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 initial management of pulmonary edema, irrespective of the type or cause, is supporting vital functions. Therefore, if the level of consciousness is decreased it may be required to proceed to tracheal intubation and mechanical ventilation to prevent airway compromise. Hypoxia (abnormally low oxygen levels) may require supplementary oxygen, but if this is insufficient then again mechanical ventilation may be required to prevent complications. Treatment of the underlying cause is the next priority; pulmonary edema secondary to infection, for instance, would require the administration of appropriate antibiotics.

Acute cardiogenic pulmonary edema often responds rapidly to medical treatment. Positioning upright may relieve symptoms. Loop diuretics such as furosemide or bumetanide are administered, often together with morphine or diamorphine to reduce respiratory distress. Both diuretics and morphine may have vasodilator effects, but specific vasodilators may be used (particularly intravenous glyceryl trinitrate or ISDN) provided the blood pressure is adequate.

Continuous positive airway pressure and bilevel positive airway pressure (BIPAP/NIPPV) has been demonstrated to reduce the need of mechanical ventilation in people with severe cardiogenic pulmonary edema, and may reduce mortality.

It is possible for cardiogenic pulmonary edema to occur together with cardiogenic shock, in which the cardiac output is insufficient to sustain an adequate blood pressure. This can be treated with inotropic agents or by intra-aortic balloon pump, but this is regarded as temporary treatment while the underlying cause is addressed.

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.

The administration of fluid therapy in individuals with pulmonary contusion is controversial. Excessive fluid in the circulatory system (hypervolemia) can worsen hypoxia because it can cause fluid leakage from injured capillaries (pulmonary edema), which are more permeable than normal. However, low blood volume (hypovolemia) resulting from insufficient fluid has an even worse impact, potentially causing hypovolemic shock; for people who have lost large amounts of blood, fluid resuscitation is necessary. A lot of the evidence supporting the idea that fluids should be withheld from people with pulmonary contusion came from animal studies, not clinical trials with humans; human studies have had conflicting findings on whether fluid resuscitation worsens the condition. Current recommendations suggest giving enough fluid to ensure sufficient blood flow but not giving any more fluid than necessary. For people who do require large amounts of intravenous fluid, a catheter may be placed in the pulmonary artery to measure the pressure within it. Measuring pulmonary artery pressure allows the clinician to give enough fluids to prevent shock without exacerbating edema. Diuretics, drugs that increase urine output to reduce excessive fluid in the system, can be used when fluid overload does occur, as long as there is not a significant risk of shock. Furosemide, a diuretic used in the treatment of pulmonary contusion, also relaxes the smooth muscle in the veins of the lungs, thereby decreasing pulmonary venous resistance and reducing the pressure in the pulmonary capillaries.

Positive pressure ventilation, in which air is forced into the lungs, is needed when oxygenation is significantly impaired. Noninvasive positive pressure ventilation including continuous positive airway pressure (CPAP) and bi-level positive airway pressure (BiPAP), may be used to improve oxygenation and treat atelectasis: air is blown into the airways at a prescribed pressure via a face mask. Noninvasive ventilation has advantages over invasive methods because it does not carry the risk of infection that intubation does, and it allows normal coughing, swallowing, and speech. However, the technique may cause complications; it may force air into the stomach or cause aspiration of stomach contents, especially when level of consciousness is decreased.

People with signs of inadequate respiration or oxygenation may need to be intubated and mechanically ventilated. Mechanical ventilation aims to reduce pulmonary edema and increase oxygenation. Ventilation can reopen collapsed alveoli, but it is harmful for them to be repeatedly opened, and positive pressure ventilation can also damage the lung by overinflating it. Intubation is normally reserved for when respiratory problems occur, but most significant contusions do require intubation, and it may be done early in anticipation of this need. People with pulmonary contusion who are especially likely to need ventilation include those with prior severe lung disease or kidney problems; the elderly; those with a lowered level of consciousness; those with low blood oxygen or high carbon dioxide levels; and those who will undergo operations with anesthesia. Larger contusions have been correlated with a need for ventilation for longer periods of time.

