Caisson disease

A caisson disease occurs when the pressure decreases rapidly (for example, when you ascend from a depth, leave the caisson or altitude chamber, or climb to a height).

At the same time, the gas, previously dissolved in blood or tissues, forms gas bubbles in the blood vessels. Typical symptoms include pain and / or neurologic disorders. Severe cases can be fatal. The diagnosis is based on clinical data. The main treatment for caisson disease is recompression. Observance of safety rules by a diver is vital for the prevention of caisson disease.

Henry's law states that the solubility of gas in a liquid is directly proportional to the pressure exerted on the gas and liquid. Thus, the amount of inert gases (eg, nitrogen, helium) in the blood and tissues increases at a higher pressure. During ascent, when the surrounding pressure decreases, gas bubbles may form. Free gas bubbles can occur in any tissue and cause local symptoms, or they can get with blood flow to distant organs. Vesicles cause symptoms by blocking the vessel, tearing or squeezing the tissue, or activating the coagulation and inflammatory cascades. Because N readily dissolves in fat, tissues with a high lipid content (eg, CNS) are particularly sensitive to rapid pressure loss.

A caisson disease occurs from about 2 to 4 cases per 10,000 dives. Risk factors include immersion in cold water, stress, fatigue, bronchial asthma, dehydration, obesity, age, physical activity, diving, fast ascents and long and / or deep water dives. Since excess N remains dissolved in the body tissues for at least 12 hours after immersion, repeated immersion on the same day requires the use of special techniques for determining adequate decompression, and the development of decompression sickness is most likely.

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Symptoms of caisson disease

Severe symptoms may appear within minutes after ascent, but in most patients the symptoms develop gradually, sometimes a prodromal period with malaise, fatigue, anorexia and headache is observed. Symptoms begin within an hour after leaving the water in approximately 50% of patients, and in 90% of cases after 6 hours. Less common symptoms may appear 24-48 hours after surfacing, especially in case of ascent to a height after scuba diving.

Decompression type I disease usually causes aggravated pain in the joints (especially in the elbow and shoulder), back and muscles. The pain intensifies during movement, it is described as "deep" and "drilling". Other symptoms include lymphadenopathy, patchiness of the skin, itching and rash.

Decompression type II disease is often manifested by paresis, numbness and tingling, neurapraxia, difficulty urinating, and impaired bladder function or intestinal function. There may be headache and fatigue, but they are nonspecific. Dizziness, tinnitus and hearing loss are possible if the inner ear is damaged. Severe symptoms include cramps, slurred speech, loss of vision, stunning and to whom. A fatal outcome is possible. Choking (respiratory decompression sickness) is a rare, but formidable manifestation; it includes shortness of breath, chest pain and cough. Massive embolism of the pulmonary vasculature can cause rapid development of vascular collapse and death.

Dysbacterial osteonecrosis is a late manifestation of decompression sickness. This is an insidious form of aseptic bone necrosis caused by prolonged or often repeated stay in rooms with high blood pressure (usually people working in compressed air and professional deepwater divers are much more likely than amateurs). Degeneration of the articular surfaces of the shoulder and hip joints can cause chronic pain and severe disability.

Classification of caisson disease

Usually distinguish 2 types of caisson disease. Type I, involving the muscles, skin and lymphatic system, is mild and, as a rule, is not life-threatening. Type II is much more serious, sometimes life-threatening and damaging various organ systems. The spinal cord is particularly vulnerable; other injured areas include the brain, respiratory (eg, pulmonary emboli), and the circulatory system (eg, heart failure, cardiogenic shock). "Lump" means local pain in the joints and muscles as a result of caisson disease, the term is often used as a synonym for any component of this disease.

