Outcomes of CDH are largely dependent on the severity of the defect and the appropriate timing of treatment. A small percentage of cases go unrecognized into adulthood. Treatment
The first step in management is orogastric tube placement and securing the airway (intubation). Ideally, the baby will never take a breath, to avoid air going into the intestines and compressing the lungs and heart. The baby will then be immediately placed on a ventilator. Extracorporeal membrane oxygenation (ECMO) has been used as part of the treatment strategy at some hospitals. ECMO acts as a heart-lung bypass. Diaphragm eventration is typically repaired thoracoscopically, by a technique called plication of the diaphragm. Plication basically involves a folding of the eventrated diaphragm which is then sutured in order to “take up the slack” of the excess diaphragm tissue. Prognosis
Congenital diaphragmatic hernia has a mortality rate of 40–62%, with outcomes being more favorable in the absence of other congenital abnormalities. Individual rates vary greatly dependent upon multiple factors: size of hernia, organs involved, additional birth defects and/or genetic problems, amount of lung growth, age and size at birth, type of treatments, timing of treatments, complications (such as infections) and lack of lung function. See also
Diaphragmatic rupture

References
External links

Congenital Diaphragmatic Hernia Study Group under University of Texas Health Science Center at Houston
DHREAMS (Diaphragmatic Hernia Research & Exploration; Advancing Molecular Science) Project  coordinated at Columbia University Medical Center
CDH International – A global initiative to stop Congenital Diaphragmatic Hernia
The fact that eTG has been found in precipitates of skin-bound IgA from skin affected by this condition has been used to conclude that dermatitis herpetiformis may be caused by a deposition of both IgA and eTG within the dermis. It is estimated that these deposits may resorb after ten years of following a gluten-free diet. Moreover, it is suggested that this condition is closely linked to genetics. This theory is based on the arguments that individuals with a family history of gluten sensitivity who still consume foods containing gluten are more likely to develop the condition as a result of the formation of antibodies to gluten. These antibodies cross-react with eTG, and IgA/eTG complexes deposit within the papillary dermis to cause the lesions of dermatitis herpetiformis. These IgA deposits may disappear after long-term (up to ten years) avoidance of dietary gluten.Gliadin proteins in gluten are absorbed by the gut and enter the lamina propria where they need to be deamidated by tissue transglutaminase (tTG). tTG modifies gliadin into a more immunogenic peptide. Classical dendritic cells (cDCs) endocytose the immunogenic peptide and if their pattern recognition receptors (PRRs) are stimulated by pathogen-associated molecular patterns (PAMPs) or danger-associated molecular pattern (DAMPs), the danger signal will influence them to secrete IL-8 (CXCL8) in the lamina propria, recruiting neutrophils. Neutrophil recruitment results in a very rapid onset of inflammation.