Pulmonary contusion or its complications such as acute respiratory distress syndrome may cause lungs to lose compliance (stiffen), so higher pressures may be needed to give normal amounts of air and oxygenate the blood adequately. Positive end-expiratory pressure (PEEP), which delivers air at a given pressure at the end of the expiratory cycle, can reduce edema and keep alveoli from collapsing. PEEP is considered necessary with mechanical ventilation; however, if the pressure is too great it can expand the size of the contusion and injure the lung. When the compliance of the injured lung differs significantly from that of the uninjured one, the lungs can be ventilated independently with two ventilators in order to deliver air at different pressures; this helps avoid injury from overinflation while providing adequate ventilation.

Specific pretreatments, drugs to prevent chemically induced lung injuries due to respiratory airway toxins, are not available. Analgesic medications, oxygen, humidification, and ventilator support currently constitute standard therapy. In fact, mechanical ventilation remains the therapeutic mainstay for acute inhalation injury. The cornerstone of treatment is to keep the PaO2 > 60 mmHg (8.0 kPa), without causing injury to the lungs with excessive O2 or volutrauma. Pressure control ventilation is more versatile than volume control, although breaths should be volume limited, to prevent stretch injury to the alveoli. Positive end-expiratory pressure (PEEP) is used in mechanically ventilated patients with ARDS to improve oxygenation. Hemorrhaging, signifying substantial damage to the lining of the airways and lungs, can occur with exposure to highly corrosive chemicals and may require additional medical interventions. Corticosteroids are sometimes administered, and bronchodilators to treat bronchospasms. Drugs that reduce the inflammatory response, promote healing of tissues, and prevent the onset of pulmonary edema or secondary inflammation may be used following severe injury to prevent chronic scarring and airway narrowing.

Although current treatments can be administered in a controlled hospital setting, many hospitals are ill-suited for a situation involving mass casualties among civilians. Inexpensive positive-pressure devices that can be used easily in a mass casualty situation, and drugs to prevent inflammation and pulmonary edema are needed. Several drugs that have been approved by the FDA for other indications hold promise for treating chemically induced pulmonary edema. These include β2-agonists, dopamine, insulin, allopurinol, and non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen. Ibuprofen is particularly appealing because it has an established safety record and can be easily administered as an initial intervention. Inhaled and systemic forms of β2-agonists used in the treatment of asthma and other commonly used medications, such as insulin, dopamine, and allopurinol have also been effective in reducing pulmonary edema in animal models but require further study. A recent study documented in the "AANA Journal" discussed the use of volatile anesthetic agents, such as sevoflurane, to be used as a bronchodilator that lowered peak airway pressures and improved oxygenation. Other promising drugs in earlier stages of development act at various steps in the complex molecular pathways underlying pulmonary edema. Some of these potential drugs target the inflammatory response or the specific site(s) of injury. Others modulate the activity of ion channels that control fluid transport across lung membranes or target surfactant, a substance that lines the air sacs in the lungs and prevents them from collapsing. Mechanistic information based on toxicology, biochemistry, and physiology may be instrumental in determining new targets for therapy. Mechanistic studies may also aid in the development of new diagnostic approaches. Some chemicals generate metabolic byproducts that could be used for diagnosis, but detection of these byproducts may not be possible until many hours after initial exposure. Additional research must be directed at developing sensitive and specific tests to identify individuals quickly after they have been exposed to varying levels of chemicals toxic to the respiratory tract.

Currently there are no clinically approved agents that can reduce pulmonary and airway cell dropout and avert the transition to pulmonary and /or airway fibrosis.

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

Management has generally been reported to be conservative, though deaths have been reported.

- Removal from water

- Observation

- Diuretics and / or Oxygen when necessary

- Episodes are generally self-limiting in the absence of other medical problems

Treatment of the underlying cause is required. Endotracheal intubation and mechanical ventilation are required in cases of severe respiratory failure (PaO2 less than 50 mmHg). Respiratory stimulants such as doxapram are rarely used, and if the respiratory failure resulted from an overdose of sedative drugs such as opioids or benzodiazepines, then the appropriate antidote (naloxone or flumazenil, respectively) will be given.

