Risk of Neonatal Sepsis With Rescue Steroids in Preterm Premature Rupture of Membranes.

Objective To evaluate whether a rescue course of corticosteroids, when given at least 14 days after the initial course, is associated with an increased risk of neonatal sepsis after preterm premature rupture of membranes (PPROM). Methods We performed a retrospective, descriptive cohort study of women with singleton gestations from 23+0 to 34+0 weeks of gestation who received a rescue course of corticosteroids within the Indiana University Health Network from January 2009 through October 2016. Patients were separated into three groups based on amniotic membrane status at the time of each corticosteroid administration: Group 1 (intact membranes at initial/intact membranes at rescue), Group 2 (intact membranes at initial/PPROM at rescue), and Group 3 (PPROM at initial/PPROM at rescue). The primary outcome (neonatal sepsis) was compared between the groups. Patient characteristics and neonatal outcomes were analyzed with Fisher's exact test for categorical variables and ANOVA for continuous variables. Relative risk (RR) was calculated by comparing those with ruptured membranes to those with intact membranes at the time of rescue course administration. Results A total of 143 patients were eligible. Neonatal sepsis occurred in 6.8% of patients in Group 1, 21.1% of patients in Group 2, and 23.8% of patients in Group 3. Groups 2 and 3 had a statistically significant higher rate of neonatal sepsis than Group 1 (p = 0.021). The RR of neonatal sepsis after a rescue course in patients with PPROM (Groups 2 and 3) was 3.31 (95% CI = 1.32, 8.29) compared to those with intact membranes at the time of rescue course administration (Group 1). Conclusion A rescue course of corticosteroids in women with PPROM at the time of rescue administration was associated with an increased risk of neonatal sepsis. This increased risk was seen in women with intact membranes as well as ruptured membranes during their initial course of steroids. Larger studies are needed to further investigate this association.

Unicuspid Aortic Valve With Severe Aortic Stenosis and Progressive Heart Failure During Pregnancy.

A 39-year-old gravida 7 para 6 woman with unicuspid aortic valve and severe symptomatic stenosis was admitted to the hospital at 15 weeks gestation. We describe maternal cardiovascular complications and their implication on obstetric and fetal care. We also describe our multidisciplinary approach to caring for this complex patient.

Quantitative EEG improves prediction of Sturge-Weber syndrome in infants with port-wine birthmark.

OBJECTIVE: Port-wine birthmark (PWB) is a common occurrence in the newborn, and general pediatricians, dermatologists, and ophthalmologists are often called on to make an assessment of risk for Sturge-Weber syndrome (SWS) due to workforce shortages in pediatric neurologists and MRI's low sensitivity for SWS brain involvement in infants. We therefore aimed to develop a quantitative EEG (qEEG) approach to safely screen young infants with PWB for SWS risk and optimal timing of diagnostic MRI. METHODS: Forty-eight infants (prior to first birthday) underwent EEG recording. Signal processing methods compared voltage between left and right sides using a previously defined pipeline and diagnostic threshold. In this test sample, we compared sensitivity/specificity of the qEEG metric against MRI performed after the first birthday. We also used likelihood ratio testing to determine whether qEEG adds incremental information beyond topographical extent of PWB, another risk marker of brain involvement. RESULTS: qEEG helped predict SWS risk in the first year of life (p = 0.031), with a sensitivity of 50% and a specificity of 81%. It added about 40% incremental information beyond PWB extent alone (p = 0.042). CONCLUSION: qEEG adds information to risk prediction in infants with facial PWB. SIGNIFICANCE: qEEG can be used to help determine whether to obtain an MRI in the first year of life. The data collected can assist in developing a predictive model risk calculator that incorporates both PWB extent and qEEG results, which can be validated and then employed in the community.

Cognitive-behavioral therapy for insomnia in knee osteoarthritis: a randomized, double-blind, active placebo-controlled clinical trial.

OBJECTIVE: Insomnia is prevalent among patients with knee osteoarthritis (OA). Research indicates that sleep disruption may amplify clinical pain by altering central pain modulation, suggesting that treatment of insomnia may improve pain. The aims of this study were to evaluate the efficacy of cognitive-behavioral therapy for insomnia (CBT-I) in patients with knee OA, to determine whether improvements in sleep predict reduced pain, and to determine whether alterations in pain modulation mediate improvements in clinical pain. METHODS: We conducted a randomized, double-blind, active placebo-controlled clinical trial of CBT-I in 100 patients with knee OA and insomnia (mean ± SD age 59.4 ± 9.5 years). Patients were randomized (1:1) to receive either 8 sessions of CBT-I or behavioral desensitization (placebo). We conducted in-home polysomnography (PSG), diary assessment, and sensory tests of pain modulation at baseline, posttreatment, 3 months, and 6 months. RESULTS: Intent-to-treat analyses demonstrated substantial improvement in sleep in both groups of patients. Patients in the CBT-I group had significantly greater reductions in wake after sleep onset (WASO), as measured by patient diary and PSG. Patients in both groups reported significant and comparable reductions in pain over 6 months, with one-third reporting a 30% reduction in pain severity. Baseline-to-posttreatment reductions in WASO as measured by diary and PSG predicted subsequent decreases in clinical pain. This effect was significantly greater for CBT-I compared with behavioral desensitization. No significant changes in laboratory measures of pain modulation were observed. CONCLUSION: Compared with active placebo, CBT-I was efficacious in reducing sleep maintenance insomnia. CBT-I decreased clinical pain, but not pain modulation, suggesting that it has the potential to augment pain management in knee OA. Future work is needed to identify the mechanisms by which improved sleep reduces clinical pain.

