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Dentistry Journal Nov 2022Childhood diseases are a continuous source of interest in all areas of general and dental medicine. Congenital, developmental, and hereditary diseases may either be... (Review)
Review
Childhood diseases are a continuous source of interest in all areas of general and dental medicine. Congenital, developmental, and hereditary diseases may either be present upon birth or appear in early childhood. Developmental anomalies, although often asymptomatic, may become grounds for different infections. Furthermore, they can indicate certain systemic disorders. Childhood age frequently brings about benign tumors and different types of traumatic lesions to the oral mucosa. Traumatic lesions can be caused by chemical, mechanical, or thermal injury. Mucocele and ranula are, by definition, traumatic injuries of the salivary glands or their ducts. Recurrent aphthous lesions are the most common type of ulcerations in childhood, and their etiology is considered multifactorial. Oral mucosal lesions in children require different treatment approaches depending on etiological factors and clinical presentation. Clinicians should have adequate knowledge of oral anatomy in order to diagnose and treat pathological conditions.
PubMed: 36354659
DOI: 10.3390/dj10110214 -
American Journal of Obstetrics and... Dec 2019The impact of infections and inflammation during pregnancy on the developing fetal brain remains incompletely defined, with important clinical and research gaps.... (Review)
Review
The impact of infections and inflammation during pregnancy on the developing fetal brain remains incompletely defined, with important clinical and research gaps. Although the classic infectious TORCH pathogens (ie, Toxoplasma gondii, rubella virus, cytomegalovirus [CMV], herpes simplex virus) are known to be directly teratogenic, emerging evidence suggests that these infections represent the most extreme end of a much larger spectrum of injury. We present the accumulating evidence that prenatal exposure to a wide variety of viral and bacterial infections-or simply inflammation-may subtly alter fetal brain development, leading to neuropsychiatric consequences for the child later in life. The link between influenza infections in pregnant women and an increased risk for development of schizophrenia in their children was first described more than 30 years ago. Since then, evidence suggests that a range of infections during pregnancy may also increase risk for autism spectrum disorder and depression in the child. Subsequent studies in animal models demonstrated that both pregnancy infections and inflammation can result in direct injury to neurons and neural progenitor cells or indirect injury through activation of microglia and astrocytes, which can trigger cytokine production and oxidative stress. Infectious exposures can also alter placental serotonin production, which can perturb neurotransmitter signaling in the developing brain. Clinically, detection of these subtle injuries to the fetal brain is difficult. As the neuropsychiatric impact of perinatal infections or inflammation may not be known for decades after birth, our construct for defining teratogenic infections in pregnancy (eg, TORCH) based on congenital anomalies is insufficient to capture the full adverse impact on the child. We discuss the clinical implications of this body of evidence and how we might place greater emphasis on prevention of prenatal infections. For example, increasing uptake of the seasonal influenza vaccine is a key strategy to reduce perinatal infections and the risk for fetal brain injury. An important research gap exists in understanding how antibiotic therapy during pregnancy affects the fetal inflammatory load and how to avoid inflammation-mediated injury to the fetal brain. In summary, we discuss the current evidence and mechanisms linking infections and inflammation with the increased lifelong risk of neuropsychiatric disorders in the child, and how we might improve prenatal care to protect the fetal brain.
