Supportive care is the treatment of choice for TTN. This may include withholding oral feeding in periods of extreme tachypnea (over 60 breaths per minute) to prevent aspiration, supplemental oxygen, and CPAP.

There is evidence to show that steroids given to babies less than 8 days old can prevent bronchopulmonary dysplasia. However, the risks of treatment may outweigh the benefits.

It is unclear if starting steroids more than 7 days after birth is harmful or beneficial. It is thus recommended that they only be used in those who cannot be taken off of a ventilator.

Treatment is directed at correcting the underlying cause. Post-surgical atelectasis is treated by physiotherapy, focusing on deep breathing and encouraging coughing. An incentive spirometer is often used as part of the breathing exercises. Walking is also highly encouraged to improve lung inflation. People with chest deformities or neurologic conditions that cause shallow breathing for long periods may benefit from mechanical devices that assist their breathing. One method is continuous positive airway pressure, which delivers pressurized air or oxygen through a nose or face mask to help ensure that the alveoli do not collapse, even at the end of a breath. This is helpful, as partially inflated alveoli can be expanded more easily than collapsed alveoli. Sometimes additional respiratory support is needed with a mechanical ventilator.

The primary treatment for acute massive atelectasis is correction of the underlying cause. A blockage that cannot be removed by coughing or by suctioning the airways often can be removed by bronchoscopy. Antibiotics are given for an infection. Chronic atelectasis is often treated with antibiotics because infection is almost inevitable. In certain cases, the affected part of the lung may be surgically removed when recurring or chronic infections become disabling or bleeding is significant. If a tumor is blocking the airway, relieving the obstruction by surgery, radiation therapy, chemotherapy, or laser therapy may prevent atelectasis from progressing and recurrent obstructive pneumonia from developing.

Surfactant appears to improve outcomes when given to infants following meconium aspiration.

It has been recommended that the throat and nose of the baby be suctioned as soon as the head is delivered. However, this is not really useful and the revised Neonatal Resuscitation Guidelines no longer recommend it. When meconium staining of the amniotic fluid is present and the baby is born depressed, it is recommended that an individual trained in neonatal intubation use a laryngoscope and endotracheal tube to suction meconium from below the vocal cords. If the condition worsens, extracorporeal membrane oxygenation (ECMO) can be useful.

Albumin-lavage has not demonstrated to benefit outcomes of MAS. Steroid use has not demonstrated to benefit the outcomes of MAS.

MAS is difficult to prevent. Amnioinfusion, a method of thinning thick meconium that has passed into the amniotic fluid through pumping of sterile fluid into the amniotic fluid, has not shown a benefit.

Most patients recover with corticosteroid therapy. A standardized approach to dosing starting at 0.75 mg/kg and weaning over 24 weeks has been shown to reduce total corticosteroid exposure without affecting outcome.

About two thirds of patients recover with corticosteroid therapy: the usual corticosteroid administered is prednisolone in Europe and prednisone in the USA; these differ by only one functional group and have the same clinical effect. The corticosteroid is initially administered in high dosage, typically 50 mg per day tapering down to zero over a six-month to one-year period. If the corticosteroid treatment is halted too quickly the disease may return. Other medications must be taken to counteract side effects of the steroid.

Most babies with ACD have normal Apgar scores at 1 and 5 minutes, but within minutes or hours present with hypoxia and upon investigation are found to have hypoxemia and pulmonary hypertension. Initial treatments address the hypoxia, usually beginning with supplemental oxygen and arrangements for urgent transport to a neonatal intensive care unit.

Therapies that have been tried to extend life include extracorporeal membrane oxygenation and nitric oxide. These are supportive therapies for persistent pulmonary hypertension; they do not treat the ACD. The objective of therapy is to keep the baby alive long enough to obtain a lung transplant.

Several patients have survived with atypical or “patchy ACDMPV” long enough to receive lung transplants. According to a 2013 case series conducted by St. Louis Children’s Hospital, four ACDMPV patients (ages 4 months, 5 months, 9 months and 20 months of age at time of transplant) with atypical presentations of ACDMPV each underwent a successful bilateral lung transplantation (BLT). As stated in the case study, “If they survive to BLT, patients with ACDMPV can have successful outcomes” and the ACDMPV patients “are alive at last follow-up at 1, 8, 9 and 12 years of age” (as of May 2013).

