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.

Oxygen is given with a small amount of continuous positive airway pressure ("CPAP"), and intravenous fluids are administered to stabilize the blood sugar, blood salts, and blood pressure. If the baby's condition worsens, an endotracheal tube (breathing tube) is inserted into the trachea and intermittent breaths are given by a mechanical device. An exogenous preparation of surfactant, either synthetic or extracted from animal lungs, is given through the breathing tube into the lungs. Some of the most commonly used surfactants are Survanta or its generic form Beraksurf, derived from cow lungs, which can decrease the risk of death in hospitalized very-low-birth-weight infants by 30%. Such small premature infants may remain ventilated for months. A study shows that an aerosol of a perfluorocarbon such as perfluoromethyldecalin can reduce inflammation in swine model of IRDS. Chronic lung disease including bronchopulmonary dysplasia are common in severe RDS. The etiology of BPD is problematic and may be due to oxygen, overventilation or underventilation. The mortality rate for babies greater than 27 weeks gestation is less than 20%

Extracorporeal membrane oxygenation (ECMO) is a potential treatment, providing oxygenation through an apparatus that imitates the gas exchange process of the lungs. However, newborns cannot be placed on ECMO if they are under 4.5 pounds (2 kg), because they have extremely small vessels for cannulation, thus hindering adequate flow because of limitations from cannula size and subsequent higher resistance to blood flow (compare with vascular resistance). Furthermore, in infants aged less than 34 weeks of gestation several physiologic systems are not well-developed, specially the cerebral vasculature and germinal matrix, resulting in high sensitivity to slight changes in pH, PaO, and intracranial pressure. Subsequently, preterm infants are at unacceptably high risk for intraventricular hemorrhage (IVH) if administered ECMO at a gestational age less than 32 weeks.

- The INSURE Method

Henrik Verder is the inventor and pioneer of the INSURE method, a very effective approach to managing preterm neonates with respiratory distress. The method itself has been shown, through meta-analysis; to successfully decrease the use of mechanical ventilation and lower the incidence of bronchopulmonary dysplasia (BPD). Since its conception in 1989 the INSURE method has been academically cited in more than 500 papers. The first randomised study about the INSURE method was published in 1994 and a second randomised study in infants less than 30 weeks gestation was published by the group in 1999. In the last 15 years Henrik has worked with lung maturity diagnostics on gastric aspirates obtained at birth. By combining this diagnostic method with INSURE, Henrik has worked to further improve the clinical outcome of RDS. The lung maturity tests used have been the microbubble test, lamellar body counts (LBC) and measurements of lecithin-sphingomyelin ratio (L/S) with chemometrics, which involved a collaboration with Agnar Höskuldsson.

Giving the mother glucocorticoids speeds the production of surfactant. For very premature deliveries, a glucocorticoid is given without testing the fetal lung maturity. The American College of Obstetricians and Gynecologists (ACOG), Royal College of Medicine, and other major organizations have recommended antenatal glucocorticoid treatment for women at risk for preterm delivery prior to 34 weeks of gestation. Multiple courses of glucocorticoid administration, compared with a single course, does not seem to increase or decrease the risk of death or neurodevelopmental disorders of the child.

In pregnancies of greater than 30 weeks, the fetal lung maturity may be tested by sampling the amount of surfactant in the amniotic fluid by amniocentesis, wherein a needle is inserted through the mother's abdomen and uterus. Several tests are available that correlate with the production of surfactant. These include the lecithin-sphingomyelin ratio ("L/S ratio"), the presence of phosphatidylglycerol (PG), and more recently, the surfactant/albumin (S/A) ratio. For the L/S ratio, if the result is less than 2:1, the fetal lungs may be surfactant deficient. The presence of PG usually indicates fetal lung maturity. For the S/A ratio, the result is given as mg of surfactant per gm of protein. An S/A ratio 55 indicates mature surfactant production(correlates with an L/S ratio of 2.2 or greater).

The standard and most important treatment is to descend to a lower altitude as quickly as possible, preferably by at least 1000 metres. Oxygen should also be given if possible. Symptoms tend to quickly improve with descent, but more severe symptoms may continue for several days. The standard drug treatments for which there is strong clinical evidence are dexamethasone and nifedipine. Phosphodiesterase inhibitors such as sildenafil and tadalafil are also effective but may worsen the headache of mountain sickness.

