Caisson disease is a complex of symptoms formed by the formation of gas bubbles in blood vessels and tissues against the background of a rapid decrease in atmospheric pressure. Pathology can be acute or chronic. It is manifested by pain in the joints, muscles, Meniere’s syndrome, dyspepsia, signs of central nervous system damage, acute pulmonary and cardiovascular insufficiency. When making a diagnosis, anamnestic data and the results of an objective examination are used, radiography, ultrasound, MRI, CT are used to assess the condition of various organs. Treatment – recompression followed by slow decompression, symptomatic drug therapy.
T70.3 Caisson disease [decompression sickness]
Caisson disease (decompression sickness, DCS) is a complex of changes that develop during the transition from high atmospheric pressure to normal, less often from normal to low. The pathology got its name from the word “caisson”, denoting a chamber created in the 40s of the XIX century and intended for work under water or in conditions of water-saturated soils. DCS is considered an occupational disease of submariners and specialists working in the conditions of caisson chambers, in some cases it is diagnosed in pilots. In recent years, due to the widespread use of diving, it has been detected in other groups of the population. According to statistics, the incidence of the disease is 2-4 cases per 10,000 dives.
The immediate cause of the caisson disease is a rapid decrease in atmospheric pressure when the depth of immersion in water changes, less often when the aircraft rises to a significant height. The faster the atmospheric pressure changes, the greater the risk of this pathology. Factors that increase the likelihood of developing the disease are considered:
- Aging of the body. As we age, the condition of all organs deteriorates. This causes a decrease in the compensatory capacity of the lungs and heart during the period of pressure changes.
- Hypothermia. It is accompanied by a slowdown in blood flow in peripheral vessels. Blood from distant parts of the body enters the pulmonary vessels more slowly, gas is less released from the blood physiologically.
- Dehydration. The viscosity of blood in this condition increases, which provokes a slowdown in blood circulation. When the external pressure changes, stasis occurs at the periphery, which is aggravated by the formation of bubbles blocking the lumen of the vessels.
- Physical activity. It potentiates a violation of the uniformity of blood flow, as a result of which conditions are created for the intensive dissolution of gases in the blood, followed by the appearance of “quiet” bubbles. A characteristic feature is the deposition of microbubbles in the joints and an increase in the likelihood of pathology during the following dives.
- Lipidemia, overweight. Fats have increased hydrophobicity, therefore, with their high content, bubbles form more actively. Adipose tissue cells intensively dissolve the inert gases that make up the respiratory mixtures.
- Hypercapnia. Develops with a low quality of the respiratory mixture or attempts to “save” it by holding your breath. An increase in the amount of CO2 provokes a shift of the acid-base state to the acidic side. Because of this, more inert gases are dissolved in the blood.
- Alcoholic intoxication. When taking alcohol, dehydration occurs. In addition, alcohol molecules cause the connection of small bubbles into larger ones and become centers around which large bubbles form, clogging blood vessels.
At elevated pressure, the gases of the respiratory mixture, due to diffusion, dissolve in significant quantities in the blood of the capillaries of the lung tissue. When the pressure decreases, the opposite phenomenon is observed – gases “exit” from the liquid, forming bubbles. The faster the pressure changes, the more intense the reverse diffusion process becomes. With a rapid rise, the patient’s blood “boils”, the gases released form many large bubbles that can block vessels of different calibers and damage various organs.
Large bubbles connect with small ones, platelets “stick” to the formed bubbles, blood clots form, attaching to the walls of small vessels and blocking their lumen. Some of the blood clots come off with fragments of the vascular wall, migrate through the bloodstream and block other vessels. With the accumulation of a large number of such formations, a gas embolism develops. With significant damage to the walls, the integrity of the arterioles is violated, hemorrhages occur.
The appearance of bubbles and the formation of their complexes with platelets triggers a cascade of biochemical reactions, as a result of which various mediators are released into the blood, intravascular coagulation occurs. Vesicles also form outside the vascular bed, in articular cavities and soft tissue structures. They increase in volume and squeeze the nerve endings, provoking pain. Pressure on soft tissue formations causes their damage with the formation of necrosis foci in muscles, tendons and internal organs.
Due to the possibility of damage to various organs, significant differences in severity and prognosis, the most rational from a practical point of view is the systematization of the types of caisson disease based on the prevailing manifestations. The clinical classification of M. I. Yakobson is a detailed version of the allocation of degrees of the disease, taking into account the symptoms. There are four forms of pathology:
- Easy. Arthralgia, myalgia, and neuralgia predominate due to compression of nerve endings by gas bubbles. A number of patients show livedo, itching, greasiness of the skin caused by blockage of small superficial veins, ducts of sebaceous and sweat glands.
- Moderate severity. Disorders of the vestibular apparatus, eyes and gastrointestinal tract, resulting from embolism of the capillaries and arterioles of the labyrinth, accumulation of gas bubbles in the vessels of the mesentery and intestines, transient spasm of the retinal arteries, prevail.
- Heavy. It is manifested by rapidly increasing symptoms of spinal cord damage, usually at the level of the mid-thoracic segments, which is due to the tendency of myelin to absorb nitrogen and weak vascularization of the mid-thoracic region, which is why actively forming vesicles do not migrate with blood, but squeeze the nerve tissue. Signs of brain involvement are detected much less frequently. Cardiac and respiratory disorders are possible.
- Lethal. It occurs with the total cessation of blood circulation in the lungs or medulla oblongata, the development of acute heart failure. It is provoked by the formation of a large number of large bubbles, simultaneously blocking many vessels.
