Consequences and prevention of hypothermia
Prolonged exposure to low temperatures in the workplace is a major risk factor. Hypothermia can provoke the development of a number of inflammatory and neurological pathologies. Primarily, these include lumbosacral radiculitis, pyelitis, and cystitis. Neuralgias of various localizations, including lesions of the facial, trigeminal, and sciatic nerves, are also frequently diagnosed.
To protect workers' health, strict preventive measures are applied:
- Providing personnel with adequate warm clothing and footwear.
- Mandatory installation of special drying facilities for work clothing at the enterprise.
- Organization of heated rooms where workers can periodically go to warm up.
- In cases of severe cold, reduction of the total work shift duration.
There are clear hygienic standards for the temperature regime in workspaces. If an employee performs light physical work, the air temperature must not drop below 10 °C. During heavy physical labor, a temperature decrease is permitted, but it must be at least 5 °C.
Individuals suffering from diseases of the peripheral nervous system, joints, muscles, kidneys, as well as the respiratory organs (including frequent colds), have strict medical contraindications to working under the risk of hypothermia.
Exposure to elevated atmospheric pressure
Specific occupational groups encounter elevated atmospheric pressure: divers and workers engaged in caisson work (construction of bridge piers, building underwater tunnels and subways, working in water-saturated soils).
Diving operations are carried out in special suits or diving gear into which compressed air is pumped under pressure. The level of this pressure must strictly compensate for the water column pressure from the water surface to the specialist's diving depth. The pressure gradient is simply calculated: a dive of every 10 meters results in a pressure increase of approximately 1 atm.
During work under high-pressure conditions, characteristic physiological changes are observed in humans. Breathing difficulties are noted, primarily affecting the exhalation phase. A sensation of severe compression and pain in the ears occurs, caused by the mechanical pushing of the tympanic membrane inward. In addition, a decreased heart rate—bradycardia—is recorded.
Hygienic regulation of labor under such conditions requires strict time limits for staying under pressure. For example, if the working pressure reaches values from 3.5 to 3.9 atm, the work shift must be forcibly shortened to no more than 2 hours 40 minutes.
Organization of caisson work
A caisson is a specialized engineering structure designed for safe underwater or underground excavation. Structurally, it consists of three main parts:
- Reinforced concrete caisson chamber — open at the bottom and lowered directly onto the seabed or riverbed.
- Metal shaft tube — mounted over a special opening in the ceiling of the chamber and serves as a channel for communication with the surface.
- Lock apparatus — located in the upper part of the shaft tube and provides a safe transition between zones with different atmospheric pressures.
The operating principle of the system is as follows: compressed air is pumped into the working chamber through the air supply pipe (pressure can reach 4 atm). Overpressure displaces water from the chamber, creating a dry zone for excavation. As the caisson sinks deeper into the rock, the shaft tube is gradually extended, and the so-called above-caisson masonry is erected on the ceiling of the chamber, forming the future bridge pier or other structure.
For lowering and raising loads and equipment, the material airlock of the lock apparatus, a winch, an above-caisson crane, and a bucket (container for extracting soil to the dump site) are used.
People move through the passenger airlock. The key process here is lock transition (pressurization/depressurization). Before the shift, the pressure in the lock is gradually increased to the working level (compression), and after the shift, it is slowly reduced to normal (decompression).
Pathogenesis and clinical presentation of decompression sickness
The most critical risk factor during caisson work is the process of transitioning from the high-pressure area to normal surface conditions. Violation of decompression rules leads to the development of a severe condition — caisson (decompression) sickness.
The pathogenesis is based on the excessive accumulation of nitrogen. Nitrogen is an inert gas; it is not used by tissues for vital activity. Its solubility in blood is directly proportional to pressure. If at normal pressure of 100 cm³ of blood, 1.2 cm³ of nitrogen is dissolved, then at 2 atm this figure rises to 2.2 cm³, at 3 atm to 3.0 cm³, and at 4 atm to 3.9 cm³.