The dual (ET and ET) endothelin receptor antagonist bosentan was approved in 2001. Sitaxentan (Thelin) was approved for use in Canada, Australia, and the European Union, but not in the United States. In 2010, Pfizer withdrew Thelin worldwide because of fatal liver complications. A similar drug, ambrisentan is marketed as Letairis in the U.S. by Gilead Sciences.

The U.S. FDA approved sildenafil, a selective inhibitor of cGMP specific phosphodiesterase type 5 (PDE5), for the treatment of PAH in 2005. It is marketed for PAH as Revatio. In 2009, they also approved tadalafil, another PDE5 inhibitor, marketed under the name Adcirca. PDE5 inhibitors are believed to increase pulmonary artery vasodilation, and inhibit vascular remodeling, thus lowering pulmonary arterial pressure and pulmonary vascular resistance.

Tadalafil is taken orally, as well as sildenafil, and it is rapidly absorbed (serum levels are detectable at 20 minutes). The T (biological half-life) hovers around 17.5 hours in healthy subjects. Moreover, if we consider pharmacoeconomic implications, patients that take tadalafil would pay two-thirds of the cost of sildenafil therapy. However, there are some adverse effects of this drug such as headache, diarrhea, nausea, back pain, dyspepsia, flushing and myalgia.

ILD is not a single disease, but encompasses many different pathological processes. Hence treatment is different for each disease.

If a specific occupational exposure cause is found, the person should avoid that environment. If a drug cause is suspected, that drug should be discontinued.

Many cases due to unknown or connective tissue-based causes are treated with corticosteroids, such as prednisolone. Some people respond to immunosuppressant treatment. Patients with a low level of oxygen in the blood may be given supplemental oxygen.

Pulmonary rehabilitation appears to be useful. Lung transplantation is an option if the ILD progresses despite therapy in appropriately selected patients with no other contraindications.

On October 16, 2014, the Food and Drug Administration approved a new drug for the treatment of Idiopathic Pulmonary Fibrosis (IPF). This drug, Ofev (nintedanib), is marketed by Boehringer Ingelheim Pharmaceuticals, Inc. This drug has been shown to slow the decline of lung function although the drug has not been shown to reduce mortality or improve lung function. The estimated cost of the drug per year is approximately $94,000.

General treatment principles are removal from exposure, protection of the airway (i.e., preemptive intubation), and treatment of hypoxemia. Concomitant airway injury with acute bronchospasm often warrants treatment with bronchodilators because of the airway obstruction.

A beneficial role for corticosteroids has not been established by controlled trials in humans. Despite the lack of controlled evidence of efficacy, anecdotal reports of benefits from systemic corticosteroid use continue to appear.

Prophylactic antibiotic drugs have not proved to be efficacious in toxic lung injury. Antibiotics should be reserved for those patients with clinical evidence of infection.

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.

A hemothorax is managed by removing the source of bleeding and by draining the blood already in the thoracic cavity. Blood in the cavity can be removed by inserting a drain (chest tube) in a procedure called a tube thoracostomy. Generally, the thoracostomy tube is placed between the ribs in the sixth or seventh intercostal space at the mid-axillary line. Usually the lung will expand and the bleeding will stop after a chest tube is inserted.

The blood in the chest can thicken as the clotting cascade is activated when the blood leaves the blood vessels and comes into contact with the pleural surface, injured lung or chest wall, or with the chest tube. As the blood thickens, it can clot in the pleural space (leading to a retained hemothorax) or within the chest tube, leading to chest tube clogging or occlusion. Chest tube clogging or occlusion can lead to worse outcomes as it prevents adequate drainage of the pleural space, contributing to the problem of retained hemothorax. In this case, patients can be hypoxic, short of breath, or in some cases, the retained hemothorax can become infected (empyema).

Retained hemothorax occurs when blood remains in the pleural space, and is a risk factor for the development of complications, including the accumulation of pus in the pleural space and fibrothorax. It is treated by inserting a second chest tube or by drainage by video-assisted thoracoscopy. Fibrolytic therapy has also been studied as a treatment.

When hemothorax is treated with a chest tube, it is important that it maintain its function so that the blood cannot clot in the chest or the tube. If clogging occurs, internal chest tube clearing can be performed using an open or closed technique. Manual manipulation, which may also be called milking, stripping, or tapping, of chest tubes is commonly performed to maintain an open tube, but no conclusive evidence has demonstrated that any of these techniques are more effective than the others, or that they improve chest tube drainage.

