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.

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.

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

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.

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

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.

Pulmonary barotrauma:

- Endotracheal intubation may be required if the airway is unstable or hypoxia persists when breathing 100% oxygen.

- Needle decompression or tube thoracostomy may be necessary to drain a pneumothorax or haemothorax

- Foley catheterization may be necessary for spinal cord AGE if the person is unable to urinate.

- Intravenous hydration may be required to maintain adequate blood pressure.

- Therapeutic recompression is indicated for severe AGE. The diving medical practitioner will need to know the vital signs and relevant symptoms, along with the recent pressure exposure and breathing gas history of the patient. Air transport should be below if possible, or in a pressurized aircraft which should be pressurised to as low an altitude as reaonably possible.

Sinus squeeze and middle ear squeeze are generally treated with decongestants to reduce the pressure differential, with anti-inflammatory medications to treat the pain. For severe pain, narcotic analgesics may be appropriate.

Suit, helmet and mask squeeze are treated as trauma according to symptoms and severity.

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.

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).

A large bubble of air in the heart (as can follow certain traumas in which air freely gains access to large veins) will present with a constant "machinery" murmur. It is important to promptly place the patient in Trendelenburg position (head down) and on their left side (left lateral decubitus position). The Trendelendburg position keeps a left-ventricular air bubble away from the coronary artery ostia (which are near the aortic valve) so that air bubbles do not enter and occlude the coronary arteries (which would cause a heart attack). Left lateral decubitus positioning helps to trap air in the non-dependent segment of the right ventricle (where it is more likely to remain instead of progressing into the pulmonary artery and occluding it). The left lateral decubitus position also prevents the air from passing through a potentially patent foramen ovale (present in as many as 30% of adults) and entering the left ventricle, from which it could then embolise to distal arteries (potentially causing occlusive symptoms such as stroke).

Administration of high percentage oxygen is recommended for both venous and arterial air embolism. This is intended to counteract ischaemia and accelerate bubble size reduction.

For venous air embolism the Trendelenburg or left lateral positioning of a patient with an air-lock obstruction of the right ventricle may move the air bubble in the ventricle and allow blood flow under the bubble.

Hyperbaric therapy with 100% oxygen is recommended for patients presenting clinical features of arterial air embolism, as it accelerates removal of nitrogen from the bubbles by solution and improves tissue oxygenation. This is recommended particularly for cases of cardiopulmonary or neurological involvement. Early treatment has greatest benefits, but it can be effective as late as 30 hours after the injury.

Prevention is a more successful strategy than treatment. By using the most conservative decompression schedule reasonably practicable, and by minimizing the number of major decompression exposures, the risk of DON may be reduced. Prompt treatment of any symptoms of decompression sickness (DCS) with recompression and hyperbaric oxygen also reduce the risk of subsequent DON.

Dysbarism refers to medical conditions resulting from changes in ambient pressure. Various activities are associated with pressure changes. underwater diving is the most frequently cited example, but pressure changes also affect people who work in other pressurized environments (for example, caisson workers), and people who move between different altitudes.

Treatment is difficult, often requiring a joint replacement. Spontaneous improvement occasionally happens and some juxta-articular lesions do not progress to collapse. Other treatments include immobilization and osteotomy of the femur. Cancellous bone grafts are of little help.

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.

Mild disease can be treated with fluids by mouth. In more significant disease spraying with mist and using a fan is useful. For those with severe disease putting them in lukewarm water is recommended if possible with transport to a hospital.

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.

If pneumothorax occurs in a smoker, this is considered an opportunity to emphasize the markedly increased risk of recurrence in those who continue to smoke, and the many benefits of smoking cessation. It may be advisable for someone to remain off work for up to a week after a spontaneous pneumothorax. If the person normally performs heavy manual labor, several weeks may be required. Those who have undergone pleurodesis may need two to three weeks off work to recover.

Air travel is discouraged for up to seven days after complete resolution of a pneumothorax if recurrence does not occur. Underwater diving is considered unsafe after an episode of pneumothorax unless a preventative procedure has been performed. Professional guidelines suggest that pleurectomy be performed on both lungs and that lung function tests and CT scan normalize before diving is resumed. Aircraft pilots may also require assessment for surgery.

Acute compartment syndrome is a medical emergency requiring immediate surgical treatment, known as a fasciotomy, to allow the pressure to return to normal. Although only one compartment is affected, fasciotomy is done to release all compartments. For instance, if only the deep posterior compartment of a leg is affected, the treatment would be fasciotomy (with medial and lateral incisions) to release all compartments of the leg in question, namely the anterior, lateral, superficial posterior and deep posterior.

An acute compartment syndrome has some distinct features such as swelling of the compartment due to inflammation and venous occlusion. Decompression of the nerve traversing the compartment might alleviate the symptoms (Rorabeck, 1984). Until definitive fasciotomy can be performed, the extremity should be placed at the level of the heart. Hypotension should also be avoided, as this decreases perfusion pressure to the compartment. Supplemental oxygen also optimizes tissue and neural oxygenation.

Prevention includes avoiding medications that can increase the risk of heat illness (e.g. antihypertensives, diuretics, and anticholinergics), gradual adjustment to heat, and sufficient fluids and electrolytes.

