Treatment of diving barotrauma depends on the symptoms. Lung over-pressure injury may require a chest drain to remove air from the pleura or mediastinum. Recompression with hyperbaric oxygen therapy is the definitive treatment for arterial gas embolism, as the raised pressure reduces bubble size, low inert gas partial pressure accelerates inert gas solution and high oxygen partial pressure helps oxygenate tissues compromised by the emboli. Care must be taken when recompressing to avoid a tension pneumothorax. Barotraumas that do not involve gas in the tissues are generally treated according to severity and symptoms for similar trauma from other causes.

Pre-hospital care for lung barotrauma includes basic life support of maintaining adequate oxygenation and perfusion, assessment of airway, breathing and circulation, neurological assessment, and managing any immediate life-threatening conditions. High-flow oxygen up to 100% is considered appropriate for diving accidents. Large-bore venous access with isotonic fluid infusion is recommended to maintain blood pressure and pulse.

Oxygen first aid treatment is useful for suspected gas embolism casualties or divers who have made fast ascents or missed decompression stops. Most fully closed-circuit rebreathers can deliver sustained high concentrations of oxygen-rich breathing gas and could be used as an alternative to pure open-circuit oxygen resuscitators. However pure oxygen from an oxygen cylinder through a Non-rebreather mask is the optimal way to deliver oxygen to a decompression illness patient.

Recompression is the most effective, though slow, treatment of gas embolism in divers. Normally this is carried out in a recompression chamber. As pressure increases, the solubility of a gas increases, which reduces bubble size by accelerating absorption of the gas into the surrounding blood and tissues. Additionally, the volumes of the gas bubbles decrease in inverse proportion to the ambient pressure as described by Boyle's law. In the hyperbaric chamber the patient may breathe 100% oxygen, at ambient pressures up to a depth equivalent of 18 msw. Under hyperbaric conditions, oxygen diffuses into the bubbles, displacing the nitrogen from the bubble and into solution in the blood. Oxygen bubbles are more easily tolerated. Diffusion of oxygen into the blood and tissues under hyperbaric conditions supports areas of the body which are deprived of blood flow when arteries are blocked by gas bubbles. This helps to reduce ischemic injury. The effects of hyperbaric oxygen also counteract the damage that can occur with reperfusion of previously ischemic areas; this damage is mediated by leukocytes (a type of white blood cell).

First aid is common for both DCS and AGE:

- Monitor the patient for responsiveness, airway, breathing and circulation, resuscitate if necessary.

- Treat for shock.

- Lay the patient on their back, or for drowsy, unconscious, or nauseated victims, on their side.

- Administer 100% oxygen as soon as possible.

- Seek immediate medical assistance, locate a hospital with hyperbaric facilities and plan for possible transport.

- Allow the patient to drink water or isotonic fluids only if responsive, stable, and not suffering from nausea or stomach pain. Administration of intravenous saline solution is preferable.

- Record details of recent dives and responses to first aid treatment and provide to the treating medical specialist. The diving details should include depth and time profiles, breathing gases used and surface intervals.

Subcutaneous emphysema is usually benign. Most of the time, SCE itself does not need treatment (though the conditions from which it results may); however, if the amount of air is large, it can interfere with breathing and be uncomfortable. It occasionally progresses to a state "Massive Subcutaneous Emphysema" which is quite uncomfortable and requires surgical drainage. When the amount of air pushed out of the airways or lung becomes massive, usually due to positive pressure ventilation, the eyelids swell so much that the patient cannot see. Also the pressure of the air may impede the blood flow to the areolae of the breast and skin of the scrotum or labia. This can lead to necrosis of the skin in these areas. The latter are urgent situations requiring rapid, adequate decompression. Severe cases can compress the trachea and do require treatment.