In some cases bleeding continues and surgery is necessary to stop the source of bleeding. For example, if the hemothorax was caused by aortic rupture in high energy trauma, surgical intervention is mandatory.

If left untreated, the condition can progress to a point where the blood accumulation begins to put pressure on the mediastinum and the trachea, effectively limiting the amount that the heart's ventricles are able to fill. The condition can cause the trachea to deviate, or move, toward the unaffected side.

Treatment for this condition entails the maintenance of intravascular volume. Additionally, the following can be done as a means of managing FES in an individual:

- Albumin can be used for volume resuscitation

- Long bone fractures should be attended to immediately (surgery)

- Mechanical ventilation

Although the etiology is unconfirmed, transient hyperammonemia is known to be caused by increased levels of ammonia in the blood stream, as well as a failure of the urea cycle to convert enough of the ammonia into urea. Since transamination of proteins is a leading producer of ammonia, protein restriction may be recommended as a therapy to reduce the symptoms of the episode. THAN can also be treated by avoiding amino acids in TPN or total parenteral nutrition or by giving a high caloric diet to limit catabolism of the tissues and therefore to minimize the breakdown of endogenous protein. The most common treatments are dialysis (both peritoneal and hemodialysis), sodium benzoate, and arginine. Sodium Benzoate combines with glycine to be excreted in the form of hippuric acid. The goal of these treatments is to convert nitrogen to a compound that can be excreted more easily.

The best treatment is to avoid the provoking allergen, as chronic exposure can cause permanent damage. Corticosteroids such as prednisolone may help to control symptoms but may produce side-effects.

The mortality rate for THAN is relatively high unless immediate treatment is obtained. The duration of hyperammonemia is directly correlated to morbidity as well as the associated neurological conditions. After the first hyperammonemic episode, there is no increased risk for future hyperammonemic episodes, and normal protein consumption can be continued.

In 2001 the American Thoracic Society, drawing on the work of the British and Canadian Thoracic Societies, established guidelines for the management of adult CAP dividing patients into four categories based on common organisms:

- Healthy outpatients without risk factors: This group (the largest) is composed of otherwise-healthy patients without risk factors for DRSP, enteric gram-negative bacteria, "pseudomonas" or other, less-common, causes of CAP. Primary microoganisms are viruses, atypical bacteria, penicillin-sensitive "streptococcus pneumoniae" and "haemophilus influenzae". Recommended drugs are macrolide antibiotics, such as azithromycin or clarithromycin, for seven to ten days.

- Outpatients with underlying illness or risk factors: Although this group does not require hospitalization, patients have underlying health problems (such as emphysema or heart failure) or are at risk for DRSP or enteric gram-negative bacteria. They are treated with a quinolone active against "streptococcus pneumoniae" (such as levofloxacin) or a β-lactam antibiotic (such as cefpodoxime, cefuroxime, amoxicillin or amoxicillin/clavulanic acid) and a macrolide antibiotic, such as azithromycin or clarithromycin, for seven to ten days.

- Hospitalized patients without risk for "pseudomonas": This group requires intravenous antibiotics, with a quinolone active against "streptococcus pneumoniae" (such as levofloxacin), a β-lactam antibiotic (such as cefotaxime, ceftriaxone, ampicillin/sulbactam or high-dose ampicillin plus a macrolide antibiotic (such as azithromycin or clarithromycin) for seven to ten days.

- Intensive-care patients at risk for "pseudomonas aeruginosa": These patients require antibiotics targeting this difficult-to-eradicate bacterium. One regimen is an intravenous antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an IV antipseudomonal fluoroquinolone such as levofloxacin. Another is an IV antipseudomonal beta-lactam such as cefepime, imipenem, meropenem or piperacillin/tazobactam, plus an aminoglycoside such as gentamicin or tobramycin, plus a macrolide (such as azithromycin) or a nonpseudomonal fluoroquinolone such as ciprofloxacin.

For mild-to-moderate CAP, shorter courses of antibiotics (3–7 days) seem to be sufficient.

Some patients with CAP will be at increased risk of death despite antimicrobial treatment. A key reason for this is the host's exaggerated inflammatory response. On one hand it is required to control the infection but on the other, it leads to bystander tissue damage. As a consequence of this recent research focuses on immunomodulatory therapy that can modulate the immune response to reduce injury to the lung and other affected organs such as the heart. Although the evidence for these agents has not resulted in their routine use, there potential benefits are highly promising.

