive rate of 14%. CONCLUSIONS: Ninety-three percent of right-sided CDH lesions and 98% of left-sided lesions have an umbilical vein ratio outside the normal range. This finding shows that deviation may a useful indicator of CDH in screening ultrasound examinations. An umbilical vein ratio less than 0.4 is predictive of liver herniation.

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Recent progress has been made using fMRI as a clinical assessment tool, often employing analogues of traditional "paper and pencil" tests. The Trail Making Test (TMT), popular for years as a neuropsychological exam, has been largely ignored in the realm of neuroimaging, most likely because its physical format and administration does not lend itself to straightforward adaptation as an fMRI paradigm. Likewise, there is relatively more ambiguity about the neural systems associated with this test than many other tests of comparable clinical use. In this study, we describe an fMRI version of Trail Making Test-B (TMTB) that maintains the core functionality of the TMT while optimizing its use for both research and clinical settings. Subjects (N=32) were administered the Functional Trail Making Test-B (f-TMTB). Brain region activations elicited by the f-TMTB were consistent with expectations given by prior TMT neurophysiological studies, including significant activations in the ventral and dorsal visual pathways and the medial pre-supplementary motor area. The f-TMTB was further evaluated for concurrent validity with the traditional TMTB using an additional sample of control subjects (N=100). Together, these results support the f-TMTB as a viable neuroimaging adaptation of the TMT that is optimized to evoke maximally robust fMRI activation with minimal time and equipment requirements.

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