The newer National Institute of Health (US) criteria for BPD (for neonates treated with more than 21% oxygen for at least 28 days) is as follows:,

- Mild

- Breathing room air at 36 weeks post-menstrual age or discharge (whichever comes first) for babies born before 32 weeks, or

- breathing room air by 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.

- Moderate

- Need for <30% oxygen at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks, or

- need for <30% oxygen to 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks gestation.

- Severe

- Need for >30% oxygen, with or without positive pressure ventilation or continuous positive pressure at 36 weeks postmenstrual age, or discharge (whichever comes first) for babies born before 32 weeks, or

- need for >30% oxygen with or without positive pressure ventilation or continuous positive pressure at 56 days postnatal age, or discharge (whichever comes first) for babies born after 32 weeks' gestation.

Prolonged high oxygen delivery in premature infants causes necrotizing bronchiolitis and alveolar septal injury, with inflammation and scarring. This results in hypoxemia. Today, with the advent of surfactant therapy and high frequency ventilation and oxygen supplementation, infants with BPD experience much milder injury without necrotizing bronchiolitis or alveolar septal fibrosis. Instead, there are usually uniformly dilated acini with thin alveolar septa and little or no interstitial fibrosis. It develops most commonly in the first 4 weeks after birth.

Transient tachypnea of the newborn (TTN, TTNB, or "transitory tachypnea of newborn") is a respiratory problem that can be seen in the newborn shortly after delivery. Amongst causes of respiratory distress in term neonates, it is the most common. It consists of a period of rapid breathing (higher than the normal range of 30-60 times per minute). It is likely due to amniotic fluid remaining in the lungs after birth. Usually, this condition resolves over 24–48 hours. Treatment is supportive and may include supplemental oxygen and antibiotics. The chest x-ray shows hyperinflation of the lungs including prominent pulmonary vascular markings, flattening of the diaphragm, and fluid in the horizontal fissure of the right lung.

TTN is a diagnosis of exclusion as it is a benign condition that can have symptoms and signs similar to more serious conditions, such as respiratory distress syndrome. A chest X-ray may show a radiopaque line - fluid - in the horizontal fissure of the right lung, fluid infiltrate throughout alveoli or fluid in individual lung lobes. The lungs may also appear hyperinflated.

May have no signs and symptoms or they may include:

- cough, but not prominent;

- chest pain (not common);

- breathing difficulty (fast and shallow);

- low oxygen saturation;

- pleural effusion (transudate type);

- cyanosis (late sign);

- increased heart rate.

It is a common misconception that atelectasis causes fever. A study of 100 post-op patients followed with serial chest X-rays and temperature measurements showed that the incidence of fever decreased as the incidence of atelectasis increased. A recent review article summarizing the available published evidence on the association between atelectasis and post-op fever concluded that there is no clinical evidence supporting this doctrine.

The most obvious sign that meconium has been passed during or before labor is the greenish or yellowish appearance of the amniotic fluid. The infant's skin, umbilical cord, or nailbeds may be stained green if the meconium was passed a considerable amount of time before birth. These symptoms alone do not necessarily indicate that the baby has inhaled in the fluid by gasping in utero or after birth. After birth, rapid or labored breathing, cyanosis, slow heartbeat, a barrel-shaped chest or low Apgar score are all signs of the syndrome. Inhalation can be confirmed by one or more tests such as using a stethoscope to listen for abnormal lung sounds (diffuse 'wet' crackles and rhonchi), performing blood gas tests to confirm a severe loss of lung function (respiratory acidosis as a consequence of hypercapnia), and using chest X-rays to look for patchy or streaked areas on the lungs. Infants who have inhaled meconium may develop respiratory distress syndrome often requiring ventilatory support. Complications of MAS include pneumothorax and persistent pulmonary hypertension of the newborn.

Clinically significant atelectasis is generally visible on chest X-ray; findings can include lung opacification and/or loss of lung volume. Post-surgical atelectasis will be bibasal in pattern. Chest CT or Bronchoscopy may be necessary if the cause of atelectasis is not clinically apparent. Direct signs of atelectasis include displacement of interlobar fissures and mobile structures within the thorax, overinflation of the unaffected ipsilateral lobe or contralateral lung, and opacification of the collapsed lobe.

Meconium aspiration syndrome (MAS) also known as neonatal aspiration of meconium is a medical condition affecting newborn infants. It occurs when meconium is present in their lungs during or before delivery. Meconium is the first stool of an infant, composed of materials ingested during the time the infant spends in the uterus.