Chronic compartment syndrome in the lower leg can be treated conservatively or surgically. Conservative treatment includes rest, anti-inflammatories, and manual decompression. Elevation of the affected limb in patients with compartment syndrome is contraindicated, as this leads to decreased vascular perfusion of the affected region. Ideally, the affected limb should be positioned at the level of the heart. The use of devices that apply external pressure to the area, such as splints, casts, and tight wound dressings, should be avoided. If symptoms persist after conservative treatment or if an individual does not wish to cease engaging in the physical activities which bring on symptoms, compartment syndrome can be treated by a surgery known as a fasciotomy. Surgery is the most effective treatment for compartment syndrome. Incisions are made in the affected muscle compartments so that they will decompress. This decompression will relieve the pressure on the venules and lymphatic vessels, and will increase bloodflow throughout the muscle. Left untreated, chronic compartment syndrome can develop into the acute syndrome and lead to permanent muscle and nerve damage.

A military study conducted in 2012 found that teaching individuals with lower leg chronic exertional compartment syndrome to change their running stride to a forefoot running technique abated symptoms. Follow up studies are needed to confirm the finding of this study.

Hyperbaric oxygen therapy has been suggested by case reports – though as of 2011 not proven in controlled randomized trials – to be an effective adjunctive therapy for crush injury, compartment syndrome, and other acute traumatic ischemias, by improving wound healing and reducing the need for repetitive surgery.

The second stage features the reabsorption of the initially extravasated fluid and albumin from the tissues, and it usually lasts 1 to 2 days. Intravascular fluid overload leads to polyuria and can cause flash pulmonary edema and cardiac arrest, with possibly fatal consequences. Death from SCLS typically occurs during this recruitment phase because of pulmonary edema arising from excessive intravenous fluid administration during the earlier leak phase. The severity of the problem depends on to the quantity of fluid supplied in the initial phase, the damage that may have been sustained by the kidneys, and the promptness with which diuretics are administered to help the patient discharge the accumulated fluids quickly. A recent study of 59 acute episodes occurring in 37 hospitalized SCLS patients concluded that high-volume fluid therapy was independently associated with poorer clinical outcomes, and that the main complications of SCLS episodes were recovery-phase pulmonary edema (24%), cardiac arrhythmia (24%), compartment syndrome (20%), and acquired infections (19%).

The prevention of episodes of SCLS has involved two approaches. The first has long been identified with the Mayo Clinic, and it recommended treatment with beta agonists such as terbutaline, phosphodiesterase-inhibitor theophylline, and leukotriene-receptor antagonists montelukast sodium.

The rationale for use of these drugs was their ability to increase intracellular cyclic AMP (adenosine monophosphate) levels, which might counteract inflammatory signaling pathways that induce endothelial permeability. It was the standard of care until the early 2000s, but was sidelined afterwards because patients frequently experienced renewed episodes of SCLS, and because these drugs were poorly tolerated due to their unpleasant side effects.

The second, more recent approach pioneered in France during the last decade (early 2000s) involves monthly intravenous infusions of immunoglobulins (IVIG), with an initial dose of 2 gr/kg/month of body weight, which has proven very successful as per abundant case-report evidence from around the world.

IVIG has long been used for the treatment of autoimmune and MGUS-associated syndromes, because of its potential immunomodulatory and anticytokine properties. The precise mechanism of action of IVIG in patients with SCLS is unknown, but it is likely that it neutralizes their proinflammatory cytokines that provoke endothelial dysfunction. A recent review of clinical experience with 69 mostly European SCLS patients found that preventive treatment with IVIG was the strongest factor associated with their survival, such that an IVIG therapy should be the first-line preventive agent for SCLS patients. According to a recent NIH survey of patient experience, IVIG prophylaxis is associated with a dramatic reduction in the occurrence of SCLS episodes in most patients, with minimal side effects, such that it may be considered as frontline therapy for those with a clear-cut diagnosis of SCLS and a history of recurrent episodes.

Treatment is decompression of the quadrilateral space, with supportive therapy in recalcitrant cases.

Taravana is a disease often found among Polynesian island natives who habitually dive deep without breathing apparatus many times in close succession, usually for food or pearls. These free-divers may make 40 to 60 dives a day, each of 30 or 40 metres (100 to 140 feet).

Taravana seems to be decompression sickness. The usual symptoms are vertigo, nausea, lethargy, paralysis and death. The word "taravana" is Tuamotu Polynesian for "to fall crazily".

Taravana is also used to describe someone who is "crazy because of the sea".

Blocking agents of the adrenoceptors alpha 1/alpha 2 are typically used to treat the effects of the vasoconstriction associated with vascular claudication. Cilostazol (trade name: Pletal) is FDA approved for intermittent claudication. It is contraindicated in patients with heart failure, and improvement of symptoms may not be evident for two to three weeks.

Neurogenic claudication can be treated surgically with spinal decompression.

It usually resolves with conservative therapy stopping oral ingestions, i.e. nil per os and a nasogastric tube, but may require colonoscopic decompression which is successful in 70% of the cases. A study published in the "New England Journal of Medicine" showed that neostigmine is a potent pharmacological way of decompressing the colon. According to the American Society for Gastrointestinal Endoscopy (ASGE), it should be considered prior to colonoscopic decompression. The use of neostigmine is not without risk since it can induce bradyarrhythmia and bronchospasms. Therefore, atropine should be within immediate reach when this therapy is used.