According to the St. Louis Children's Hospital (the Level I pediatric trauma center and pediatric teaching hospital for the Washington University School of Medicine), which is noted worldwide for its record in pediatric pulmonary transplantation, a type of artificial lung device, the Quadrox, was used after ECMO as a bridge to a dual lung transplant in ten-month-old Eleni Scott of the St. Louis suburb of Florissant, Missouri, who after transplantation returned to her home. Doctors have said it is too early to presume it will continue to work here or work in other pediatric patients as an experiment, much less a successful, curative standard therapy, but the infant has survived thus far, meaning that there might be hope for sufferers of this rare condition. For more information, please see the link to the news release.

Preventing alveolar overdistension – Alveolar overdistension is mitigated by using small tidal volumes, maintaining a low plateau pressure, and most effectively by using volume-limited ventilation.

Preventing cyclic atelectasis (atelectotrauma) – Applied positive end-expiratory pressure (PEEP) is the principal method used to keep the alveoli open and lessen cyclic atelectasis.

Open lung ventilationn – Open lung ventilation is a ventilatory strategy that combines small tidal volumes (to lessen alveolar overdistension) and an applied PEEP above the low inflection point on the pressure-volume curve (to lessen cyclic atelectasis).

High frequency ventilation is thought to reduce ventilator-associated lung injury, especially in the context of ARDS and acute lung injury.

Permissive hypercapnia and hypoxaemia allow the patient to be ventilated at less aggressive settings and can thererfore mitigate all forms of ventilator associated lung injury

The use of steroids (Dexamethasone) coupled with an antibiotic (Amoxicillin) will support the kitten in a number of ways, the steroid enhancing maturation and the antibiotic addressing the possibility of underlying infection and compensating for the immuno-depressant properties of the steroid. The steroid will also encourage the kitten to feed more energetically, keeping its weight up. Several breeders believe that Taurine plays a part in the condition, and it may be that some cases are Taurine-related. These breeders give the queen large doses of Taurine (1000 mg) daily until the kittens recover – apparently within a few days. Given that most FCKS cases take weeks rather than days to recover, this supplement may be relevant.

Treatment is difficult to define given the number of different causes and the wealth of anecdotal information collected by and from cat breeders. Treatments have hitherto been based on the assumption that FCKS is caused by a muscular spasm, and their effectiveness is impossible to assess because some kittens will recover spontaneously without intervention.

Diaphragmatic spasm is easily tested for and treated by short term interruption of the Phrenic nerve. The nerve runs down the outside of the neck where the neck joins to the shoulder, within a bundle of muscles and tendons at this junction. The cluster can be pinched gently and held for a few seconds each time. Kittens with spasmodic FCKS will show almost immediate improvement, but the treatment may need to be repeated several times over a few days as the spasm may have a tendency to recur. [Um für diapragmatisch Sparmus zu prüfen, Sie müssen der Phrenikus finden (es heisst auch der Zwerchfellnerv), der lauft am aussen des Hals, wo der Hals trifft die Schulter. Da gibt es mehrere Muskeln und Sehnen–da es unmoeglich ist die Nerv allein zu finden bzw. kneifen, müssen Sie die ganze Menge zusammen ruhig kneifen für ein paar Sekunden. Wenn es doch diapragmatisch Spasmus ist und Sie das Phrenikus gut kneifest (manchmal aber nicht immer werde die Katze mit den hinteren Beinen kicken), sollen Sie sofort eine Verbesserung anschauen. Es kann sein, dass die Spasmus wieder kommt nachher im kommenden Tage—in dem Fall müssen Sie es nochmal machen. Wenn Sie aber keine Verbesserung siehst, ist der Problem dann leider etwas anders.]

Continuous positive air pressure (CPAP) is used in human babies with lung collapse, but this is impossible with kittens. It is possible that the success of some breeders in curing kittens by splinting the body, thus putting pressure on the ribcage, was successful as it has created the effect of positive air pressure, thus gradually re-inflating the lungs by pulling them open rather than pushing them open as is the case with CPAP.

Treatment of infants suffering birth asphyxia by lowering the core body temperature is now known to be an effective therapy to reduce mortality and improve neurological outcome in survivors, and hypothermia therapy for neonatal encephalopathy begun within 6 hours of birth significantly increases the chance of normal survival in affected infants.

There has long been a debate over whether newborn infants with birth asphyxia should be resuscitated with 100% oxygen or normal air. It has been demonstrated that high concentrations of oxygen lead to generation of oxygen free radicals, which have a role in reperfusion injury after asphyxia. Research by Ola Didrik Saugstad and others led to new international guidelines on newborn resuscitation in 2010, recommending the use of normal air instead of 100% oxygen.

The rate of BPD varies among institutions, which may reflect neonatal risk factors, care practices (e.g., target levels for acceptable oxygen saturation), and differences in the clinical definitions of BPD.