Nutrition in Wound Care Management: A Comprehensive Overview.

Wound care is a multidisciplinary specialty requiring many physiologic and immunologic processes as well as physical, social, and societal factors to achieve successful wound closure. Most wounds are treated with combinations of antimicrobials, protective barriers, and topical growth agents, including skin and biologic grafts.The role of nutrition in wound healing may be overlooked in the wound care patient. Like the specialty, it is often multifaceted, with many nutritional components playing a variety of roles in the wound healing process. Suboptimal nutrition can alter immune function, collagen synthesis, and wound tensile strength, all of which are essential in the wound healing process. It is also important to remember that not all wounds are equal: a burn is different from a diabetic foot ulcer, which is different from a pressure ulcer. Nonetheless, nutrition is a common denominator for all wound patients, and what is studied in 1 wound population is often relevant in another. Due to the complexities of monitoring and measuring both wound healing and dietary intake, randomized, controlled trials of wound care patients are difficult to conduct, and much of the data concerning nutrition in wound care relies on combined supplements. In summary, it appears that some nutrients are necessary only if deficient, whereas others may become conditionally essential and serve a therapeutic role. All of the nutrients discussed should be viewed as a component of a broader, complete diet. This article is a summary of wound healing and the roles of a variety of macronutrients and micronutrients in the process.

EEG evolution in Sturge-Weber syndrome.

The EEG in Sturge-Weber syndrome (SWS) was theorized over 50 years ago as changing over time from normality to focal asymmetry to lastly epileptiform. We sought to validate these findings in a larger cohort today. Children with confirmed SWS and routine EEG at our center were evaluated retrospectively. An EEG score (0-3) was created and linked to patient current age, overall neurologic function, and seizure frequency. Eighty-one EEGs from 44 patients with SWS (mean age 2.0 years (range: 0.2-37.9 years)) were evaluated and assigned an EEG score. The mean age for patients with an EEG score of 0-1 (normal or focal slowing) was 3.2 years (SEM 0.6), whereas those with an EEG score of 2-3 (focal sharp waves or frequent spike-wave bursts) was 8.7 years (SEM 1.7) (p=0.006). There was no correlation between the EEG score and either the SWS overall neuroscore or seizure subscore (measuring frequency). The EEG in patients with SWS does appear to evolve over time, becoming more abnormal with more frequent epileptiform activity, as suspected in smaller studies decades ago. This progressive change, however, did not correlate with the child's neurologic function or seizure frequency.

Clinical correlates of insomnia in patients with acute coronary syndrome.

This study sought to examine the prevalence of insomnia and its association with depression, anxiety, and medical comorbidities in patients after an acute coronary syndrome (ACS). Insomnia increases risk of recurrent cardiac events in ACS patients, but little is known about the prevalence and clinical correlates of insomnia in this setting. Patients (n = 102, 58.3 ± 10.6 years-old) admitted for ACS to a cardiology service at an urban academic medical center completed the Insomnia Severity Index, Epworth Sleepiness Scale, and measures of depression and anxiety. A subset (n = 20) completed ambulatory polysomnography (PSG) in their homes several weeks after discharge. Moderate or severe insomnia was reported by 37% of patients during hospitalization and was associated with 76 minutes more wake after sleep onset measured by home PSG. Although depression and insomnia were strongly associated, about 1 in 4 patients with insomnia did not report significant depressive symptoms. Sleep apnea was documented in 80% of patients on PSG, but insomnia was not associated with sleep apnea, periodic limb movements, demographic factors, or medical conditions other than liver disease. Insomnia is present in over one-third of ACS patients during hospitalization, but at-risk patients could not be readily identified by demographic or medical factors or by depression symptoms.

Nocturnal heart rate variability is lower in temporomandibular disorder patients than in healthy, pain-free individuals.

AIMS: To determine whether patients with a painful myofascial temporomandibular disorder (TMD) have diminished nocturnal heart rate variability (HRV), a marker of autonomic nervous system (ANS) dysfunction, relative to healthy, pain-free controls. METHODS: Participants with myofascial TMD and healthy, pain-free volunteers underwent nocturnal polysomnography studies during which HRV indices were measured. Multiple linear regression analyses were used to determine whether TMD status exerted unique effects on HRV. RESULTS: Ninety-five participants (n = 37 TMD; n = 58 controls) were included in the analyses. The TMD group had a lower standard deviation of R-R intervals (89.81 ± 23.54 ms versus 107.93 ± 34.42 ms, P ⋜ .01), a lower root mean squared successive difference (RMSSD) of R-R intervals (54.78 ± 27.37 ms versus 81.88 ± 46.43 ms, P < .01), and a lower high frequency spectral power (2336.89 ± 1224.64 ms² versus 2861.78 ± 1319 ms², P = .05) than the control group. The ratio of the low-frequency (LF) to the high-frequency (HF) spectral power was higher in the TMD group (2.47 ± 2 versus 1.38 ± 0.65, P < .01). The differences in RMSSD (91.21 ms versus 112.03 ms, P = .05) and LF:HF ratio (0.71 versus 0.32, P < .01) remained significant after controlling for age and psychological distress. CONCLUSION: Myofascial TMD patients revealed lower nocturnal HRV than healthy, pain-free controls. Further research should focus on processes that address this ANS imbalance, which may potentially lead to effective therapeutic interventions.