Topics: Animals; Astrocytes; Autism Spectrum Disorder; Bipolar Disorder; Cytokines; Depressive Disorder; Female; Humans; Inflammation; Mental Disorders; Microglia; Neural Stem Cells; Neurons; Oxidative Stress; Placenta; Pregnancy; Pregnancy Complications; Pregnancy Complications, Infectious; Prenatal Exposure Delayed Effects; Schizophrenia; Serotonin
PubMed: 31207234
DOI: 10.1016/j.ajog.2019.06.013 -
American Journal of Obstetrics and... May 2023Normal birth is a eustress reaction, a beneficial hedonic stress with extremely high catecholamines that protects us from intrauterine hypoxia and assists in the rapid... (Review)
Review
Normal birth is a eustress reaction, a beneficial hedonic stress with extremely high catecholamines that protects us from intrauterine hypoxia and assists in the rapid shift to extrauterine life. Occasionally the cellular O requirement becomes critical and an O deficit in blood (hypoxemia) may evolve to a tissue deficit (hypoxia) and finally a risk of organ damage (asphyxia). An increase in H concentration is reflected in a decrease in pH, which together with increased base deficit is a proxy for the level of fetal O deficit. Base deficit (or its negative value, base excess) was introduced to reflect the metabolic component of a low pH and to distinguish from the respiratory cause of a low pH, which is a high CO concentration. Base deficit is a theoretical estimate and not a measured parameter, calculated by the blood gas analyzer from values of pH, the partial pressure of CO, and hemoglobin. Different brands of analyzers use different calculation equations, and base deficit values can thus differ by multiples. This could influence the diagnosis of metabolic acidosis, which is commonly defined as a pH <7.00 combined with a base deficit ≥12.0 mmol/L in umbilical cord arterial blood. Base deficit can be calculated as base deficit in blood (or actual base deficit) or base deficit in extracellular fluid (or standard base deficit). The extracellular fluid compartment represents the blood volume diluted with the interstitial fluid. Base deficit in extracellular fluid is advocated for fetal blood because a high partial pressure of CO (hypercapnia) is common in newborns without concomitant hypoxia, and hypercapnia has a strong influence on the pH value, then termed respiratory acidosis. An increase in partial pressure of CO causes less increase in base deficit in extracellular fluid than in base deficit in blood, thus base deficit in extracellular fluid better represents the metabolic component of acidosis. The different types of base deficit for defining metabolic acidosis in cord blood have unfortunately not been noticed by many obstetrical experts and organizations. In addition to an increase in H concentration, the lactate production is accelerated during hypoxia and anaerobic metabolism. There is no global consensus on definitions of normal cord blood gases and lactate, and different cutoff values for abnormality are used. At a pH <7.20, 7% to 9% of newborns are deemed academic; at <7.10, 1% to 3%; and at <7.00, 0.26% to 1.3%. From numerous studies of different eras and sizes, it can firmly be concluded that in the cord artery, the statistically defined lower pH limit (mean -2 standard deviations) is 7.10. Given that the pH for optimal enzyme activity differs between different cell types and organs, it seems difficult to establish a general biologically critical pH limit. The blood gases and lactate in cord blood change with the progression of pregnancy toward a mixed metabolic and respiratory acidemia because of increased metabolism and CO production in the growing fetus. Gestational age-adjusted normal reference values have accordingly been published for pH and lactate, and they associate with Apgar score slightly better than stationary cutoffs, but they are not widely used in clinical practice. On the basis of good-quality data, it is reasonable to set a cord artery lactate cutoff (mean +2 standard deviations) at 10 mmol/L at 39 to 40 weeks' gestation. For base deficit, it is not possible to establish statistically defined reference values because base deficit is calculated with different equations, and there is no consensus on which to use. Arterial cord blood represents the fetus better than venous blood, and samples from both vessels are needed to validate the arterial origin. A venoarterial pH gradient of <0.02 is commonly used to differentiate arterial from venous samples. Reference values for pH in cord venous blood have been determined, but venous blood comes from the placenta after clearance of a surplus of arterial CO, and base deficit in venous blood then overestimates the metabolic component of fetal acidosis. The ambition to increase neonatal hemoglobin and iron depots by delaying cord clamping after birth results in falsely acidic blood gas and lactate values if the blood sampling is also delayed. Within seconds after birth, sour metabolites accumulated in peripheral tissues and organs will flood into the central circulation and further to the cord arteries when the newborn starts to breathe, move, and cry. This influence of "hidden acidosis" can be avoided by needle puncture of unclamped cord vessels and blood collection immediately after birth. Because of a continuing anaerobic glycolysis in the collected blood, it should be analyzed within 5 minutes to not result in a falsely high lactate value. If the syringe is placed in ice slurry, the time limit is 20 minutes. For pH, it is reasonable to wait no longer than 15 minutes if not in ice. Routine analyses of cord blood gases enable perinatal audits to gain the wisdom of hindsight, to maintain quality assurance at a maternity unit over years by following the rate of neonatal acidosis, to compare results between hospitals on regional or national bases, and to obtain an objective outcome measure in clinical research. Given that the intrapartum cardiotocogram is an uncertain proxy for fetal hypoxia, and there is no strong correlation between pathologic cardiotocograms and fetal acidosis, a cord artery pH may help rather than hurt a staff person subjected to a malpractice suit based on undesirable cardiotocogram patterns. Contrary to common beliefs and assumptions, up to 90% of cases of cerebral palsy do not originate from intrapartum events. Future research will elucidate whether cell injury markers with point-of-care analysis will become valuable in improving the dating of perinatal injuries and differentiating hypoxic from nonhypoxic injuries.