This procedure involves removal of amniotic fluid periodically throughout the pregnancy under the assumption that the extra fluid in the recipient twin can cause preterm labor, perinatal mortality, or tissue damage. In the case that the fluid does not reaccumulate, the reduction of amniotic fluid stabilizes the pregnancy. Otherwise the treatment is repeated as necessary. There is no standard procedure for how much fluid is removed each time. There is a danger that if too much fluid is removed, the recipient twin could die. This procedure is associated with a 66% survival rate of at least one fetus, with a 15% risk of cerebral palsy and average delivery occurring at 29 weeks gestation.

This procedure involves the tearing of the dividing membrane between fetuses such that the amniotic fluid of both twins mixes under the assumption that pressure is different in either amniotic sac and that its equilibration will ameliorate progression of the disease. It has not been proven that pressures are different in either amniotic sac. Use of this procedure can preclude use of other procedures as well as make difficult the monitoring of disease progression. In addition, tearing the dividing membrane has contributed to cord entanglement and demise of fetuses through physical complications.

Transient tachypnea of the newborn occurs in approximately 1 in 100 preterm infants and 3.6-5.7 per 1000 term infants. It is most common in infants born by Cesarian section without a trial of labor after 35 weeks' gestation. Male infants and infants with an umbilical cord prolapse or perinatal asphyxia are at higher risk. Parental risk factors include use of pain control or anesthesia during labor, asthma, and diabetes.

VALI does not need to be distinguished from progressive ALI/ARDS because management is the same in both. Additionally, definitive diagnosis of VALI may not be possible because of lack of sign or symptoms.

The World Health Organization recommends that women with severe hypertension during pregnancy should receive treatment with anti-hypertensive agents. Severe hypertension is generally considered systolic BP of at least 160 or diastolic BP of at least 110. Evidence does not support the use of one anti-hypertensive over another. The choice of which agent to use should be based on the prescribing clinician's experience with a particular agent, its cost, and its availability. Diuretics are not recommended for prevention of preeclampsia and its complications. Labetolol, Hydralazine and Nifedipine are commonly used antihypertensive agents for hypertension in pregnancy. ACE inhibitors and angiotensin receptor blockers are contraindicated as they affect fetal development.

The goal of treatment of severe hypertension in pregnancy is to prevent cardiovascular, kidney, and cerebrovascular complications. The target blood pressure has been proposed to be 140–160 mmHg systolic and 90–105 mmHg diastolic, although values are variable.

In the past, treatment options were limited to supportive medical therapy. Nowadays neonatal encephalopathy is treated using hypothermia therapy.

The intrapartum and postpartum administration of magnesium sulfate is recommended in severe pre-eclampsia for the prevention of eclampsia. Further, magnesium sulfate is recommended for the treatment of eclampsia over other anticonvulsants. Magnesium sulfate acts by interacting with NMDA receptors.

Treatment options include

- gefitinib - epidermal growth factor receptor tyrosine kinase inhibitor

- indomethacin

- corticosteroids

- octreotide

- radiation therapy

- bronchoscopy as is often done in the post traumatic setting.

Hypothermia treatment induced by head cooling or systemic cooling administered within 6 hours of birth for 72 hours has proven beneficial in reducing death and neurological impairments at 18 months of age. This treatment does not completely protect the injured brain and may not improve the risk of death in the most severely hypoxic-ischemic neonates and has also not been proven beneficial in preterm infants. Combined therapies of hypothermia and pharmacological agents or growth factors to improve neurological outcomes are most likely the next direction for damaged neonatal brains, such as after a stroke.

Treatment remains controversial with regards to the risk/benefit ratio, which differs significantly from treatment of stroke in adults. Presence or possibility of organ or limb impairment and bleeding risks are possible with treatments using antithrombotic agents.

Atelectasis may be an acute or chronic condition. In acute atelectasis, the lung has recently collapsed and is primarily notable only for airlessness. In chronic atelectasis, the affected area is often characterized by a complex mixture of airlessness, infection, widening of the bronchi (bronchiectasis), destruction, and scarring (fibrosis).

Intrauterine hypoxia occurs when the fetus is deprived of an adequate supply of oxygen. It may be due to a variety of reasons such as prolapse or occlusion of the umbilical cord, placental infarction and maternal smoking. Intrauterine growth restriction (IUGR) may cause or be the result of hypoxia. Intrauterine hypoxia can cause cellular damage that occurs within the central nervous system (the brain and spinal cord). This results in an increased mortality rate, including an increased risk of sudden infant death syndrome (SIDS). Oxygen deprivation in the fetus and neonate have been implicated as either a primary or as a contributing risk factor in numerous neurological and neuropsychiatric disorders such as epilepsy, ADHD, eating disorders and cerebral palsy.