Caisson's disease

Decompression sickness occurs when there is a rapid decrease in pressure (for example, when surfacing from depth, exiting a caisson or pressure chamber, or ascending to altitude).

In this case, gas previously dissolved in the blood or tissues forms gas bubbles in the blood vessels. Characteristic symptoms include pain and/or neurological impairment. Severe cases can be fatal. Diagnosis is based on clinical findings. The main treatment for decompression sickness is recompression. Compliance with safety rules by the diver is vital to prevent decompression sickness.

Henry's Law states that the solubility of a gas in a liquid is directly proportional to the pressure exerted on the gas and liquid. Thus, the amount of inert gases (e.g., nitrogen, helium) in the blood and tissues increases at higher pressures. During ascent, as the surrounding pressure decreases, gas bubbles may form. Free gas bubbles may form in any tissue and cause local symptoms, or they may travel via the bloodstream to distant organs. Bubbles cause symptoms by blocking a vessel, rupturing or compressing tissue, or activating the coagulation and inflammatory cascades. Because N is readily soluble in fat, tissues with a high lipid content (e.g., the central nervous system) are particularly sensitive to rapid pressure reduction.

The incidence of decompression sickness is approximately 2 to 4 cases per 10,000 dives. Risk factors include cold water diving, stress, fatigue, asthma, dehydration, obesity, age, physical exertion, flying after diving, rapid ascents, and long and/or deep dives. Since excess N remains dissolved in body tissues for at least 12 hours after a dive, repeated dives on the same day require special techniques to determine adequate decompression, and decompression sickness is more likely to develop.

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Symptoms of decompression sickness

Severe symptoms may appear within minutes of surfacing, but most patients develop symptoms gradually, sometimes with a prodromal period of malaise, fatigue, anorexia, and headache. Symptoms begin within an hour of surfacing in approximately 50% of patients, and after 6 hours in 90%. Rarely, symptoms may appear 24–48 hours after surfacing, especially if the patient ascends to altitude after diving.

Type I decompression sickness typically causes increasing pain in the joints (especially the elbows and shoulders), back, and muscles. The pain worsens with movement and is described as “deep” and “boring.” Other symptoms include lymphadenopathy, mottling of the skin, itching, and rash.

Type II decompression sickness often presents with paresis, numbness and tingling, neurapraxia, difficulty urinating, and bladder or bowel dysfunction. Headache and fatigue may be present but are nonspecific. Dizziness, tinnitus, and hearing loss may occur if the inner ear is affected. Severe symptoms include seizures, slurred speech, visual loss, confusion, and coma. Death may occur. Asphyxiation (respiratory decompression sickness) is a rare but serious manifestation; it includes shortness of breath, chest pain, and cough. Massive pulmonary embolism may cause rapid vascular collapse and death.

Dysbaric osteonecrosis is a late manifestation of decompression sickness. It is an insidious form of aseptic bone necrosis caused by prolonged or repeated exposure to high-pressure environments (usually in people working in compressed air and in professional deep-sea divers much more often than in amateurs). Degeneration of the articular surfaces of the shoulder and hip joints can cause chronic pain and severe disability.

Classification of decompression sickness

There are generally two types of decompression sickness. Type I, involving muscles, skin, and the lymphatic system, is mild and usually not life-threatening. Type II is much more severe, sometimes life-threatening, and affects multiple organ systems. The spinal cord is particularly vulnerable; other areas affected include the brain, respiratory (eg, pulmonary emboli), and circulatory systems (eg, heart failure, cardiogenic shock). "Aches" refers to the localized joint and muscle pain resulting from decompression sickness, and is often used synonymously for any component of the disease.

Differential diagnosis of gas embolism and decompression sickness

Peculiarities	Gas embolism	Caisson disease
Symptoms	Characteristic: unconsciousness, often with convulsions (any unconscious diver should be considered to have gas embolism, and recompression should be performed as quickly as possible). Less characteristic: milder cerebral manifestations, mediastinal or subcutaneous emphysema, pneumothorax	Extremely variable: aches (pain, most often inside or around a joint), neurological manifestations of almost any type or degree, suffocation (respiratory distress syndrome with the development of vascular collapse - an extremely dangerous situation); occur both separately and with other symptoms
Onset of the disease	Sudden onset during or shortly after surfacing	Gradual or sudden onset after surfacing or 24 hours after a dive* to a depth >10 m (>33 ft) or exposure to a pressure >2 atm
Possible reasons	Common: Breath holding or airway obstruction during ascent, even from depths of several feet, or decompression at elevated pressure	Typical: Scuba diving or pressurized environments beyond the no-stop limit or failure to follow decompression stop schedule. Rare: Scuba diving or a pressurized environment within the no-stop limit or with a decompression stop schedule; a low-pressure environment (e.g., cabin depressurization at altitude)
Mechanism	Common: Overinflation of the lungs causing free gas to enter the pulmonary vessels, with subsequent embolism of the cerebral vessels. Rare: Pulmonary, cardiac or systemic obstruction of the circulation by free gas from any source.	Formation of bubbles from excess gas dissolved in blood or tissues when external pressure decreases
Urgent Care	Emergency measures (e.g., maintaining airway patency, hemostasis, cardiovascular resuscitation) are essential. Rapid transportation of the victim to the nearest recompression chamber. Inhalation of 100% O2 in a horizontal position through a tightly fitting mask. Plenty of fluids if the patient is conscious, if not - intravenous infusions	The same

*- Often with repeated diving.

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Diagnosis of decompression sickness

Diagnosis is based on clinical findings. CT and MRI may show changes in the brain or spinal cord, but they have low sensitivity and treatment should usually be initiated based on the clinical picture. Sometimes arterial gas embolism occurs in the same way.

In dysbaric osteonecrosis, direct radiography may show degenerative joint changes that cannot be distinguished from those caused by other joint diseases; MRI can usually resolve these diagnostic difficulties.

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Treatment of decompression sickness

Approximately 80% of patients make a full recovery.

Initially, 100% O is given at a high flow, washing out N, increasing the pressure gradient between the lungs and vessels and, thus, accelerating the reabsorption of embolic bubbles.

Recompression therapy is indicated for all patients, except perhaps those whose symptoms are limited to itching, mottling, and fatigue; they should be observed for deterioration. Other patients are transported to the nearest facility with recompression equipment. Because the time to initiation of treatment is the major determinant of outcome, transport should not be delayed even if the situation appears nonthreatening or for nonlife-saving procedures. If air evacuation is required, low altitude is preferred: less than 2,000 ft (609 m) in unpressurized aircraft, or a cabin pressurized to sea level. Commercial flights typically have cabin pressures equivalent to 8,000 ft (2,438 m), which may worsen the patient's condition. Flying on a commercial flight shortly after scuba diving may precipitate symptoms.

Prevention of decompression sickness

Significant bubble formation can be avoided in most cases by limiting the depth and duration of the dive to a range that does not require decompression stops during the ascent (called a "non-stop" dive), or by ascending with decompression stops as recommended in published guidelines (e.g., the decompression table in the U.S. Navy Diving Manual). Many divers now use a portable dive computer that continuously monitors depth, time at depth, and calculates a decompression schedule. In addition, many divers make a decompression stop of several minutes at approximately 4.6 m (15 ft) below the surface.

In approximately 50% of cases, decompression sickness develops despite a correctly calculated permissible "non-stop" regime, and the widespread introduction of computers does not reduce its incidence. The reason may be that the published tables and computer programs do not take into account all the variability of risk factors among divers, or not all divers follow the recommendations accurately enough.