Postpartum fatigue and evidence-based interventions

The aim of this article is to review postpartum fatigue, especially as it relates to the occurrence and pathophysiology of three common postpartum conditions known to contribute to fatigue: anemia, infection/inflammation, and thyroid dysfunction. Fatigue is an unrelenting condition that affects physical and mental health, and it has implications for everyday activities, motivation, and social interactions. Although individuals of all ages and both genders are at risk for developing fatigue, postpartum fatigue is particularly challenging, because the new mother has demanding life tasks to accomplish during this period of time. Postpartum fatigue may impact postpartum maternal role attainment and may place a woman at increased risk for postpartum depression. Although several treatable physiological conditions common during the postpartum period are known to increase fatigue, none of these conditions is a part of the usual assessment of healthy postpartum women. For many women, subtle fatigue may develop, linger or worsen, and even lead to depression, with both the woman and her care provider unaware.     

Clinical management of the organ donor

There is a critical mismatch between available organs for transplant and acutely or critically ill patients with end-stage organ disease. Patients who may benefit from organ transplantation far outnumber available organs. The causes for this imbalance are multiple. One cause is family refusal to donate. A second cause is nonrecognition or delay in determination of brain death. A third cause is donor loss due to profound cardiopulmonary and metabolic instability consequent to brain-stem herniation and brain death. Family refusal may be addressed by education, public awareness, as well as close attention to social, cultural and ethical issues, and optimal communication with donor families. Brain death may be consequent to traumatic brain injury, ischemic versus hemorrhagic stroke, as well as massive cerebral anoxia/ischemic following cardiac arrest. Nonrecognition or delay in brain death determination may be addressed by clinician education and frequent clinical assessment to detect early stages of brain-stem herniation refractory to aggressive measures for control of intracranial pressure. Donor loss due to profound cardiopulmonary and metabolic instability may be addressed by aggressive, mechanism-based treatment for clinical instability based on affected body system, as well as measures to support metabolic activity at the cellular and tissue level in the brain-dead organ donor. This article explores cerebral physiology related to impending brain death and catastrophic intracranial pressure elevations. In addition, physiologic consequences of brain death are correlated with affected body systems and mechanism-based therapies to support organ function pending transplantation. Ethical/legal issues are explored as related to patient autonomy and optimal family outcomes. Effective family communication, astute clinical assessment, and optimal clinical management of the organ donor are illustrated using a case study approach, highlighting the role of the advanced practice nurse in donor management.     

c-Jun NH(2)-terminal kinase (JNK)1 and JNK2 signaling pathways have divergent roles in CD8(+) T cell-mediated antiviral immunity

c-Jun NH(2)-terminal kinases (JNK) play important roles in T helper cell (Th) proliferation, differentiation, and maintenance of Th1/Th2 polarization. To determine whether JNKs are involved in antiviral T cell immunity, and whether JNK1 and JNK2 bear biological differences, we investigated the immune responses of JNK1-deficient and JNK2-deficient mice to lymphocytic choriomeningitis virus (LCMV). After LCMV infection, wild-type (JNK(+/+)) mice had a 5- to 10-fold increase in splenic CD8(+) T cells. In contrast, infected JNK1(-/-) mice showed a significantly lower virus-specific CD8(+) T cell expansion. However, JNK1(-/-) mice cleared LCMV infection with similar kinetics as JNK(+/+) mice. Splenic T cells from LCMV-infected JNK1(-/-) animals produced interferon gamma after stimulation with viral peptides. However, fewer JNK1(-/-) T cells acquired an activated phenotype (CD44(hi)) and more JNK1(-/-)CD8(+)CD44(hi) cells underwent apoptosis than JNK(+/+) cells at the peak of the primary response. In contrast, LCMV-infected JNK2(-/-) mice generated more virus-specific CD8(+) T cells than JNK(+/+) mice. These results indicate that JNK1 and JNK2 signal pathways have distinct roles in T cell responses during a viral infection. JNK1 is involved in survival of activated T cells during immune responses, and JNK2 plays a role in control of CD8(+) T cell expansion in vivo.     

Congenital anomalies in the offspring of nurses: association with area of employment during pregnancy

The purpose of this study was to determine whether registered nurses in specific areas of employment during pregnancy had a higher risk for congenital anomalies in their offspring. An offspring cohort (n = 22,611) was created through linkage of the British Columbia Vital Statistics Agency live and stillbirth records from 1986 to 2000, to a female cohort database of registered nurses. Of these, 16,005 (70.8%) were registered in a specific area of employment when pregnant. Odds ratios were calculated using generalized estimating equations (GEE), binary logistic regression with adjustment for sex, mother's age, and year of birth. Elevated risks of congenital anomalies were found for the singleton offspring of nurses employed in the following areas: operating rooms and pediatric nursing units (heart anomalies); maternal newborn units (integument); emergency room (respiratory system); and psychiatry (upper alimentary tract). Further research is needed to determine whether these are chance or consistent findings and whether exposure patterns might provide biological plausibility.     

