CONTENT MODULE 3

June 25, 2024
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VIBRATION DISEASE.

ALTITUDE SICKNESS AND DECOMPRESSION SICKNESS

 

I. VIBRATION DISEASE

(health effects of vibration, diagnosis and treatment of vibration disease)

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Vibration disease (VD) is a professional disease, the main etiological factor of which is industrial vibration. The favourable background for the development of the disease there are the following concomitant occupational factors of risk: noise, super cooling, significant muscle tension of shoulder, forced position of body.

Usually vibration disease is met among the workers of machine building, metallurgical, aircraft, shipbuilding, mineral resource industries, and also in transport and agriculture. Mainly among those workers, whose character of work is related with the long influence of vibration during the use of hand mechanic tools of percussion action.

Occupational Vibration – A Short History

·                1839 – Pneumatic tools were first used in French mines

·                1862 – Primary Raynaud’s Phenomenon (Raynaud’s Disease) identified.

·                1911 – Professor Loriga first described vascular spasm in the hands of Italian miners using pneumatic tools.

·                1918 – Alice Hamilton studied miners using drills in limestone quarries describing spastic anaemia of the hands.

·                1930-40s – Cases of white finger were identified studies in fettlers, riveters, boot and shoe industry workers and users of electrical powered rotating tools

·                1950s – Research links signs and symptoms ierves, bones, joints and muscles with vibrating tools.

·                1968-69 – After 12-14 years of continuous chain saw use widespread complaints of VWF (Vibration white finger) in operators.

·                1975 – Scale for assessing the extent of vascular injury associated with vibration white finger published by Taylor-Pelmear

·                1985 – VWF becomes a prescribed disease for Industrial Injuries Disablement Benefit purposes

·                1987Stockholm scale for assessment of VWF published. Standard for measurement of vibration published in BS 6842.

·               

 

The vibration is the mechanic oscillations that repeat periodically and are characterized by the frequency measured in hertz (Hz), vibrovelocity (m/s) and amplitude (cm).

There are three types of vibration: low-frequency (8 – 15 Hz), medium-frequency (16 – 64 Hz), high-frequency (more than 64 Hz).

Dangerous for the development of disease is the vibration with the frequency 16 – 250 Hz. The women are very sensible to the vibration (the influence to the fetus is very dangerous), the teenagers, people elder than 40 and people with neural disorder also are very sensible. Mostly this illness is revealed (40%) among the workers, whose length of service is 10-15 years.

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The main parameters determining the vibration are the oscillation frequency, vibration velocity and the amplitude. Oscillation frequency is measured in hertz, vibration velocity in meters per second. Strength of vibration on the human body depends on the amount of absorbed energy, which is expressed in the vibration velocity. A derivative of vibration in time – vibration acceleration, which measured in meters per second squared

According to the character of influence to the organism there is local, general and combined vibration.

During the local vibration the transmission of mechanic oscillations to the body is realized through the arms. Most often this etiologic factor we can see among the face-workers, chasers, drillers, tunnellers, polishers, grinders, wood-cutters.

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The sources of the general vibration are the vibroplatform, the table vibrator, the forming and concrete-laying machines, the floor of weaving-mills, agricultural machines (tractors, combines), excavators, vehicles (airplanes, helicopters, sea and river ships).

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The combined vibration is a combination of local and general. For its turn, it can be with the advantage of local influence during the work with hand tools, when the transmission of vibration on the worker’s body is realized not only through the arms, but also through the legs, breast, back and other parts of body, depending on the posture during the work and the construction of instrument. In other cases the general influence can prevail, for example, during the work on vibroplatforms with simultaneous floating of concrete mix.