During safe (slow) decompression, excess nitrogen gradually passes from tissues into the blood in a dissolved state and is safely removed from the body via the lungs. If the ascent is too rapid, the dissolved gas does not have time to eliminate. It lingers in the tissues (especially in adipose tissue and the white matter of the brain) and transitions into a gaseous state. Gas bubbles (emboli) form in the blood and tissues. They cause blockage of blood vessels, mechanical compression of surrounding tissues, and even rupture of capillaries.
The clinical picture of mild to moderate severity includes:
- Specific muscle and joint pains in the extremities, known among workers as "bends".
- Pruritus (itching) and the appearance of a marbled skin pattern.
- Girdle pains in the abdomen and chest.
- Increased heart rate (tachycardia) and respiration (tachypnea).
- Dizziness and epistaxis (nosebleeds).
Treatment and rehabilitation
The only effective emergency measure for the onset of symptoms of decompression sickness is immediate recompression. The victim is urgently placed in a therapeutic airlock (decompression chamber), which, according to safety regulations, must always be located in the immediate vicinity of the work site.
The pressure in the chamber is quickly raised to the working level at which the person was working. Due to this, the gas bubbles in the tissues are compressed, and nitrogen diffuses back into the blood, returning to a dissolved state. Then the process of therapeutic decompression begins — an extremely slow reduction of pressure to eliminate nitrogen through the alveoli.
The therapeutic pressure reduction regimen is stricter than standard lock transition:
- In severe cases, pressure is reduced by 0.1 atm every 10 minutes.
- In mild cases, by 0.1 atm every 5 minutes.
In the post-compression period, the patient is under medical observation for a duration of 3 to 12 hours. To accelerate nitrogen elimination, massage and moderate physical exercises are actively used, which can be started while still in the therapeutic lock.
Briefly: answers to topical questions
What is the clinical picture of severe decompression sickness?
The clinical picture of severe acute decompression sickness is caused by the formation of gas bubbles in arterial blood and vascular embolism. Symptoms include the following manifestations:
- Brain vessel damage — causes dizziness, stupor, vomiting, weakness, fainting, paresis, paralysis, and loss of consciousness.
- Pulmonary vessel embolism — leads to asphyxia, retrosternal pain, sharp cough, and dyspnea.
- Spinal cord injury — accompanied by paralysis of the extremities, urinary and defecation disorders.
In severe cases, fatal outcome is possible within a few minutes after decompression.
What are the long-term consequences and chronic complications of past decompression sickness?
Chronic complications of decompression sickness develop with prolonged exposure to elevated pressure and systematic formation of venous gas bubbles. The main long-term consequences include:
- Involvement of tubular bones — appearance of rarefaction foci with perifocal sclerosis.
- Joint involvement — development of deforming osteoarthritis.
- Impaired bone nutrition — occurs due to the blockage of small blood vessels (Haversian canals) by gas emboli.
These pathological changes form the picture of chronic decompression disorders in individuals who are regularly exposed to pressure drops.
What gases are used in modern breathing mixtures for the prevention of nitrogen narcosis and decompression sickness?
In the given deep-sea diving example, a helium breathing mixture with an oxygen content of 2% was used. At high pressure, nitrogen can exert a narcotic effect, and during rapid decompression, it presents the main danger, as its bubbles cause gas embolism.
Class and exam questions
What happens to the body during a rapid ascent from depth?
Due to a sharp drop in pressure, the nitrogen dissolved in tissues does not have time to be eliminated through the lungs and forms gas bubbles (emboli). This leads to vessel blockage, capillary rupture, and mechanical compression of tissues.
In which tissues does nitrogen accumulate the most?
Excess nitrogen predominantly accumulates and is retained in adipose tissue and the white matter of the brain.
What does first aid for decompression sickness entail?
The victim must be immediately placed in a therapeutic airlock, the pressure quickly raised to the initial working level, and then a very slow therapeutic decompression performed.
What else to study on this topic
- Clinical presentation of severe forms of decompression sickness and localization of emboli
- Specifics of medical examinations for clearance to perform diving operations
- Requirements for ventilation and the quality of supplied compressed air in a caisson
- Physiological mechanisms of bradycardia under increased atmospheric pressure
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