Complications
Children with this condition are at a higher risk of developing the following complications:
Failure to thrive
Recurrent chest infections
Endocarditis
Epilepsy
Stroke
Arrhythmia
Heart failure
Premature deathChildren whose PAVSD is caused by DiGeorge syndrome (also known as 22q11.2 deletion syndrome) are more likely to suffer from the post-surgical complications (especially respiratory ones) associated with surgeries that treat this defect.Women with PAVSD are at a slightly higher risk of being infertile and having miscarriages or children with a congenital heart defect.Airway hyperresponsiveness is a commonly seen co-morbidity among those afflicted with PAVSD. Pathogenesis
Pulmonary atresia in PAVSD takes place during the first 8 weeks of fetal life, when the pulmonary valve that is supposed to form, fails to form, this doesnt allow blood to flow through the pulmonary artery from the right ventricle. The ventricular septal defect associated with PAVSD lets the right ventricule form.In some cases of PAVSD, major aortopulmonary collateral arteries develop; in a normal fetus, these arteries usually develop but then start deteriorating after pulmonary arteries grow, in fetuses with PAVSD, the pulmonary arteries dont develop, and this gives a chance to the major aortopulmonary collateral arteries to develop fully. Pathophysiology
The mildest variant of pulmonary atresia with ventricular septal defect involves pulmonary atresia with normally developed main pulmonary artery and branch pulmonary arteries, the blood that flows to the lungs from the right side of the heart goes to the left side of the heart through the ventricular septum which then flows through the patent ductus arteriosus.
These surface receptors allow a bridge to be formed which binds to host endothelial cells. Lipases allow for the degradation of lipids on the skin surface and its expression can be directly correlated with its ability of the bacteria to produce abscesses. Diagnosis
Observing the skins physical appearance, or swabbing a culture of the lesion for S. aureus. Nasal swabs from the patients immediate family members are necessary to identify them as being asymptomatic nasal carriers of S. aureus. Histology
The epidermis is composed of four layers, stratum basale, stratum spinosum, stratum granulosum, and stratum corneum. The cleavage plane can be found either subcorneally or within the upper stratum granulosum. The roof of the pustule is parakeratotic stratum corneum, and the floor is formed of keratinocytes, which may or may not be acantholytic. Neutrophils begin to fill the pustule. Toxins are produced by S. aureus and target desmoglein, which is a desmosomal cell-cell adhesion molecule found in the upper levels of the epidermis. This correlates with the subcorneal localization of the bullae. Uncommon variants
Erythema multiforme
Systemic lupus erythematosus
Stevens–Johnson syndrome
Pemphigus vulgaris

Differential
HPV
Insect bites
Burns
Herpes simplex 1/2

Prevention
Since the common pathogens involved with impetigo are bacteria naturally found on the skin, most prevention (especially in children), is targeted towards appropriate hygiene, wound cleaning, and minimizing scratching (i.e. by keeping nails trimmed and short). Avoiding close contact and sharing of items such as towels with potentially infected individuals is also recommended. Management
Antibiotic creams are the preferred treatment for mild cases of impetigo, despite their limited systemic absorption.