Note that, in neonates, sepsis is difficult to diagnose clinically. They may be relatively asymptomatic until hemodynamic and respiratory collapse is imminent, so, if there is even a remote suspicion of sepsis, they are frequently treated with antibiotics empirically until cultures are sufficiently proven to be negative. In addition to fluid resuscitation and supportive care, a common antibiotic regimen in infants with suspected sepsis is a beta-lactam antibiotic (usually ampicillin) in combination with an aminoglycoside (usually gentamicin) or a third-generation cephalosporin (usually cefotaxime—ceftriaxone is generally avoided in neonates due to the theoretical risk of kernicterus.) The organisms which are targeted are species that predominate in the female genitourinary tract and to which neonates are especially vulnerable to, specifically Group B Streptococcus, "Escherichia coli", and "Listeria monocytogenes" (This is the main rationale for using ampicillin versus other beta-lactams.) Of course, neonates are also vulnerable to other common pathogens that can cause meningitis and bacteremia such as "Streptococcus pneumoniae" and "Neisseria meningitidis". Although uncommon, if anaerobic species are suspected (such as in cases where necrotizing enterocolitis or intestinal perforation is a concern, clindamycin is often added.

Granulocyte-macrophage colony stimulating factor (GM-CSF) is sometimes used in neonatal sepsis. However, a 2009 study found that GM-CSF corrects neutropenia if present but it has no effect on reducing sepsis or improving survival.

Trials of probiotics for prevention of neonatal sepsis have generally been too small and statistically underpowered to detect any benefit, but a randomized controlled trial that enrolled 4,556 neonates in India reported that probiotics significantly reduced the risk of developing sepsis. The probiotic used in the trial was "Lactobacillus plantarum".

A very large meta-analysis investigated the effect of probiotics on preventing late-onset sepsis (LOS) in neonates. Probiotics were found to reduce the risk of LOS, but only in babies who were fed human milk exclusively. It is difficult to distinguish if the prevention was a result of the probiotic supplementation or if it was a result of the properties of human milk. It is also still unclear if probiotic administration reduces LOS risk in extremely low birth weight infants due to the limited number of studies that investigated it. Out of the 37 studies included in this systematic review, none indicated any safety problems related to the probiotics. It would be beneficial to clarify the relationship between probiotic supplementation and human milk for future studies in order to prevent late onset sepsis in neonates.

Treatment of CAP in children depends on the child's age and the severity of illness. Children under five are not usually treated for atypical bacteria. If hospitalization is not required, a seven-day course of amoxicillin is often prescribed, with co-trimaxazole an alternative when there is allergy to penicillins. Further studies are needed to confirm the efficacy of newer antibiotics. With the increase in drug-resistant Streptococcus pneumoniae, antibiotics such as cefpodoxime may become more popular. Hospitalized children receive intravenous ampicillin, ceftriaxone or cefotaxime, and a recent study found that a three-day course of antibiotics seems sufficient for most mild-to-moderate CAP in children.

Individual susceptibility to HAPE is difficult to predict. The most reliable risk factor is previous susceptibility to HAPE, and there is likely to be a genetic basis to this condition, perhaps involving the gene for angiotensin converting enzyme (ACE). Recently, scientists have found the similarities between low amounts of 2,3-BPG (also known as 2,3-DPG) with the occurrence of HAPE at high altitudes. Persons with sleep apnea are susceptible due to irregular breathing patterns while sleeping at high altitudes.

Medication is used to relieve fever, seizures, and weight loss or dehydration. When medication is use for opiate withdrawal in newborn babies is deemed necessary, opiates are the treatment of choice; they are slowly tapered down to wean the baby off opiates. Phenobarbital is sometimes used as an alternative but is less effective in suppressing seizures; however, phenobarbital is superior to diazepam for neonatal opiate withdrawal symptoms. In the case of sedative-hypnotic neonatal withdrawal, phenobarbital is the treatment of choice. Clonidine is an emerging add-on therapy.

Opioids such as neonatal morphine solution and methadone are commonly used to treat clinical symptoms of opiate withdrawal, but may prolong neonatal drug exposure and duration of hospitalization. A study demonstrated a shorter wean duration in infants treated with methadone compared to those treated with diluted tincture of opium. When compared to morphine, methadone has a longer half-life in children, which allows for less frequent dosing intervals and steady serum concentrations to prevent neonatal withdrawal symptoms.