Differential diagnosis of gas embolism and caisson disease

Features	Gas embolism	Caisson disease
Symptoms	Characteristic: the unconscious state, often with convulsions (any unconscious underwater should presume a gas embolism, it is necessary to perform the recompression as soon as possible). Less characteristic: more moderate cerebral manifestations, emphysema of the mediastinum or subcutaneous emphysema, pneumothorax	Extremely variable: aches (pain, most often inside or near the joint), neurological manifestations of virtually any type or degree, asphyxiation (respiratory distress syndrome with the development of vascular collapse is an extremely dangerous situation); occur both individually and with other symptoms
Onset of disease	Sudden onset during or soon after surfacing	Gradual or sudden onset after ascent or after 24 hours after immersion * to a depth> 10 m (> 33 ft) or stay in a medium with a pressure> 2 atm
Possible reasons	Usually: breathing or airway obstruction during ascent, even from a depth of several feet, or decompression at elevated pressure	Usually: scuba diving or media with increased pressure outside the non-stop limit or non-compliance with the decompression stop scheme. Rarely: scuba diving or environment with increased pressure within a non-stop limit or with a decompression stop scheme; medium with low pressure (for example, depressurization of the aircraft cabin at altitude)
Mechanism	Often: overdischarge of the lungs, causing free gas into the pulmonary vessels, followed by embolism of the brain vessels. Rarely: pulmonary, cardiac or systemic obstruction of blood circulation by free gas from any source	Formation of blisters from excess dissolved in the blood or tissues of gas with a decrease in external pressure
Urgent care	Extreme measures are extremely important (for example, to provide airway patency, hemostasis, cardiovascular resuscitation). Rapid transportation of the victim to the nearest recompression chamber. Inhalation 100% O 2 in a horizontal position through a tight fitting mask. Abundant drink if the patient is conscious, if not - intravenous infusions	Same

* - Often when re-immersed.

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Diagnosis of caisson disease

The diagnosis is based on clinical data. CT and MRI can reflect changes in the brain or spinal cord, but they are of low sensitivity, and treatment should usually be started on the basis of a clinical picture. Sometimes arterial gas embolism also occurs.

With dysbaric osteonecrosis, direct radiography can show degenerative joint changes that can not be distinguished from changes caused by other joint diseases; MRI usually resolves these diagnostic difficulties.

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Treatment of caisson disease

Approximately 80% of patients completely recover.

Initially, 100% of the O is produced by a large flow, washing out N, increasing the gradient between the lungs and blood vessels and thus accelerating the reabsorption of embolic bubbles.

Recompression therapy is indicated to all patients, perhaps, in addition to those whose symptoms are limited by itching, spotting of the skin and fatigue; they should be observed in case of deterioration. Other patients are transported to the nearest institution with recompression equipment. Since the start time of treatment is the main determining factor in the outcome of the disease, transportation can not be postponed, even if the situation does not seem threatening or for the sake of non-vital procedures. If evacuation is required by air, a low altitude is preferred: less than 609 m (<2000 ft) in a leaking air vehicle, or the creation of sea level pressure in the cabin. On commercial flights, cabin pressure is usually equal to a pressure of 2438 m (8000 ft), which can worsen a patient's condition. Flight by commercial flight shortly after scuba diving can provoke the manifestation of symptoms.

Prevention of caisson disease

The significant formation of gas bubbles in most cases can be avoided by limiting the depth and duration of immersion to a range that does not require decompression stops during ascent (the so-called non-stop mode) or floating with decompression stops in accordance with the recommendations of published guidelines (for example, decompression table in the US Navy Diving Guide). Now, many divers use a portable computer when submerged, which continuously monitors depth, depth time and calculates decompression scheme. In addition, many submariners make a decompression stop for a few minutes at about 4.6 m (15 ft) from the surface.

In about 50% of cases, decompression sickness develops despite the correctly calculated permissible non-stop regime, and widespread adoption of computers does not reduce its frequency. The reason may be that the published tables and computer programs do not take into account the entire variability of risk factors among divers, or not all divers quite adhere to the recommendations.