Orthopedics - Oleksa A.P. 2006

Occupational diseases of the musculoskeletal system
Bone and joint changes in caisson disease

Caisson disease is quite well studied. It occurs in emergency situations involving the forced violation of safety regulations and when a person transitions too rapidly from conditions of high pressure to normal atmospheric pressure. Under METABOLISM/18.html">The Influence of high pressure, body Tissues become saturated with gases—primarily nitrogen, in accordance with the law of partial pressures. With a gradual reduction in pressure (decompression), the remaining gases dissolved in the body are progressively eliminated from the tissues into the Blood via diffusion, and subsequently exhaled from the blood through the Lungs.

In cases of rapid decompression, the lungs are unable to release nitrogen quickly enough; consequently, free gas bubbles form in the blood and various body tissues. “The blood boils,” and these bubbles cause gas embolisms, infarctions, ruptures of Blood Vessels and various tissues, leading to scattered aseptic necroses. The higher the pressure and the shorter the transition to normal atmospheric pressure, the more severe and potentially life-threatening the resulting injuries are.

It has been established that fats dissolve 5 to 6 times more nitrogen than an equivalent volume of Blood Plasma or other bodily fluids. Consequently, adipose tissue and the Bone Marrow of tubular bones are the most severely affected.

Free gas also accumulates in the joint cavities, periarticular tissues, and beneath the fascia, giving rise to the characteristic pain of caisson disease. This pain begins one to two hours after transitioning from the caisson to normal atmospheric pressure, is predominantly localized in the knee and elbow joints, shins, and forearms, and persists for 1 to 3 days.

Acute decompression sickness manifests 10 to 15 minutes or later following decompression—that is, during the period of gas bubble formation—resulting in joint pain.

Based on its clinical manifestations, caisson disease is classified into mild, moderate, and severe forms.

The mild form is characterized by exceptionally intense pain in the area of one or more joints. This pain is caused by ischemia in the embolized tissue region (periosteum, bone, joint, fascia, Muscle, or nerve). Persistent pain most frequently occurs in the knee, shoulder, wrist, elbow, and ankle joints. The pain lacks a precise localization and is felt diffusely around the joint, radiating in all directions and intensifying upon Palpation and limb flexion.

In moderate and severe forms, the auditory Organs and gastrointestinal tract are affected, and hemorrhages occur.

Chronic decompression sickness may be primary, resulting from chronic pressure fluctuations, or secondary, occurring after acute decompression sickness and manifesting as aseptic necrosis. Treatment consists of recompression.

Drawing on extensive radiological data, S. A. Reinberg established that the most pronounced changes in caisson disease appear in the proximal ends of the femoral and humeral bones as multiple aseptic osteonecroses with significant secondary reactive manifestations.

The HEAD, neck, and trochanteric region of the femora, as well as the metaepiphyses of the humeri, lose their trabecular Structure and exhibit cystic radiolucencies in certain areas surrounded by a sclerotic rim. When the articular ends of the bones are affected, the articular cartilages are drawn into the pathological process. The articular surfaces change accordingly, manifesting as deforming arthroses of the large joints—sometimes multiple—which distinguishes them from conventional osteoarthroses.

Occasionally, radiological examination reveals calcified and ossified formations resembling intra-articular and intracapsular chondromatous bodies. These share the same origin as other soft-tissue calcifications in caisson disease, stemming from necrosis of adipose elements.

Another highly diagnostic radiological sign of caisson disease is alterations in the bone marrow, referred to as medullary calcifications, which appear as cloud-like or shell-like calcified structures.

Additionally, submarine personnel or deep-sea miners sometimes exhibit vertebral changes such as brevyspondylia or platyspondylia without damage to the cartilaginous discs; radiological signs in the bones appear some time after the onset of caisson disease. The same condition later develops in professionals due to continuous pressure fluctuations. Therefore, to detect spinal changes in a timely manner and prevent their progression, periodic occupational medical examinations should be conducted.

In acute cases of caisson disease, symptomatic treatment is administered to eliminate general and local manifestations. Therefore, the primary measure is strict adherence to decompression protocols when exiting the caisson. To halt the release of gas from tissues, emergency recompression must be performed, followed by gradual decompression in accordance with established guidelines.