Vibration has negative influence on all the tissues of the organism, but most of all on the neural and bone tissue; the last is a good conductor and resonator of vibration. The most sensitive to it are nerve endings, mostly receptors that are located in the skin of distal sections of hands and foots. In the transmission of irritations the important place has the vestibular apparatus. The high-frequency vibration influences negatively to the acoustic. It is proved that the high-frequency vibration causes the vasoconstrictor effect and the most unfavourable action (vasospasm) causes the vibration with the frequency 100 – 250 Hz. Low-frequency vibration and big amplitudes of body changes and its organs in space are related with irritation of vestibular apparatus. And the significant role in the reaction of organism to the action of pathogenic factor plays the resonance frequency, biologically peculiar to the organism in whole, and to separate organs and tissues in particular. It is known that for the body of man it is equal to 6 Hz, for head and stomach to 8 Hz. First of all, under the influence of low-frequency vibration (till 16 Hz), appear the functional disorders of organism, that is considered as the condition of naupathia (the sickness of movement). It often may be observed at the employees of different kind of transport: railway, sea, air.

 

The body is susceptible to non-acoustic vibration transmitted by direct contact with oscillating surfaces. As with sound, frequency is important: vibration below 2 Hz and above 1500 Hz is not thought to be harmful; motion between 5Hz and 20 Hz is considered potentially most damaging. Vibration can be measured in various ways, but is normally expressed as acceleration in metres per second squared (m/s2) averaged over the three axes. As vibration at frequencies below 2 Hz and above 1500 Hz is not thought to cause damage, weighting is applied to measurements of vibration magnitude to allow for this frequency dependence of the risk of harm.

Vibration is usually measured in three orthogonal directions at the interfaces between the body and the vibrating surface

 

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PATHOPHYSIOLOGY

Workers using hand-held vibratory tools are exposed to 3 major stressors: vibration, noise generated from the machines, and environmental cold. In general, typical levels of tool vibration are more than 0.316 m/s2, while tool noise levels are generally more than 95 dB (air). ChronicaIIy repeated action of the stressors on the human body may overload and impair not only the peripheral systems but also the central nervous system, including the higher center of the autonomic nervous system, in addition to the acoustic nerves.

4) In the input overloading state, excitation of the hypothalamus and the limbic lobe in the cortex, where the higher center of the autonomic nervous system exists, results in an increase in circulating catecholamines from the adrenal medulla. This process may result in a very large increase in vasoconstriction and stimulation of the heart, leading to hypoxia and lack of nutrition in the target tissues. The peripheral circulatory and nervous disorders reveal, in particular, Raynaud’s phenomenon in the fingers. Among the cardiovascular manifestations are sinus bradycardia, enlarged heart and increased left ventricular ejection fraction at rest. Blood pressure runs on the low side. These symptoms and signs of the cardiovascular system are similar to those frequently observed in endurance athletes. Well-trained athletes are adapted to physical training and possess, at rest, sinus bradycardia, cardiomegaly, comparatively lower blood pressure, increased stroke volume and left ventricular ejection fraction, increased cardiac output, and electrocardiographic abnormalities. Thus, it is emphasized that the clinical features of the vibration syndrome can include adaptive responses to the stressors, in addition to direct injuries induced by vibration. The pathophysiological mechanism of Raynaud’s phenomenon in the fingers, one of the typical symptoms and signs of the disease, has not yet been clarified. Raynaud suggested in 1862 that the vasospasm was mediated through central sympathetic nervous impulses. Contradictory to this, Lewis advanced a theory in 1929 that an attack of Raynaud’s phenomenon was produced only by defects in the nerve endings with no role of central sympathetic nervous impul-

ses. From this controversy, many experimental and clinical data have been presented.

HEALTH EFFECTS OF VIBRATION

Vibration and noise often emanate from the same source. Vibration may reach the body through a number of pathways, but consideration  of adverse health effects centres on whole body vibration and hand arm vibration. As with noise, the risk of harm is a function of both the  magnitude of exposure and of its duration: “doses” are therefore adjusted to a standard reference period of eight hours to allow comparison, and this figure is termed A(8). Measuring vibration is complex and should only be undertaken by those with specialist training.