Treatment depends on the drug involved, the infant's overall health, abstinence scores and whether the baby was born full-term or premature. Clinicians will watch the newborn carefully for up to a week after birth for signs of withdrawal, feeding problems, and weight gain. Babies who vomit or who are very dehydrated may need to get fluids through a vein (IV).

Some babies with severe symptoms need medicines such as methadone and morphine to treat withdrawal symptoms. These babies may need to stay in the hospital for weeks or months after birth. The goal of treatment is to prescribe the infant a drug similar to the one the mother used during pregnancy and slowly decrease the dose over time. This helps wean the baby off the drug and relieves some withdrawal symptoms.

If the symptoms are severe, especially if other drugs were used, a second medicine such as phenobarbital or clonidine may be added. Breastfeeding may also be helpful if the mother is in a methadone or buprenorphine treatment program without other drug use.

Babies with this condition often have severe diaper rash or other areas of skin breakdown. This requires treatment with special ointment or cream. Babies may also have problems with feeding or slow growth. These problems may require higher-calorie feedings that provide greater nutrition and smaller portions given more often. Objectives of management are to minimize negative outcomes and promote normal development.

Non-selective beta-blockers are the most effective in reducing the frequency and severity of PSH episodes. They help decrease the effect of circulating catecholamines and lower metabolic rates, which are high in patients during PSH episodes. Beta-blockers also help in reducing fever, diaphoresis, and in some cases dystonia. Propanolol is a common beta-blocker administered due to the fact that it penetrates the blood-brain barrier relatively well. Typically it is administered in doses of twenty milligrams to sixty milligrams every four to six hours in the treatment of PSH.

"Fire-eater's lung" is an important variant of hydrocarbon pneumonitis, which typically involves adolescents or young adults who are exposed through mishap during flame-blowing performances using a variety of different flammable materials. The substances used overlap with some of the pediatric exposures (kerosene, gasoline) but can also include other hydrocarbons such as jet fuel and, in France, an aromatic hydrocarbon enriched petroleum-distillate called "kerdan". There has also been a case of citronella oil aspiration in a fire-eater. As with hydrocarbon pneumonitis in children, fire-eater's lung can also be complicated by pneumatocele. Although the term "acute lipoid pneumonia" has been used to refer to the "fire-eater's lung" syndrome, this is a misnomer.

The two most common medications used in the treatment of paroxysmal sympathetic hyperactivity are morphine sulfate and beta-blockers. Morphine is useful in helping halt episodes that have started to occur. Beta-blockers are helpful in preventing the occurrence of 'sympathetic storms'. Other drugs that have been used and have in some cases been helpful are dopamine agonists, other various opiates, benzodiazepines, clonidine, and baclofen. Chlorpromazine and haloperidol, both dopamine antagonists, in some cases have worsened PSH symptoms. These drugs are in use currently for treatment; exact pathways are not known and wide-range helpfulness is speculative.

Interstitial lung disease (ILD), or diffuse parenchymal lung disease (DPLD), is a group of lung diseases affecting the interstitium (the tissue and space around the air sacs of the lungs). It concerns alveolar epithelium, pulmonary capillary endothelium, basement membrane, perivascular and perilymphatic tissues. It may occur when an injury to the lungs triggers an abnormal healing response. Ordinarily, the body generates just the right amount of tissue to repair damage. But in interstitial lung disease, the repair process goes awry and the tissue around the air sacs (alveoli) becomes scarred and thickened. This makes it more difficult for oxygen to pass into the bloodstream. The term ILD is used to distinguish these diseases from obstructive airways diseases.

In children, several unique forms of ILD exist which are specific for the young age groups. The acronym chILD is used for this group of diseases and is derived from the English name, Children’s Interstitial Lung Diseases – chILD.

Prolonged ILD may result in pulmonary fibrosis, but this is not always the case. Idiopathic pulmonary fibrosis is interstitial lung disease for which no obvious cause can be identified (idiopathic), and is associated with typical findings both radiographic (basal and pleural based fibrosis with honeycombing) and pathologic (temporally and spatially heterogeneous fibrosis, histopathologic honeycombing and fibroblastic foci).

In 2013 interstitial lung disease affected 595,000 people globally. This resulted in 471,000 deaths.