If the diver has not been exposed to excessive depth and decompression and presents as DON, there may be a predisposition for the condition. Diving should be restricted to shallow depths. Divers who have suffered from DON are at increased risk of future fracture of a juxta-articular lesion during a dive, and may face complications with future joint replacements. Because of the young age of the population normally affected, little data is available regarding joint replacement complications.

There is the potential for worsening of DON for any diving where there might be a need for decompression, experimental or helium diving. Physically stressful diving should probably be restricted, both in sport diving and work diving due to the possibility of unnecessary stress to the joint. Any diving should be less than 40 feet/12 meters. These risks are affected by the degree of disability and by the type of lesion (juxta-articular or shaft).

Treatment varies with the type of vascular disease; in the case of renal artery disease, information from a meta-analysis indicated that balloon angioplasty results in improvement of diastolic blood pressure and a reduction in antihypertensive drug requirements. In the case of peripheral artery disease, preventing complications is important; without treatment, sores or gangrene (tissue death) may occur. Among the treatments are:

- Quitting smoking

- Lowering cholesterol

- Lower blood pressure

- Lower blood glucose

- Physical activity

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.

A very large range of medical conditions can cause circulatory collapse. These include, but are not limited to:

- Surgery, particularly on patients who have lost blood.

- Blood clots, including the use of some platelet-activating factor drugs in some animals and humans

- Dengue Fever

- Severe dehydration

- Shock (including, among other types, many cases of cardiogenic shock- e.g., after a myocardial infarction or during heart failure; distributive shock, hypovolemic shock, resulting from large blood loss; and severe cases of septic shock)

- Heart Disease (myocardial infarction- heart attack; acute or chronic congestive or other heart failure, ruptured or dissecting aneurysms; large, especially hemorrhagic, stroke; some untreated congenital heart defects; failed heart transplant)

- Superior mesenteric artery syndrome

- Drugs that affect blood pressure

- Drinking seawater

- As a complication of dialysis

- Intoxicative inhalants

The effects of a circulatory collapse vary based on the type of collapse it is. Peripheral collapses usually involve abnormally low blood pressure and result in collapsed arteries and/or veins, leading to oxygen deprivation to tissues, organs, and limbs.

Acute collapse can result from heart failure causing the primary vessels of the heart to collapse, perhaps combined with cardiac arrest.

Prevention of pulmonary contusion is similar to that of other chest trauma. Airbags in combination with seat belts can protect vehicle occupants by preventing the chest from striking the interior of the vehicle during a collision, and by distributing forces involved in the crash more evenly across the body. However, in rare cases, an airbag causes pulmonary contusion in a person who is not properly positioned when it deploys. Child restraints such as carseats protect children in vehicle collisions from pulmonary contusion. Equipment exists for use in some sports to prevent chest and lung injury; for example, in softball the catcher is equipped with a chest protector. Athletes who do not wear such equipment, such as basketball players, can be trained to protect their chests from impacts. Protective garments can also prevent pulmonary contusion in explosions. Although traditional body armor made from rigid plates or other heavy materials protects from projectiles generated by a blast, it does not protect against pulmonary contusion, because it does not prevent the blast's shock wave from being transferred to the lung. Special body armor has been designed for military personnel at high risk for blast injuries; these garments can prevent a shock wave from being propagated across the chest wall to the lung, and thus protect wearers from blast lung injuries. These garments alternate layers of materials with high and low acoustic impedance (the product of a material's density and a wave's velocity through it) in order to "decouple" the blast wave, preventing its propagation into the tissues.

Collapsed veins are a common result of chronic use of intravenous injections. They are particularly common where injecting conditions are less than ideal, such as in the context of drug abuse.

Veins may become temporarily blocked if the internal lining of the vein swells in response to repeated injury or irritation. This may be caused by the needle, the substance injected, or donating plasma. Once the swelling subsides, the circulation will often become re-established.

Permanent vein collapse occurs as a consequence of:

- Long-term injecting

- Repeated injections, especially with blunt needles

- Poor technique

- Injection of substances which irritate the veins; in particular, injection of liquid methadone intended for oral use.

Smaller veins may collapse as a consequence of too much suction being used when pulling back against the plunger of the syringe to check that the needle is in the vein. This will pull the sides of the vein together and, especially if they are inflamed, they may stick together causing the vein to block. Removing the needle too quickly after injecting can have a similar effect.

Collapsed veins may never recover. Many smaller veins are created by the body to circulate the blood, but they are not adequate for injections or IVs.