There is tentative evidence that in those with respiratory failure identified before arrival in hospital, continuous positive airway pressure can be useful when started before conveying to hospital.

Acute respiratory distress syndrome is usually treated with mechanical ventilation in the intensive care unit (ICU). Mechanical ventilation is usually delivered through a rigid tube which enters the oral cavity and is secured in the airway (endotracheal intubation), or by tracheostomy when prolonged ventilation (≥2 weeks) is necessary. The role of non-invasive ventilation is limited to the very early period of the disease or to prevent worsening respiratory distress in individuals with atypical pneumonias, lung bruising, or major surgery patients, who are at risk of developing ARDS. Treatment of the underlying cause is crucial. Appropriate antibiotic therapy must be administered as soon as microbiological culture results are available, or clinical infection is suspected (whichever is earlier). Empirical therapy may be appropriate if local microbiological surveillance is efficient. The origin of infection, when surgically treatable, must be removed. When sepsis is diagnosed, appropriate local protocols should be enacted.

Individuals can benefit from a variety of physical therapy interventions. Persons with neurological/neuromuscular abnormalities may have breathing difficulties due to weak or paralyzed intercostal, abdominal and/or other muscles needed for ventilation. Some physical therapy interventions for this population include active assisted cough techniques, volume augmentation such as breath stacking, education about body position and ventilation patterns and movement strategies to facilitate breathing.

Inhaled nitric oxide (NO) selectively widens the lung's arteries which allows for more blood flow to open alveoli for gas exchange. Despite evidence of increased oxygenation status, there is no evidence that inhaled nitric oxide decreases morbidity and mortality in people with ARDS. Furthermore, nitric oxide may cause kidney damage and is not recommended as therapy for ARDS regardless of severity.

In those who are not palliative the primary treatment of shortness of breath is directed at its underlying cause. Extra oxygen is effective in those with hypoxia; however, this has no effect in those with normal blood oxygen saturations, even in those who are palliative.

Supportive care is the mainstay of therapy in TRALI. Oxygen supplementation is employed in all reported cases of TRALI and aggressive respiratory support is needed in 72 percent of patients. Intravenous administration of fluids, as well as vasopressors, are essential for blood pressure support. Use of diuretics, which are indicated in the management of transfusion associated circulatory overload (TACO), should be avoided in TRALI. Corticosteroids can be beneficial.

Treatments for primary pulmonary hypertension such as prostacyclins and endothelin receptor antagonists can be fatal in people with PVOD due to the development of severe pulmonary edema, and worsening symptoms after initiation of these medications may be a clue to the diagnosis of pulmonary veno occlusive disease.

The definitive therapy is lung transplantation, though transplant rejection is always a possibility, in this measures must be taken in terms of appropriate treatment and medication.

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.

Patients with HACE should be brought to lower altitudes and provided supplemental oxygen, and rapid descent is sometimes needed to prevent mortality. Early recognition is important because as the condition progresses patients are unable to descend without assistance. Dexamethasone should also be administered, although it fails to ameliorate some symptoms that can be cured by descending to a lower altitude. It can also mask symptoms, and they sometimes resume upon discontinuation. Dexamethasone's prevention of angiogenesis may explain why it treats HACE well. Three studies that examined how mice and rat brains react to hypoxia gave some credence to this idea.

If available, supplemental oxygen can be used as an adjunctive therapy, or when descent is not possible. FiO2 should be titrated to maintain arterial oxygen saturation of greater than 90%, bearing in mind that oxygen supply is often limited in high altitude clinics/environments.

In addition to oxygen therapy, a portable hyperbaric chamber (Gamow bag) can by used as a temporary measure in the treatment of HACE. These devices simulate a decrease in altitude of up to 7000 ft, but they are resource intensive and symptoms will often return after discontinuation of the device. Portable hyperbaric chambers should not be used in place of descent or evacuation to definitive care.

Diuretics may be helpful, but pose risks outside of a hospital environment. Sildenafil and tadalafil may help HACE, but there is little evidence of their efficacy. Theophylline is also theorized to help the condition.