Topics: Infant, Newborn; Pregnancy; Female; Humans; Lactic Acid; Reference Values; Hypercapnia; Carbon Dioxide; Ice; Acidosis; Fetal Blood; Infant, Newborn, Diseases; Fetal Diseases; Umbilical Cord; Hypoxia; Hydrogen-Ion Concentration
PubMed: 37164495
DOI: 10.1016/j.ajog.2022.07.001 -
Cells Aug 2020With a worldwide incidence of 15 million cases, preterm birth is a major contributor to neonatal mortality and morbidity, and concomitant social and economic burden... (Review)
Review
With a worldwide incidence of 15 million cases, preterm birth is a major contributor to neonatal mortality and morbidity, and concomitant social and economic burden Preterm infants are predisposed to life-long neurological disorders due to the immaturity of the brain. The risks are inversely proportional to maturity at birth. In the majority of extremely preterm infants (<28 weeks' gestation), perinatal brain injury is associated with exposure to multiple inflammatory perinatal triggers that include antenatal infection (i.e., chorioamnionitis), hypoxia-ischemia, and various postnatal injurious triggers (i.e., oxidative stress, sepsis, mechanical ventilation, hemodynamic instability). These perinatal insults cause a self-perpetuating cascade of peripheral and cerebral inflammation that plays a critical role in the etiology of diffuse white and grey matter injuries that underlies a spectrum of connectivity deficits in survivors from extremely preterm birth. This review focuses on chorioamnionitis and hypoxia-ischemia, which are two important antenatal risk factors for preterm brain injury, and highlights the latest insights on its pathophysiology, potential treatment, and future perspectives to narrow the translational gap between preclinical research and clinical applications.
Topics: Brain Injuries; Cell- and Tissue-Based Therapy; Chorioamnionitis; Female; Gestational Age; Humans; Hypothermia, Induced; Hypoxia-Ischemia, Brain; Incidence; Infant, Newborn; Infant, Premature; Pregnancy; Premature Birth; Time Factors
PubMed: 32785181
DOI: 10.3390/cells9081871 -
American Journal of Obstetrics and... Mar 2024Perineal trauma after vaginal birth is common, with approximately 9 of 10 women being affected. Second-degree perineal tears are twice as likely to occur in primiparous... (Review)
Review
Perineal trauma after vaginal birth is common, with approximately 9 of 10 women being affected. Second-degree perineal tears are twice as likely to occur in primiparous births, with a incidence of 40%. The incidence of obstetrical anal sphincter injury is approximately 3%, with a significantly higher rate in primiparous than in multiparous women (6% vs 2%). Obstetrical anal sphincter injury is a significant risk factor for the development of anal incontinence, with approximately 10% of women developing symptoms within a year following vaginal birth. Obstetrical anal sphincter injuries have significant medicolegal implications and contribute greatly to healthcare costs. For example, in 2013 and 2014, the economic burden of obstetrical anal sphincter injuries in the United Kingdom ranged between £3.7 million (with assisted vaginal birth) and £9.8 million (with spontaneous vaginal birth). In the United States, complications associated with trauma to the perineum incurred costs of approximately $83 million between 2007 and 2011. It is therefore crucial to focus on improvements in clinical care to reduce this risk and minimize the development of perineal trauma, particularly obstetrical anal sphincter injuries. Identification of risk factors allows modification of obstetrical practice with the aim of reducing the rate of perineal trauma and its attendant associated morbidity. Risk factors associated with second-degree perineal trauma include increased fetal birthweight, operative vaginal birth, prolonged second stage of labor, maternal birth position, and advanced maternal age. With obstetrical anal sphincter injury, risk factors include induction of labor, augmentation of labor, epidural, increased fetal birthweight, fetal malposition (occiput posterior), midline episiotomy, operative vaginal birth, Asian ethnicity, and primiparity. Obstetrical practice can be modified both antenatally and intrapartum. The evidence suggests that in the antenatal period, perineal massage can be commenced in the third trimester of pregnancy to increase muscle elasticity and allow stretching of the perineum during birth, thereby reducing the risk of tearing or need for episiotomy. With regard to the intrapartum period, there is a growing body of evidence from the United Kingdom, Norway, and Denmark suggesting that the implementation of quality improvement initiatives including the training of clinicians in manual perineal protection and mediolateral episiotomy can reduce the incidence of obstetrical anal sphincter injury. With episiotomy, the International Federation of Gynecology and Obstetrics recommends restrictive rather than routine use of episiotomy. This is particularly the case with unassisted vaginal births. However, there is a role for episiotomy, specifically mediolateral or lateral, with assisted vaginal births. This is specifically the case with nulliparous vacuum and forceps births, given that the use of mediolateral or lateral episiotomy has been shown to significantly reduce the incidence of obstetrical anal sphincter injury in these groups by 43% and 68%, respectively. However, the complications associated with episiotomy including perineal pain, dyspareunia, and sexual dysfunction should be acknowledged. Despite considerable research, interventions for reducing the risk of perineal trauma remain a subject of controversy. In this review article, we present the available data on the prevention of perineal trauma by describing the risk factors associated with perineal trauma and interventions that can be implemented to prevent perineal trauma, in particular obstetrical anal sphincter injury.