No treatment is known to speed the healing of a pulmonary contusion; the main care is supportive. Attempts are made to discover injuries accompanying the contusion, to prevent additional injury, and to provide supportive care while waiting for the contusion to heal. Monitoring, including keeping track of fluid balance, respiratory function, and oxygen saturation using pulse oximetry is also required as the patient's condition may progressively worsen. Monitoring for complications such as pneumonia and acute respiratory distress syndrome is of critical importance. Treatment aims to prevent respiratory failure and to ensure adequate blood oxygenation. Supplemental oxygen can be given and it may be warmed and humidified. When the contusion does not respond to other treatments, extracorporeal membranous oxygenation may be used, pumping blood from the body into a machine that oxygenates it and removes carbon dioxide prior to pumping it back in.

Vascular disease is a class of diseases of the blood vessels – the arteries and veins of the circulatory system of the body. It is a subgroup of cardiovascular disease. Disorders in this vast network of blood vessels, can cause a range of health problems which can be severe or prove fatal.

Treatment depends substantially of the type of ICH. Rapid CT scan and other diagnostic measures are used to determine proper treatment, which may include both medication and surgery.

- Tracheal intubation is indicated in people with decreased level of consciousness or other risk of airway obstruction.

- IV fluids are given to maintain fluid balance, using isotonic rather than hypotonic fluids.

First described by Preiser in 1910 in 5 patients, all with previous history of wrist trauma, and scaphoid fractures in 3 of them.

Surgery is required if the hematoma is greater than , if there is a structural vascular lesion or lobar hemorrhage in a young patient.

- A catheter may be passed into the brain vasculature to close off or dilate blood vessels, avoiding invasive surgical procedures.

- Aspiration by stereotactic surgery or endoscopic drainage may be used in basal ganglia hemorrhages, although successful reports are limited.

The prevalence of Mönckeberg's arteriosclerosis increases with age and is more frequent in diabetes mellitus, chronic kidney disease, systemic lupus erythematosus, chronic inflammatory conditions, hypervitaminosis D and rare genetic disorders, such as Keutel syndrome. The prevalence of Monckeberg's arteriosclerosis in the general population has been estimated as 1.5; however the validity of this criterion is questionable.

Preiser disease, or (idiopathic) avascular necrosis of the scaphoid, is a rare condition where ischemia and necrosis of the scaphoid bone occurs without previous fracture. It is thought to be caused by repetitive microtrauma or side effects of drugs (e.g., steroids or chemotherapy) in conjunction with existing defective vascular supply to the proximal pole of the scaphoid. MRI coupled with CT and X-ray are the methods of choice for diagnosis.

Preiser's disease is initially treated by immobilising the wrist with a cast. However, in most cases the avascular scaphoid will start to collapse leading to degeneration within the wrist joints. This often requires surgical intervention to prevent the progression of arthris. Two commonly performed procedures are:

1. Proximal row carpectomy (PRC), which involves removing the first row of the carpal bones, i.e. the scaphoid, lunate and triquetrum. The wrist is immobilised in a cast for six weeks after the surgery and then physiotherapy is started.

2. Scaphoid excision and 4-corner fusion, which is a procedure consisting of the removal of the scaphoid and fixation of the remaining wrist bones with a plate (called a "spider plate") or wires in order to provide stability. The plate usually is left inside the patient's wrist, while the wires (usually K-wires) have to be removed in a second surgery. This procedure of partial wrist fusion allows for limited wrist movement, whereas total wrist fusion immobilizes the wrist permanently. Following surgery it can take several months for affected patients to regain strength.

Unfortunately both of these operations are salvage procedures and movements in the wrist will be significantly reduced.

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.

VALI is most common in patients receiving mechanical ventilation for acute lung injury or acute respiratory distress syndrome (ALI/ARDS).

Possible reasons for predisposition to VALI include:

- An injured lung may be at risk for further injury

- Cyclic atelectasis is particularly common in an injured lung

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

Often Mönckeberg's arteriosclerosis is discovered as an incidental finding in an X-ray radiograph, on mammograms, in autopsy, or in association with investigation of some other disease, such as diabetes mellitus or chronic kidney disease. Typically calcification is observed in the arteries of the upper and lower limb although it has been seen in numerous other medium size arteries. In the radial or ulnar arteries it can cause "pipestem" arteries, which present as a bounding pulse at the end of the calcific zone. It may also result in "pulselessness." Epidemiological studies have used the ratio of ankle to brachial blood pressure (ankle brachial pressure index, ABPI or ABI) as an indicator of arterial calcification with ABPI >1.3 to >1.5 being used as a diagnostic criterion depending on the study.