In severe cases of subcutaneous emphysema, catheters can be placed in the subcutaneous tissue to release the air. Small cuts, or "blow holes", may be made in the skin to release the gas. When subcutaneous emphysema occurs due to pneumothorax, a chest tube is frequently used to control the latter; this eliminates the source of the air entering the subcutaneous space. If the volume of subcutaneous air is increasing, it may be that the chest tube is not removing air rapidly enough, so it may be replaced with a larger one. Suction may also be applied to the tube to remove air faster. The progression of the condition can be monitored by marking the boundaries with a special pencil for marking on skin.

Since treatment usually involves dealing with the underlying condition, cases of spontaneous subcutaneous emphysema may require nothing more than bed rest, medication to control pain, and perhaps supplemental oxygen. Breathing oxygen may help the body to absorb the subcutaneous air more quickly.

Treatment of diving disorders depends on the specific disorder or combination of disorders, but two treatments are commonly associated with first aid and definitive treatment where diving is involved. These are first aid oxygen administration at high concentration, which is seldom contraindicated, and generally recommended as a default option in diving accidents where there is any significant probability of hypoxia, and hyperbaric oxygen therapy (HBO), which is the definitive treatment for most incidences of decompression illness. Hyperbaric treatment on other breathing gases is also used for treatment of decompression sickness if HBO is inadequate.

High incidence of relapse after hyperbaric oxygen treatment due to delayed cerebral edema.

Small spontaneous pneumothoraces do not always require treatment, as they are unlikely to proceed to respiratory failure or tension pneumothorax, and generally resolve spontaneously. This approach is most appropriate if the estimated size of the pneumothorax is small (defined as <50% of the volume of the hemithorax), there is no breathlessness, and there is no underlying lung disease. It may be appropriate to treat a larger PSP conservatively if the symptoms are limited. Admission to hospital is often not required, as long as clear instructions are given to return to hospital if there are worsening symptoms. Further investigations may be performed as an outpatient, at which time X-rays are repeated to confirm improvement, and advice given with regard to preventing recurrence (see below). Estimated rates of resorption are between 1.25% and 2.2% the volume of the cavity per day. This would mean that even a complete pneumothorax would spontaneously resolve over a period of about 6 weeks. There is, however, no high quality evidence comparing conservative to non conservative management.

Secondary pneumothoraces are only treated conservatively if the size is very small (1 cm or less air rim) and there are limited symptoms. Admission to the hospital is usually recommended. Oxygen given at a high flow rate may accelerate resorption as much as fourfold.

The administration of oxygen as a medical intervention is common in diving medicine, both for first aid and for longer term treatment.

In a large PSP (>50%), or in a PSP associated with breathlessness, some guidelines recommend that reducing the size by aspiration is equally effective as the insertion of a chest tube. This involves the administration of local anesthetic and inserting a needle connected to a three-way tap; up to 2.5 liters of air (in adults) are removed. If there has been significant reduction in the size of the pneumothorax on subsequent X-ray, the remainder of the treatment can be conservative. This approach has been shown to be effective in over 50% of cases. Compared to tube drainage, first-line aspiration in PSP reduces the number of people requiring hospital admission, without increasing the risk of complications.

Aspiration may also be considered in secondary pneumothorax of moderate size (air rim 1–2 cm) without breathlessness, with the difference that ongoing observation in hospital is required even after a successful procedure. American professional guidelines state that all large pneumothoraces – even those due to PSP – should be treated with a chest tube. Moderately sized iatrogenic traumatic pneumothoraces (due to medical procedures) may initially be treated with aspiration.

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.

Treatment of the flail chest initially follows the principles of advanced trauma life support. Further treatment includes:

- Good pain management includes intercostal blocks and avoiding opioid pain medication as much as possible. This allows much better ventilation, with improved tidal volume, and increased blood oxygenation.

- Positive pressure ventilation, meticulously adjusting the ventilator settings to avoid pulmonary barotrauma.

- Chest tubes as required.

- Adjustment of position to make the person most comfortable and provide relief of pain.

