Screening for critical congenital heart defect should be done on all newborns after 24hours or shortly before discharge. Oxygen saturation is measured in the right hand and either foot.A screening is considered positive if:

Oxygen saturation <90% in either extremity,
Oxygen saturation 90-94% in both extremities on 3 measurements separated by an hour each,
Oxygen saturation difference >3% between both extremities on 3 measurements separated by an hour each. Management
Treatment for blue baby syndrome will depend on the underlying cause. When evaluating a patient for cyanosis or respiratory distress, vital signs should be monitored, especially the patients heart rate and oxygen saturation. It is beneficial to have vascular access established. In newborns, the pulse oximeter is typically placed on the right hand to determine pre-ductal oxygenation, referring to oxygenation before the ductus arteriosus (connection between aorta and pulmonary artery). This gives the oxygenation level the heart and brain receive. Traditionally, supplemental oxygen is given in an escalating manner beginning with free-flowing oxygen, progressing to positive pressure ventilation or continuous positive airway pressure, and ending with mechanical intubation. The goal oxygen saturation is between 85 and 95%. If an infant requires supplemental oxygen for a prolonged time it should be heated and humidified to avoid heat loss. Cyanotic heart disease
Some babies born with cyanotic heart disease are treated with prostaglandin E1 after birth to keep the ductus arteriosus open and allow for more oxygenated blood to be pumped to the body. Many also receive oxygen therapy to increase the percentage of oxygen in the blood.
Doses of trazodone lower than those effective for antidepressant action are frequently used for the effective treatment of insomnia. Low doses exploit trazodones potent actions as a 5-HT2A receptor antagonist, and its properties as an antagonist of H1 and α1-adrenergic receptors, but do not adequately exploit its SERT or 5-HT2C inhibition properties, which are weaker. Since insomnia is one of the most frequent residual symptoms of depression after treatment with an SSRI, a hypnotic is often necessary for patients with a major depressive episode. Not only can a hypnotic potentially relieve the insomnia itself, but treating insomnia in patients with major depression may also increase remission rates due to improvement of other symptoms such as loss of energy and depressed mood. Thus, the ability of low doses of trazodone to improve sleep in depressed patients may be an important mechanism whereby trazodone can augment the efficacy of other antidepressants.Trazodones potent α1-adrenergic blockade may cause some side effects like orthostatic hypotension and sedation. Conversely, along with 5-HT2A and H1 receptor antagonism, it may contribute to its efficacy as a hypnotic. Trazodone lacks any affinity for the muscarinic acetylcholine receptors, so does not produce anticholinergic side effects. mCPP, a non-selective serotonin receptor modulator and serotonin releasing agent, is an active metabolite of trazodone and has been suggested to possibly play a role in its therapeutic benefits. However, research has not supported this hypothesis and mCPP might actually antagonize the efficacy of trazodone as well as produce additional side effects. Pharmacokinetics
Absorption
Trazodone is well-absorbed after oral administration.