Meconium is normally stored in the infant's intestines until after birth, but sometimes (often in response to fetal distress and hypoxia) it is expelled into the amniotic fluid prior to birth, or during labor. If the baby then inhales the contaminated fluid, respiratory problems may occur.

Alveolar capillary dysplasia (ACD, sometimes denoted ACDMPV when including misalignment of the pulmonary veins) is a type of diffuse developmental disorder of the lung. The other two diffuse developmental disorders are congenital acinar dysplasia and congenital alveolar dysplasia (CAD).

ACD or ACDMPV is the best studied diffuse developmental disorder. It is a very rare congenital malformation involving abnormal development of the capillary vascular system around the alveoli of the lungs. It is a rare cause of persistent pulmonary hypertension in infants. It also may be a rare cause of pulmonary hypoplasia.

Babies with ACD may appear normal at birth but within minutes or hours they develop respiratory distress with persistent pulmonary hypertension. ACD does not respond to standard therapies that resolve simple pulmonary hypertension. The lack of response is an important diagnostic clue.

Alveolar disease is visible on chest radiography as small, ill-defined nodules of homogeneous density centered on the acini or bronchioles. The nodules coalesce early in the course of disease, such that the nodules may only be seen as soft fluffy edges in the periphery.

When the nodules are centered on the hilar regions, the chest x-ray may develop what is called the "butterfly," or "batwing" appearance. The nodules may also have a segmental or lobar distribution. Air alveolograms and air bronchograms can also be seen.

These findings appear soon after the onset of symptoms and change rapidly thereafter.

A segmental or lobar pattern may be apparent after aspiration pneumonia, atelectasis, lung contusion, localized pulmonary edema, obstructive pneumonia, pneumonia, pulmonary embolism with infarction, or tuberculosis.

"Organizing" refers to unresolved pneumonia (in which the alveolar exudate persists and eventually undergoes fibrosis) in which fibrous tissue forms in the alveoli. The phase of resolution and/or remodeling following bacterial infections is commonly referred to as organizing pneumonia, both clinically and pathologically.

The classic presentation of COP is the development of nonspecific systemic (e.g., fevers, chills, night sweats, fatigue, weight loss) and respiratory (e.g. difficulty breathing, cough) symptoms in association with filling of the lung alveoli that is visible on chest x-ray. This presentation is usually so suggestive of an infection that the majority of patients with COP have been treated with at least one failed course of antibiotics by the time the true diagnosis is made.

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.

Alveolar lung diseases, are a group of diseases that mainly affect the alveoli of the lungs.

Ventilator-associated lung injury (VALI) is an acute lung injury that develops during mechanical ventilation and is termed ventilator-induced lung injury (VILI) if it can be proven that the mechanical ventilation caused the acute lung injury. In contrast, ventilator-associated lung injury (VALI) exists if the cause cannot be proven. VALI is the appropriate term in most situations because it is virtually impossible to prove what actually caused the lung injury in the hospital.

ACD commonly is diagnosed postmortem, by a pathologist.

Sometimes ACD is diagnosed clinically. This is common when there is a family history of ACD, but rare otherwise. A clinical differential diagnosis of ACD excludes fetal atelectasis.

ACD is not detectable by prenatal imaging. However, some babies with ACD have associated congenital malformations that are detectable by imaging. The identification of genes involved in ACD offers the potential for prenatal testing and genetic counseling.

There are various causes for intrauterine hypoxia (IH). The most preventable cause is maternal smoking. Cigarette smoking by expectant mothers has been shown to have a wide variety of deleterious effects on the developing fetus. Among the negative effects are carbon monoxide induced tissue hypoxia and placental insufficiency which causes a reduction in blood flow from the uterus to the placenta thereby reducing the availability of oxygenated blood to the fetus. Placental insufficiency as a result of smoking has been shown to have a causal effect in the development of pre-eclampsia. While some previous studies have suggested that carbon monoxide from cigarette smoke may have a protective effect against preeclampsia, a recent study conducted by the Genetics of Pre-Eclampsia Consortium (GOPEC) in the United Kingdom found that smokers were five times more likely to develop pre-eclampsia.

Nicotine alone has been shown to be a teratogen which affects the autonomic nervous system, leading to increased susceptibility to hypoxia-induced brain damage.

Maternal anemia in which smoking has also been implicated is another factor associated with IH/BA. Smoking by expectant mothers causes a decrease in maternal nucleated red blood cells (NRBC), thereby reducing the amount of red blood cells available for oxygen transport.