Topics: Pregnancy; Female; Humans; Birth Weight; Episiotomy; Parity; Parturition; Lacerations; Anal Canal; Risk Factors; Perineum; Obstetric Labor Complications
PubMed: 37635056
DOI: 10.1016/j.ajog.2022.06.021 -
Frontiers in Endocrinology 2021Neonatal hypoglycemia is a common condition. A transient reduction in blood glucose values is part of a transitional metabolic adaptation following birth, which resolves... (Review)
Review
Neonatal hypoglycemia is a common condition. A transient reduction in blood glucose values is part of a transitional metabolic adaptation following birth, which resolves within the first 48 to 72 h of life. In addition, several factors may interfere with glucose homeostasis, especially in case of limited metabolic stores or increased energy expenditure. Although the effect of mild transient asymptomatic hypoglycemia on brain development remains unclear, a correlation between severe and prolonged hypoglycemia and cerebral damage has been proven. A selective vulnerability of some brain regions to hypoglycemia including the second and the third superficial layers of the cerebral cortex, the dentate gyrus, the subiculum, the CA1 regions in the hippocampus, and the caudate-putamen nuclei has been observed. Several mechanisms contribute to neuronal damage during hypoglycemia. Neuronal depolarization induced by hypoglycemia leads to an elevated release of glutamate and aspartate, thus promoting excitotoxicity, and to an increased release of zinc to the extracellular space, causing the extensive activation of poly ADP-ribose polymerase-1 which promotes neuronal death. In this review we discuss the cerebral glucose homeostasis, the mechanisms of brain injury following neonatal hypoglycemia and the possible treatment strategies to reduce its occurrence.
Topics: Brain; Brain Injuries; Cell Death; Epilepsy; Glucose; Glutamic Acid; Homeostasis; Humans; Hypoglycemia; Infant, Newborn; Infant, Newborn, Diseases; Neurons; Oxidative Stress; Poly (ADP-Ribose) Polymerase-1; Receptors, Glutamate; Risk Factors; Zinc
PubMed: 33796072
DOI: 10.3389/fendo.2021.634305 -
Ideggyogyaszati Szemle Jul 2022The incidence of brachial plexus palsy (BPP) has decreased recently, but the indivi-d-ual's quality of life is endangered. To provide better chan-ces to BPP neonates and... (Review)
Review
BACKGROUND AND PURPOSE
The incidence of brachial plexus palsy (BPP) has decreased recently, but the indivi-d-ual's quality of life is endangered. To provide better chan-ces to BPP neonates and infants, the Department of Developmental Neurology worked out, introduced, and applied a complex early therapy, including nerve point stimulation.
METHODS
After diagnosing the severity of BPP, early intensive and complex therapy should be started. Appro-x-imately after a week or ten days following birth, the slightest form (neurapraxia) normalizes without any intervention, and signs of recovery can be detected around this period. The therapy includes the unipolar nerve point electro-stimulation and the regular application of those elemen-tary sensorimotor patterns, which activate both extremities simultaneously.
RESULTS
With the guideline worked out and applied in the Department of Developmental Neurology, full recovery can be achieved in 50% of the patients, and even in the most severe cases (nerve root lesion), functional upper limb usage can be detected with typically developing body-scheme.
CONCLUSION
Immediately starting complex treatment based on early diagnosis alters the outcome of BPP, providing recovery in the majority of cases and enhancing the everyday arm function of those who only partially benefit from the early treatment.