- Aggressive pulmonary toilet

Surgical fixation can help in significantly reducing the duration of ventilatory support and in conserving the pulmonary function.

A person may be intubated with a double lumen tracheal tube. In a double lumen endotracheal tube, each lumen may be connected to a different ventilator. Usually one side of the chest is affected more than the other, so each lung may require drastically different pressures and flows to adequately ventilate.

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.

The tissues in the mediastinum will slowly resorb the air in the cavity so most pneumomediastinums are treated conservatively. Breathing high flow oxygen will increase the absorption of the air.

If the air is under pressure and compressing the heart, a needle may be inserted into the cavity, releasing the air.

Surgery may be needed to repair the hole in the trachea, esophagus or bowel.

If there is lung collapse, it is imperative the affected individual lies on the side of the collapse, although painful, this allows full inflation of the unaffected lung.

Treatment for the "Decompression Sickness" and the "Arterial Gas Embolism" components of DCI may differ significantly. Refer to the separate treatments under those articles.

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.

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

Treatment of TBI varies based on the location and severity of injury and whether the patient is stable or having trouble breathing, but ensuring that the airway is patent so that the patient can breathe is always of paramount importance. Ensuring an open airway and adequate ventilation may be difficult in people with TBI. Intubation, one method to secure the airway, may be used to bypass a disruption in the airway in order to send air to the lungs. If necessary, a tube can be placed into the uninjured bronchus, and a single lung can be ventilated. If there is a penetrating injury to the neck through which air is escaping, the trachea may be intubated through the wound. Multiple unsuccessful attempts at conventional (direct) laryngoscopy may threaten the airway, so alternative techniques to visualize the airway, such as fiberoptic or video laryngoscopy, may be employed to facilitate tracheal intubation. If the upper trachea is injured, an incision can be made in the trachea (tracheotomy) or the cricothyroid membrane (cricothyrotomy, or cricothyroidotomy) in order to ensure an open airway. However, cricothyrotomy may not be useful if the trachea is lacerated below the site of the artificial airway. Tracheotomy is used sparingly because it can cause complications such as infections and narrowing of the trachea and larynx. When it is impossible to establish a sufficient airway, or when complicated surgery must be performed, cardiopulmonary bypass may be used—blood is pumped out of the body, oxygenated by a machine, and pumped back in. If a pneumothorax occurs, a chest tube may be inserted into the pleural cavity to remove the air.

People with TBI are provided with supplemental oxygen and may need mechanical ventilation. Employment of certain measures such as Positive end-expiratory pressure (PEEP) and ventilation at higher-than-normal pressures may be helpful in maintaining adequate oxygenation. However, such measures can also increase leakage of air through a tear, and can stress the sutures in a tear that has been surgically repaired; therefore the lowest possible airway pressures that still maintain oxygenation are typically used. Mechanical ventilation can also cause pulmonary barotrauma when high pressure is required to ventilate the lungs. Techniques such as pulmonary toilet (removal of secretions), fluid management, and treatment of pneumonia are employed to improve pulmonary compliance (the elasticity of the lungs).

While TBI may be managed without surgery, surgical repair of the tear is considered standard in the treatment of most TBI. It is required if a tear interferes with ventilation; if mediastinitis (inflammation of the tissues in the mid-chest) occurs; or if subcutaneous or mediastinal emphysema progresses rapidly; or if air leak or large pneumothorax is persistent despite chest tube placement. Other indications for surgery are a tear more than one third the circumference of the airway, tears with loss of tissue, and a need for positive pressure ventilation. Damaged tissue around a rupture (e.g. torn or scarred tissue) may be removed in order to obtain clean edges that can be surgically repaired. Debridement of damaged tissue can shorten the trachea by as much as 50%. Repair of extensive tears can include sewing a flap of tissue taken from the membranes surrounding the heart or lungs (the pericardium and pleura, respectively) over the sutures to protect them. When lung tissue is destroyed as a result of TBI complications, pneumonectomy or lobectomy (removal of a lung or of one lobe, respectively) may be required. Pneumonectomy is avoided whenever possible due to the high rate of death associated with the procedure. Surgery to repair a tear in the tracheobronchial tree can be successful even when it is performed months after the trauma, as can occur if the diagnosis of TBI is delayed. When airway stenosis results after delayed diagnosis, surgery is similar to that performed after early diagnosis: the stenotic section is removed and the cut airway is repaired.