The perinatal brain injury occurring as a result of birth asphyxia, manifesting within 48 hours of birth, is a form of hypoxic ischemic encephalopathy.

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.

Spasm in the diaphragm leads to the muscle 'locking up' so that all breathing effort falls to the intercostal muscles. The resulting loss of movement causes the lungs to deflate gradually. This is easily diagnosed and treated (see Treatment below) by short-term interruption of the Phrenic nerve.

Perinatal asphyxia, neonatal asphyxia or birth asphyxia is the medical condition resulting from deprivation of oxygen to a newborn infant that lasts long enough during the birth process to cause physical harm, usually to the brain. Hypoxic damage can occur to most of the infant's organs (heart, lungs, liver, gut, kidneys), but brain damage is of most concern and perhaps the least likely to quickly or completely heal. In more pronounced cases, an infant will survive, but with damage to the brain manifested as either mental, such as developmental delay or intellectual disability, or physical, such as spasticity.

It results most commonly from a drop in maternal blood pressure or some other substantial interference with blood flow to the infant's brain during delivery. This can occur due to inadequate circulation or perfusion, impaired respiratory effort, or inadequate ventilation. Perinatal asphyxia happens in 2 to 10 per 1000 newborns that are born at term, and more for those that are born prematurely. WHO estimates that 4 million neonatal deaths occur yearly due to birth asphyxia, representing 38% of deaths of children under 5 years of age.

Perinatal asphyxia can be the cause of hypoxic ischemic encephalopathy or intraventricular hemorrhage, especially in preterm births. An infant suffering severe perinatal asphyxia usually has poor color (cyanosis), perfusion, responsiveness, muscle tone, and respiratory effort, as reflected in a low 5 minute Apgar score. Extreme degrees of asphyxia can cause cardiac arrest and death. If resuscitation is successful, the infant is usually transferred to a neonatal intensive care unit.

There has long been a scientific debate over whether newborn infants with 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.

There is considerable controversy over the diagnosis of birth asphyxia due to medicolegal reasons. Because of its lack of precision, the term is eschewed in modern obstetrics.

Twin-to-twin transfusion syndrome (TTTS), also known as feto-fetal transfusion syndrome (FFTS) and twin oligohydramnios-polyhydramnios sequence (TOPS) is a complication of disproportionate blood supply, resulting in high morbidity and mortality. It can affect monochorionic multiples, that is, multiple pregnancies where two or more fetuses share a chorion and hence a single placenta. Severe TTTS has a 60–100% mortality rate.

Perinatal mortality (PNM), also perinatal death, refers to the death of a fetus or neonate and is the basis to calculate the perinatal mortality rate. Variations in the precise definition of the perinatal mortality exist specifically concerning the issue of inclusion or exclusion of early fetal and late neonatal fatalities. The World Health Organization defines perinatal mortality as the "number of stillbirths and deaths in the first week of life per 1,000 total births, the perinatal period commences at 22 completed weeks (154 days) of gestation and ends seven completed days after birth", but other definitions have been used.

The UK figure is about 8 per 1,000 and varies markedly by social class with the highest rates seen in Asian women. Globally about 2.6 million neonates died in 2013 before the first month of age down from 4.5 million in 1990.

Neo-natal and Later lung collapse may be due to lung infection, or possibly to a malfunction in the epiglottis, causing the in-breath to draw air into the digestive tract rather than the lungs. A short term malfunction of this sort may be perpetuated by the resulting colic creating a feedback loop that interrupts the correct breathing process.

Autopsy and analysis of lung aspirate in a group of flat-chested kittens bred by a US Vet showed the presence of Herpes virus.

Swelling (especially in the hands and face) was originally considered an important sign for a diagnosis of pre-eclampsia. However, because swelling is a common occurrence in pregnancy, its utility as a distinguishing factor in pre-eclampsia is not high. Pitting edema (unusual swelling, particularly of the hands, feet, or face, notable by leaving an indentation when pressed on) can be significant, and should be reported to a health care provider.

In general, none of the signs of pre-eclampsia are specific, and even convulsions in pregnancy are more likely to have causes other than eclampsia in modern practice. Further, a symptom such as epigastric pain may be misinterpreted as heartburn. Diagnosis, therefore, depends on finding a coincidence of several pre-eclamptic features, the final proof being their regression after delivery.

Preterm birth is the most common cause of perinatal mortality, causing almost 30 percent of neonatal deaths. Infant respiratory distress syndrome, in turn, is the leading cause of death in preterm infants, affecting about 1% of newborn infants. Birth defects cause about 21 percent of neonatal death.