Although AMS is not life-threatening, HACE is usually fatal within 24 hours if untreated. Without treatment, the patient will enter a coma and then die. In some cases, patients have died within a few hours, and a few have survived for two days. Descriptions of fatal cases often involve climbers who continue ascending while suffering from the condition's symptoms.

Recovery varies between days and weeks, but most recover in a few days. After the condition is successfully treated, it is possible for climbers to reascend. Dexamethesone should be discontinued, but continual acetazolamide is recommended. In one study, it took patients between one week and one month to display a normal CT scan after suffering from HACE.

The only reliable treatment, and in many cases the only option available, is to descend. Attempts to treat or stabilize the patient "in situ" (at altitude) are dangerous unless highly controlled and with good medical facilities. However, the following treatments have been used when the patient's location and circumstances permit:

- Oxygen may be used for mild to moderate AMS below and is commonly provided by physicians at mountain resorts. Symptoms abate in 12 to 36 hours without the need to descend.

- For more serious cases of AMS, or where rapid descent is impractical, a Gamow bag, a portable plastic hyperbaric chamber inflated with a foot pump, can be used to reduce the effective altitude by as much as . A Gamow bag is generally used only as an aid to evacuate severe AMS patients, not to treat them at altitude.

- Acetazolamide 250 mg twice daily dosing assists in AMS treatment by quickening altitude acclimatization. A study by the Denali Medical Research Project concluded: "In established cases of acute mountain sickness, treatment with acetazolamide relieves symptoms, improves arterial oxygenation, and prevents further impairment of pulmonary gas exchange."

- The folk remedy for altitude sickness in Ecuador, Peru and Bolivia is a tea made from the coca plant. See mate de coca.

- Steroids can be used to treat the symptoms of pulmonary or cerebral edema, but do not treat the underlying AMS.

- Two studies in 2012 showed that Ibuprofen 600 milligrams three times daily was effective at decreasing the severity and incidence of AMS; it was not clear if HAPE or HACE was affected.

In people with stable OHS, the most important treatment is weight loss—by diet, through exercise, with medication, or sometimes weight loss surgery (bariatric surgery). This has been shown to improve the symptoms of OHS and resolution of the high carbon dioxide levels. Weight loss may take a long time and is not always successful. Bariatric surgery is avoided if possible, given the high rate of complications, but may be considered if other treatment modalities are ineffective in improving oxygen levels and symptoms. If the symptoms are significant, nighttime positive airway pressure (PAP) treatment is tried; this involves the use of a machine to assist with breathing. PAP exists in various forms, and the ideal strategy is uncertain. Some medications have been tried to stimulate breathing or correct underlying abnormalities; their benefit is again uncertain.

While many people with obesity hypoventilation syndrome are cared for on an outpatient basis, some deteriorate suddenly and when admitted to the hospital may show severe abnormalities such as markedly deranged blood acidity (pH<7.25) or depressed level of consciousness due to very high carbon dioxide levels. On occasions, admission to an intensive care unit with intubation and mechanical ventilation is necessary. Otherwise, "bi-level" positive airway pressure (see the next section) is commonly used to stabilize the patient, followed by conventional treatment.

Increased water intake may also help in acclimatization to replace the fluids lost through heavier breathing in the thin, dry air found at altitude, although consuming excessive quantities ("over-hydration") has no benefits and may cause dangerous hyponatremia.

Positive airway pressure, initially in the form of "continuous" positive airway pressure (CPAP), is a useful treatment for obesity hypoventilation syndrome, particularly when obstructive sleep apnea co-exists. CPAP requires the use during sleep of a machine that delivers a continuous positive pressure to the airways and preventing the collapse of soft tissues in the throat during breathing; it is administered through a mask on either the mouth and nose together or if that is not tolerated on the nose only (nasal CPAP). This relieves the features of obstructive sleep apnea and is often sufficient to remove the resultant accumulation of carbon dioxide. The pressure is increased until the obstructive symptoms (snoring and periods of apnea) have disappeared. CPAP alone is effective in more than 50% of people with OHS.