Air in subcutaneous tissue does not usually pose a lethal threat; small amounts of air are reabsorbed by the body. Once the pneumothorax or pneumomediastinum that causes the subcutaneous emphysema is resolved, with or without medical intervention, the subcutaneous emphysema will usually clear. However, spontaneous subcutaneous emphysema can, in rare cases, progress to a life-threatening condition, and subcutaneous emphysema due to mechanical ventilation may induce ventilatory failure.

Vehicle occupants who wear seat belts have a lower incidence of TBI after a motor vehicle accident. However, if the strap is situated across the front of the neck (instead of the chest), this increases the risk of tracheal injury. Design of medical instruments can be modified to prevent iatrogenic TBI, and medical practitioners can use techniques that reduce the risk of injury with procedures such as tracheotomy.

In order to begin a rehabilitation program for a flail chest it is important to treat the person's pain so they are able to perform the proper exercises. Due the underlying conditions that the flail segment has caused onto the respiratory system, chest physiotherapy is important to reduce further complications. Proper positioning of the body is key, including postural alignment for proper drainage of mucous secretions. The therapy will consist of a variety of postural positioning and changes in order to increase normal breathing. Along with postural repositioning, a variety of breathing exercises are also very important in order to allow the chest wall to reposition itself back to normal conditions. Breathing exercises will also include coughing procedures. Furthermore, range of motion exercises are given to reduce the atrophy of the musculature. With progression, resistance exercises are added to the regimen to the shoulder and arm of the side containing the injury. Moreover, trunk exercises will be introduced while sitting and will progress to during standing.

Hip flexion exercises can be done to expand the thorax. This is done by lying supine on a flat surface, flexing the knees and hips and bringing them in toward the chest. The knees should come in toward the chest while the person inhales, and exhale when the knees are lowered. This exercise can be done in 3 sets of 6-8 repetitions with a pause in between sets. The person should always make sure to maintain controlled breaths.

Eventually, the person will be progressed to walking and posture correction while walking. Before, the person is discharged from the hospital the person should be able to perform mobility exercises to the core and should have attained good posture.

Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long-term effects. However, permanent long-term injury from DCS is possible. Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed had ongoing symptoms of Type II DCS, and 7% from Type I DCS. Long-term follow-ups showed similar results, with 16% having permanent neurological sequelae.

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.

Administration of oxygen at 15 litres per minute by face mask or bag valve mask is often sufficient, but tracheal intubation with mechanical ventilation may be necessary. Suctioning of pulmonary oedema fluid should be balanced against the need for oxygenation. The target of ventilation is to achieve 92% to 96% arterial saturation and adequate chest rise. Positive end-expiratory pressure will generally improve oxygenation. Drug administration via peripheral veins is preferred over endotracheal administration. Hypotension remaining after oxygenation may be treated by rapid crystalloid infusion. Cardiac arrest in drowning usually presents as asystole or pulseless electrical activity. Ventricular fibrillation is more likely to be associated with complications of pre-existing coronary artery disease, severe hypothermia, or the use of epinephrine or norepinephrine.

High pressure nervous syndrome is rarely of importance to recreational divers. Breathing any gas at great depths (hundreds of feet) can cause seizures. Interestingly it was discovered because divers were using gas mixtures without nitrogen to be able to go to great depths without experiencing nitrogen narcosis. It turns out that nitrogen prevents HPNS. The answer? Add very small amounts of nitrogen to gas mixes when diving at great depth, small enough to avoid nitrogen narcosis, but sufficient to prevent HPNS.