There is ongoing research on the treatment of ARDS by interferon (IFN) beta-1a to aid in preventing leakage of vascular beds. Traumakine (FP-1201-lyo), is a recombinant human IFN beta-1a drug developed by Faron pharmaceuticals, is undergoing international phase-III clinical trials after an open-label, early-phase trial showed a 81% reduction-in-odds of 28-day mortality in ICU patients with ARDS. The drug is known to function by enhancing lung CD73 expression and increasing production of anti-inflammatory adenosine, such that vascular leaking and escalation of inflammation are reduced.

Treatment is directed at correcting the underlying cause. Post-surgical atelectasis is treated by physiotherapy, focusing on deep breathing and encouraging coughing. An incentive spirometer is often used as part of the breathing exercises. Walking is also highly encouraged to improve lung inflation. People with chest deformities or neurologic conditions that cause shallow breathing for long periods may benefit from mechanical devices that assist their breathing. One method is continuous positive airway pressure, which delivers pressurized air or oxygen through a nose or face mask to help ensure that the alveoli do not collapse, even at the end of a breath. This is helpful, as partially inflated alveoli can be expanded more easily than collapsed alveoli. Sometimes additional respiratory support is needed with a mechanical ventilator.

The primary treatment for acute massive atelectasis is correction of the underlying cause. A blockage that cannot be removed by coughing or by suctioning the airways often can be removed by bronchoscopy. Antibiotics are given for an infection. Chronic atelectasis is often treated with antibiotics because infection is almost inevitable. In certain cases, the affected part of the lung may be surgically removed when recurring or chronic infections become disabling or bleeding is significant. If a tumor is blocking the airway, relieving the obstruction by surgery, radiation therapy, chemotherapy, or laser therapy may prevent atelectasis from progressing and recurrent obstructive pneumonia from developing.

A kitten that has difficulty in breathing is very likely also to suffer from colic (which can cause weight loss in the early development of a normal kitten), and a very small daily (or twice daily) dose of liquid paraffin (one or two drops placed on the tongue of the kitten, or 0.1 ml) should help to alleviate this problem. FCKS kittens who do not maintain weight are usually among the group which die, but many of them may simply be unable to feed properly due to colic, becoming increasingly weak and lethargic, and fading due to malnutrition as much as to the thoracic problems.

Colic has many causes, but in a kitten with respiratory difficulty it is possible that a malfunction during the breathing process leads the kitten to swallow air instead of taking it into its lungs. The GI tract fills with air while the lungs do not receive a proper air supply, preventing them from inflating fully. Pressure from the stomach exacerbates the condition. Treating for colic with liquid paraffin seems to shorten recovery time from 4–10 weeks to a matter of days.

It is most commonly caused by:

- Oesophageal rupture, for example in Boerhaave syndrome

- Asthma or other conditions leading to alveolar rupture

- Bowel rupture, where air in the abdominal cavity tracts up into the chest.

It has also been associated with:

- "Mycoplasma pneumoniae" pneumonia

- obesity

It can be induced to assist thoracoscopic surgery. It can be caused by a pulmonary barotrauma resulting when a person moves to or from a higher pressure environment, such as when a SCUBA diver, a free-diver or an airplane passenger ascends or descends.

In rare cases, pneumomediastinum may also arise as a result of blunt chest trauma (e.g. car accidents, fights, over pressure of breathing apparatus), while still evolving in the same fashion as the spontaneous form.

Pneumomediastinum is most commonly seen in otherwise healthy young male patients and may not be prefaced by a relevant medical history of similar ailments.

If the symptoms are severe enough, treatment may be needed. These range from medical management over mechanical ventilation (both continuous positive airway pressure (CPAP), or bi-level positive airway pressure (BiPAP) to tracheal stenting and surgery.

Surgical techniques include aortopexy, tracheopexy, tracheobronchoplasty, and tracheostomy. The role of the nebulised recombinant human deoxyribonuclease (rhDNase) remains inconclusive.

Treatment depends on the underlying cause. Treatments include iced saline, and topical vasoconstrictors such as adrenalin or vasopressin. Selective bronchial intubation can be used to collapse the lung that is bleeding. Also, endobronchial tamponade can be used. Laser photocoagulation can be used to stop bleeding during bronchoscopy. Angiography of bronchial arteries can be performed to locate the bleeding, and it can often be embolized. Surgical option is usually the last resort, and can involve, removal of a lung lobe or removal of the entire lung. Non–small-cell lung cancer can also be treated with erlotinib or gefitinib. Cough suppressants can increase the risk of choking.

The course of treatment and the success rate is dependent on the type of TMA. Some patients with atypical HUS and TTP have responded to plasma infusions or exchanges, a procedure which replaces proteins necessary for the complement cascade that the patient does not have; however, this is not a permanent solution or treatment, especially for patients with congenital predispositions.