In some occasions, the oxygen levels are persistently too low (oxygen saturations below 90%). In that case, the hypoventilation itself may be improved by switching from CPAP treatment to an alternate device that delivers "bi-level" positive pressure: higher pressure during inspiration (breathing in) and a lower pressure during expiration (breathing out). If this too is ineffective in increasing oxygen levels, the addition of oxygen therapy may be necessary. As a last resort, tracheostomy may be necessary; this involves making a surgical opening in the trachea to bypass obesity-related airway obstruction in the neck. This may be combined with mechanical ventilation with an assisted breathing device through the opening.

All cases of decompression sickness should be treated initially with 100% oxygen until hyperbaric oxygen therapy (100% oxygen delivered in a high-pressure chamber) can be provided. Mild cases of the "bends" and some skin symptoms may disappear during descent from high altitude; however, it is recommended that these cases still be evaluated. Neurological symptoms, pulmonary symptoms, and mottled or marbled skin lesions should be treated with hyperbaric oxygen therapy if seen within 10 to 14 days of development.

Recompression on air was shown to be an effective treatment for minor DCS symptoms by Keays in 1909. Evidence of the effectiveness of recompression therapy utilizing oxygen was first shown by Yarbrough and Behnke, and has since become the standard of care for treatment of DCS. Recompression is normally carried out in a recompression chamber. At a dive site, a riskier alternative is in-water recompression.

Oxygen first aid has been used as an emergency treatment for diving injuries for years. If given within the first four hours of surfacing, it increases the success of recompression therapy as well as decreasing the number of recompression treatments required. Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as a means of supplying oxygen if dedicated equipment is not available.

It is beneficial to give fluids, as this helps reduce dehydration. It is no longer recommended to administer aspirin, unless advised to do so by medical personnel, as analgesics may mask symptoms. People should be made comfortable and placed in the supine position (horizontal), or the recovery position if vomiting occurs. In the past, both the Trendelenburg position and the left lateral decubitus position (Durant's maneuver) have been suggested as beneficial where air emboli are suspected, but are no longer recommended for extended periods, owing to concerns regarding cerebral edema.

The duration of recompression treatment depends on the severity of symptoms, the dive history, the type of recompression therapy used and the patient's response to the treatment. One of the more frequently used treatment schedules is the US Navy Table 6, which provides hyperbaric oxygen therapy with a maximum pressure equivalent to of seawater for a total time under pressure of 288 minutes, of which 240 minutes are on oxygen and the balance are air breaks to minimise the possibility of oxygen toxicity.

A multiplace chamber is the preferred facility for treatment of decompression sickness as it allows direct physical access to the patient by medical personnel, but monoplace chambers are more widely available and should be used for treatment if a multiplace chamber is not available or transportation would cause significant delay in treatment, as the interval between onset of symptoms and recompression is important to the quality of recovery. It may be necessary to modify the optimum treatment schedule to allow use of a monoplace chamber, but this is usually better than delaying treatment. A US Navy treatment table 5 can be safely performed without air breaks if a built-in breathing system is not available. In most cases the patient can be adequately treated in a monoplace chamber at the receiving hospital.

Generally, high-altitude pulmonary edema (HAPE) or AMS precede HACE. In patients with AMS, the onset of HACE is usually indicated by vomiting, headache that does not respond to non-steroidal anti-inflammatory drugs, hallucinations, and stupor. In some situations, however, AMS progresses to HACE without these symptoms. HACE must be distinguished from conditions with similar symptoms, including stroke, intoxication, psychosis, diabetic symptoms, meningitis, or ingestion of toxic substances. It should be the first diagnosis ruled out when sickness occurs while ascending to a high altitude.

HACE is generally preventable by ascending gradually with frequent rest days while climbing or trekking. Not ascending more than daily and not sleeping at a greater height than more than the previous night is recommended. The risk of developing HACE is diminished if acetazolamide or dexamethasone are administered. Generally, the use of acetazolamide is preferred, but dexamethasone can be used for prevention if there are side effects or contraindications. Some individuals are more susceptible to HACE than others, and physical fitness is not preventative. Age and sex do not by themselves affect vulnerability to HACE.