To assess the threat to the patient’s life and determine the optimal treatment tactics in traumatology and orthopedics, a simplified classification is also used, including two types of acute DCS. The first type is characterized by damage to peripheral structures (skin, musculoskeletal system). The second is accompanied by changes on the part of the nervous, respiratory, cardiovascular, digestive systems, in the absence of treatment, a fatal outcome is possible. In addition, there is a chronic variant of caisson disease, which can develop in the presence of acute pathology in the anamnesis or without previous acute events; it is diagnosed in people who have worked for a long time in caisson conditions.
In the case of a severe lesion, manifestations may occur already in the first minutes after surfacing, but more often the clinical picture of decompression sickness is formed gradually. In half of the patients, symptoms are detected within an hour. After 6 hours, signs of pathology are detected in 90% of patients. Delayed onset of symptoms is rarely observed (for 1-2 days). With a mild form, there are pains in the joints, bone structures, muscle tissue, and back area. Pain syndrome is usually more pronounced in the shoulder and elbow joints. Patients describe the sensations as “drilling”, “deep”, intensifying with movements. There is often a rash, itching of the skin, increased greasiness, marbling of the color of the skin. Possible enlargement of lymph nodes.
With moderate caisson disease, Meniere’s syndrome is observed, due to damage to the balance organ and including dizziness, headache, pallor, sweating, nausea, vomiting. Disorders of the gastrointestinal tract are manifested by pain, vomiting and diarrhea. Retinal vascular spasm is accompanied by the appearance of photomorphopsies, “flies” and “fog” in front of the eyes. The severe form is characterized by lower spastic paraplegia, pelvic disorders, impaired sensitivity in the lower half of the body according to the conductor type. Sometimes there are hemiparesis or hemiplegia, headaches, speech disorders, psychotic disorders of a transient nature.
Cardiovascular and respiratory symptoms are found in severe form and reach the greatest severity in the lethal variant of the disease. Weakness, pallor, shortness of breath, intense chest pain, cough, falling blood pressure are determined. With the progression of symptoms, pulmonary edema develops, breathing becomes frequent, shallow, the pulse slows down, the skin becomes bluish or pale gray. Lung and myocardial infarctions are possible. The lethal form is accompanied by acute heart failure, asphyxia due to blockage of pulmonary circulation or violation of the regulation of respiration by the medulla oblongata.
The most common manifestation of chronic decompression sickness is deforming arthrosis caused by the repeated impact of small bubbles on bone and joint structures. The opinions of scientists regarding cardiac myodegeneration, early atherosclerosis and frequent diseases of the middle ear in people engaged in caisson work differ. Some experts consider these pathologies to be the result of repeated subclinical DCS, others – the result of the influence of other factors that arise when staying at great depth.
The type and severity of complications are determined by the form of the disease, the timeliness and adequacy of therapeutic measures. The most common consequences of acute decompression sickness are considered to be chronic Meniere’s syndrome and aeropathic myelosis. Other possible complications are pneumonia, myocarditis, endocarditis, cardiodystrophy, cardiosclerosis, paresis, paralysis, sensitivity disorders, aseptic osteonecrosis.
The acute form of caisson disease is diagnosed based on the patient’s complaints, anamnestic data and the results of an external examination. Radiographs may show gas bubbles in joints, muscle tissue, fascia, tendon sheaths. To determine the state of the central nervous system, tomographic examinations of the spinal cord and brain are prescribed. Confirmation of the diagnosis is the improvement of the patient’s condition during recompression. The examination program for the development of complications is determined by the nature of the alleged pathology, may include ECG, echocardiography, radiography, ultrasound, MRI and CT of various organs.
The therapy of the disease, depending on the form and severity of the symptoms of complications, is carried out by resuscitators, traumatologists, occupational pathologists and other specialists. With mild skin, muscle and joint manifestations, observation in dynamics is permissible. In other cases, urgent recompression in a pressure chamber is indicated. Initially, the pressure is increased to the values corresponding to the depth of immersion of the patient. If the victim is in a serious condition, the pressure is applied above the initial one. The minimum duration of recompression is 30 minutes, while the symptoms persist, the procedure is continued until the patient’s condition normalizes. Then a slow decompression is carried out, reducing the pressure by 0.1 atmosphere every 10 minutes. After reducing the pressure to 2 atmospheres, oxygen inhalation is used to accelerate the nitrogen removal process. If signs of DCS appear after normalization of pressure, repeated recompression is performed.
According to the indications, symptomatic therapy is prescribed. Infusions of glucose solution, plasma, salt solutions are carried out. Pharmaceutical preparations are used to normalize and stimulate the activity of the cardiovascular system. If necessary, vasodilators are included in the treatment plan. In case of intense pain syndrome, non-narcotic analgesics are used. Narcotic pharmaceuticals are not indicated because of the possible depressing effect on the respiratory center. For myalgia and arthralgia, local warming and painkillers are recommended. After leaving the pressure chamber, physiotherapy procedures are carried out: sollux, diathermy, therapeutic baths.
Prognosis and prevention
The outcome of DCS is determined by the severity of the lesion and the time of the onset of recompression. 80% of patients have a complete recovery. Fatal outcomes are observed quite rarely, usually with an emergency ascent or lack of specialized care. Prevention of caisson disease includes the use of high-quality equipment for diving and professional work at depth, strict compliance with the rules of ascent, taking into account the data of specially developed tables, regular medical examinations, exclusion of factors that increase the risk of DCS. Preventive measures also involve establishing a sufficient time interval between the first and subsequent dives or flights by air transport, limiting the time spent in high-pressure conditions for divers and caisson workers.
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