Topics: Brachial Plexus; Brachial Plexus Neuropathies; Early Diagnosis; Humans; Infant; Infant, Newborn; Neonatal Brachial Plexus Palsy; Paralysis; Quality of Life
PubMed: 35916611
DOI: 10.18071/isz.75.0247 -
International Journal of Molecular... Feb 2021Preterm birth is associated with a high risk of morbidity and mortality including brain damage and cerebral palsy. The development of brain injury in the preterm infant... (Review)
Review
Preterm birth is associated with a high risk of morbidity and mortality including brain damage and cerebral palsy. The development of brain injury in the preterm infant may be influenced by many factors including perinatal asphyxia, infection/inflammation, chronic hypoxia and exposure to treatments such as mechanical ventilation and corticosteroids. There are currently very limited treatment options available. In clinical trials, magnesium sulfate has been associated with a small, significant reduction in the risk of cerebral palsy and gross motor dysfunction in early childhood but no effect on the combined outcome of death or disability, and longer-term follow up to date has not shown improved neurological outcomes in school-age children. Recombinant erythropoietin has shown neuroprotective potential in preclinical studies but two large randomized trials, in extremely preterm infants, of treatment started within 24 or 48 h of birth showed no effect on the risk of severe neurodevelopmental impairment or death at 2 years of age. Preclinical studies have highlighted a number of promising neuroprotective treatments, such as therapeutic hypothermia, melatonin, human amnion epithelial cells, umbilical cord blood and vitamin D supplementation, which may be useful at reducing brain damage in preterm infants. Moreover, refinements of clinical care of preterm infants have the potential to influence later neurological outcomes, including the administration of antenatal and postnatal corticosteroids and more accurate identification and targeted treatment of seizures.
Topics: Anti-Inflammatory Agents; Brain Injuries; Humans; Infant, Newborn; Infant, Premature; Infant, Premature, Diseases
PubMed: 33562339
DOI: 10.3390/ijms22041671 -
JAMA Jan 2020The tort liability system is intended to serve 3 functions: compensate patients who sustain injury from negligence, provide corrective justice, and deter negligence....
IMPORTANCE
The tort liability system is intended to serve 3 functions: compensate patients who sustain injury from negligence, provide corrective justice, and deter negligence. Deterrence, in theory, occurs because clinicians know that they may experience adverse consequences if they negligently injure patients.
OBJECTIVE
To review empirical findings regarding the association between malpractice liability risk (ie, the extent to which clinicians face the threat of being sued and having to pay damages) and health care quality and safety.
DATA SOURCES AND STUDY SELECTION
Systematic search of multiple databases for studies published between January 1, 1990, and November 25, 2019, examining the relationship between malpractice liability risk measures and health outcomes or structural and process indicators of health care quality.
DATA EXTRACTION AND SYNTHESIS
Information on the exposure and outcome measures, results, and acknowledged limitations was extracted by 2 reviewers. Meta-analytic pooling was not possible due to variations in study designs; therefore, studies were summarized descriptively and assessed qualitatively.
MAIN OUTCOMES AND MEASURES
Associations between malpractice risk measures and health care quality and safety outcomes. Exposure measures included physicians' malpractice insurance premiums, state tort reforms, frequency of paid claims, average claim payment, physicians' claims history, total malpractice payments, jury awards, the presence of an immunity from malpractice liability, the Centers for Medicare & Medicaid Services' Medicare malpractice geographic practice cost index, and composite measures combining these measures. Outcome measures included patient mortality; hospital readmissions, avoidable admissions, and prolonged length of stay; receipt of cancer screening; Agency for Healthcare Research and Quality patient safety indicators and other measures of adverse events; measures of hospital and nursing home quality; and patient satisfaction.
RESULTS
Thirty-seven studies were included; 28 examined hospital care only and 16 focused on obstetrical care. Among obstetrical care studies, 9 found no significant association between liability risk and outcomes (such as Apgar score and birth injuries) and 7 found limited evidence for an association. Among 20 studies of patient mortality in nonobstetrical care settings, 15 found no evidence of an association with liability risk and 5 found limited evidence. Among 7 studies that examined hospital readmissions and avoidable initial hospitalizations, none found evidence of an association between liability risk and outcomes. Among 12 studies of other measures (eg, patient safety indicators, process-of-care quality measures, patient satisfaction), 7 found no association between liability risk and these outcomes and 5 identified significant associations in some analyses.
CONCLUSIONS AND RELEVANCE
In this systematic review, most studies found no association between measures of malpractice liability risk and health care quality and outcomes. Although gaps in the evidence remain, the available findings suggested that greater tort liability, at least in its current form, was not associated with improved quality of care.
Topics: Humans; Insurance, Liability; Liability, Legal; Malpractice; Obstetrics; Outcome Assessment, Health Care; Postoperative Complications; Quality of Health Care
PubMed: 31990319
DOI: 10.1001/jama.2019.21411