Ankylosaurid dinosaur tail clubs evolved through stepwise acquisition of key features

Ankylosaurid ankylosaurs were quadrupedal, herbivorous dinosaurs with abundant dermal ossifications. They are best known for their distinctive tail club composed of stiff, interlocking vertebrae (the handle) and large, bulbous osteoderms (the knob), which may have been used as a weapon. However, tail clubs appear relatively late in the evolution of ankylosaurids, and seemed to have been present only in a derived clade of ankylosaurids during the last 20 million years of the Mesozoic Era. New evidence from mid Cretaceous fossils from China suggests that the evolution of the tail club occurred at least 40 million years earlier, and in a stepwise manner, with early ankylosaurids evolving handle‐like vertebrae before the distal osteoderms enlarged and coossified to form a knob.     

Identification of the Pregnant Woman Who Is Using Drugs: Implications for Perinatal and Neonatal Care

Neonatal abstinence syndrome (NAS) is a set of drug withdrawal symptoms that affect the central nervous, gastrointestinal, and respiratory systems in the newborn when separated from the placenta at birth. Maternal substance use of opioids, benzodiazepines, barbiturates, and alcohol can cause NAS. Universal drug screening via questioning pregnant women is recommended, but identification of drug use is incomplete with this method. This article provides resources for the identification and management of drug use during pregnancy for midwives who provide care not only during the prenatal period but also during the intrapartum and postpartum periods. The impact of drug use on newborns can be significant and may require pharmacologic assistance with the transition to extrauterine life. Challenges involved in caring for the woman who is using drugs during pregnancy include ordering toxicology screens on the newborn, alerting social services, and educating the woman about her newborn's progress. Several measures to comfort a newborn with NAS may help to enable a mother to provide the best care for her newborn.     

Mammary Hypoplasia: Not Every Breast Can Produce Sufficient Milk

Breast milk is considered the optimal form of nutrition for newborn infants. Current recommendations are to breastfeed for 6 months. Not all women are able to breastfeed. Mammary hypoplasia is a primary cause of failed lactogenesis II, whereby the mother is unable to produce an adequate milk volume. Women with mammary hypoplasia often have normal hormone levels and innervation but lack sufficient glandular tissue to produce an adequate milk supply to sustain their infant. The etiology of this rare condition is unclear, although there are theories that refer to genetic predisposition and estrogenic environmental exposures in select agricultural environments. Women with mammary hypoplasia may not exhibit the typical breast changes associated with pregnancy and may fail to lactate postpartum. Breasts of women with mammary hypoplasia may be widely spaced (1.5 inches or greater), asymmetric, or tuberous in nature. Awareness of the history and clinical signs of mammary hypoplasia during the prenatal period and immediate postpartum increases the likelihood that women will receive the needed education and physical and emotional support and encouragement. Several medications and herbs demonstrate some efficacy in increasing breast milk production in women with mammary hypoplasia.     

Human exposure to environmental contaminants and congenital anomalies: a critical review

Congenital anomalies are an important cause of infant mortality and disability. Developmental exposure to environmental contaminants is thought to increase the risk for congenital anomalies. Herein, we describe a critical review of the literature conducted between February and March 2014 yielding 3057 references from which 97 unique relevant articles published from 2003 through 2014 were evaluated. Common congenital anomalies including hypospadias, cryptorchidism, anogenital distance (AGD), congenital heart defects and oral clefts were well represented in the literature whereas other outcomes such as neural tube defects, limb deficiency defects and gastroschisis were rarely described. While definitions used for congenital anomalies and methods of ascertainment were usually consistent across studies, inconsistencies were frequently found in grouping of different congenital heart defects. Despite strong links between some congenital anomalies and parental occupation, these studies are unable to provide clear insight into the specific chemicals responsible owing to lack of direct measures of exposure. In comparison, data are mixed for contaminant exposures at concentrations representative of results from contemporary biomonitoring studies. Of the environmental contaminants studied, the association between phthalate exposures and developmental abnormalities of the male reproductive tract received the greatest attention. Important limitations of the literature studied relate to adequacy of sample size, absence of or weaknesses in exposure assessment methodologies, failure to account for biological plausibility and grouping of congenital anomalies with divergent mechanisms. We conclude that the literature is inadequate at this time to support a conclusion that exposure to environmental contaminants are or are not associated with increased risks for congenital anomalies in the general population.