Monday, April 23, 2012


Pediatric bipolar disorder (PBD) (Pediatrics in Review Vol.32 No.11 November 2011, DOI: 10.1542/pir.32-11-502)
The clinical presentation of PBD often does not meet the Diagnostic and Statistical Manual of Mental Disorders criteria for bipolar disorder (BD), which was developed in adults and not adapted for children. The diagnosis becomes difficult because symptom presentation is variable and largely dependent on developmental age. Although discrete episodes of mania and depression that define BD in adults may match the presentation of some patients who have BD in adolescence, patients who have BD of childhood and prepubertal onset may or may not manifest these clear-cut episodes. The duration of episodes in children may be as short as 1 to 2 days. Mood symptoms can be chronic, can present as predominantly mixed episodes, or can continuously cycle rapidly, with severe irritability or aggression as the usual presenting symptoms. Disruptive behavior, hyperarousal,racing thoughts, elation, and grandiosity also may characterize the moods. A major depressive presentation is associated with a significant risk for developing subsequent BD. Poor psychosocial skills as well as cognitive and attention deficits may manifest along with mood and behavior changes. The chronic relapsing mode of PBD may extend into early adulthood. Complicating the diagnosis of PBD is the high rate of comorbidity with attention deficit hyperactivity disorder (ADHD) and psychiatric disorders such as anxiety, conduct, substance abuse, and oppositional defiant disorders. Research has suggested that physical, sexual, and emotional childhood traumas that occur at a time of sensitivity of the maturing central nervous system may predispose to and modulate the clinical expression and course of the PBD

Update in Surfactant Therapy(NeoReviews 2011;12;e625-e634, DOI: 10.1542/neo.12-11-e625)
Evidence for Use of Exogenous Surfactant in Neonatal Lung Diseases Other Than RDS

Meconium Aspiration
Meconium inactivates components of surfactant, thereby reducing the effectiveness of endogenous surfactant. Airway obstruction, inflammation, protein leak, and retained fetal lung fluid all contribute to the pathogenesis of meconium aspiration syndrome
The potential advantages to providing exogenous surfactant therapy include restoration of alveolar surfactant with the potential for improved distribution owing to retained fetal lung fluid and alveolar edema fluid as discussed above. However, the clinical trials to date only demonstrate a reduction in the need for ECMO

Congenital Diaphragmatic Hernia
CDH is characterized by pulmonary hypoplasia, poor lung compliance and likely altered numbers of alveolar type 1 and 2
epithelial cells.
In CDH lung as maldeveloped, rather than immature. The severe respiratory compromise associated with CDH is exacerbated by left ventricular and pulmonary arterial hypoplasia, arterial intimal remodeling, and pulmonary ypertension,
as well as altered alveolar epithelial cell populations. This more complex description of CDH pathophysiology and the variable timing of surfactant administration postnatally may help to explain why surfactant replacement has not shown a consistent benefit to date
Bronchiolitis
RSV binds to Toll-like receptors on epithelial cells lining the upper and lower airways and initiates a brisk inflammatory response that contributes to epithelial cell injury and reduced surfactant production. Epithelial cell dysfunction, inflammatory cytokines, and epithelial barrier injury lead to alveolar edema and contribute to surfactant abnormalities and respiratory failure in infants with bronchiolitis. The evidence base supporting the widespread use of surfactant for bronchiolitis is insufficient at this time and additional randomized controlled trials are warranted.
Genetic Disorders of the Surfactant System
They are mutations in SP-B, SP-C, and ABCA3.
They present as Neonatal respiratory distress occurring in term and late preterm infants with no other risk factors for respiratory disease
Infants with genetic disorders of the surfactant system are often indistinguishable from late preterm infants with RDS or from term infants with surfactant dysfunction due to neonatal pneumonia. Unless the treating physician is aware of a prenatal diagnosis or family history of one of these genetic disorders, it is understandable that these infants will initially be treated with surfactant due to their clinical presentation. However, there is no evidence base supporting the continued
use of surfactant in these patients 

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