 

Classification of vibration disease:

1.                  From influence of local vibration.

2.                  From influence of “combined” vibration

3.                  From influence of general vibration

According to the intensity’s degree of pathologic process symbolically mark out 4 stages of disease:

I – initial;

II – moderately expressed (dystrophic disorders);

III – expressed (irreversible organic changes);

IV – generalized

  Clinical syndromes:

1)                Angiodistonic (Vegetative-vascular disease in the limbs, impaired capillary blood circulation (atonic or spastic-atonic state))

2)                Angiospastic (White finger attack, spasms of the capillaries, skin temperature violation, marked reduction of vibration sensitivity preferentially localized to the hands and feet)

3)                syndrome of vegetative polyneuritis (Pain phenomena, violation of skin sensitivity, reduced skin temperature, vegetative symptoms);

4)                syndrome of vegetative myofascitis (Painful phenomena, vascular disorders, changes in sensitivity by peripheral or segmental type)

5)                syndrome of somatic neuritis (cubital, median), plexitis, radiculitis;

6)                diencephalic with neurocirculatory disturbance;

7)                 vestibular

 

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Sensory decrement by theperipheral type

 

WHOLE BODY VIBRATION

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Interest in the effects of whole body vibration (WBV) stems from the middle of the 20th century when mechanisation, particularly of transport,  became more prevalent. Vibration is transmitted either from a machine platform through the feet, or from a seat through the buttocks. Exposure is most likely to occur with vehicle use and this includes road, off road, rail, air, and maritime use: it  is estimated that as many as 9 million people in  the United Kingdom are regularly exposed to whole body vibration. The disorders reported in groups exposed in this way include gastric problems, vestibular dysfunction, circulatory changes, menstrual disturbance, and psychological effects. However, the main problem associated with whole body vibration is back pain, and the UK Health and Safety Executive estimates that up to 21 000 cases may be caused by exposure, with a further 13 500-31 500 cases of exacerbation of a pre- existing condition. The evidence base for a causal link between whole body vibration and back paievertheless remains weak, and has recently been comprehensively reviewed.

Sources of WBV: Drivers of some mobile machines, including certain tractors, fork lift trucks and quarrying or earth-moving machinery, may be exposed to WBV and shocks, which are associated with back pain. Other work factors, such as posture and heavy lifting, are also known to contribute to back problems for drivers, however further study is needed into the impact of WBV.

 

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Use of a vibrating tool for road breaking

Health effects of WBV

While there is a shortage of conclusive evidence to provide a definite close-effect relationship between whole-body vibration and injury or health damage, we can, from the limited scientific studies, subjective data, biodynamic models and our knowledge of the physical properties of the human body, establish some of the likely health effects.

Ø spinal column disease and complaints are perhaps the most common diseases associated with the long-term exposure to whole-body vibration, where the back is especially sensitive to the 4-12Hz vibration range

Ø digestive system diseases are often observed in persons exposed to whole-body vibration over a long period of time. This is associated with the resonance movement of the stomach at frequencies between 4 and 5Hz

Ø and cardiovascular system effects resulting from prolonged exposure to whole-body vibration at frequencies below 20Hz. These result in hyperventilation, increased heart rate, oxygen intake, pulmonary ventilation and respiratory rate.

Ø

The vibrational energy waves, much the same as noise, are transferred from the energy source – a hand tool or vehicle – into the body of the exposed operator. This is then transmitted through the body tissues, organs and skeletal systems of the individual before it is dampened and dissipated.

Fortunately the human body can tolerate certain levels of vibrational energy but when exposed over a long period of time it begins to deteriorate and fail causing a disruption in the body’s natural processes and systems. The health effects experienced by employees vary considerably and factors such as situation, age, lifestyle (smokers), posture, ergonomic design and resonance all have an influence on the ill health effects of the vibration exposure.

Each part of the human body has its own natural frequency of vibration. The extent to which the human body is affected depends on the vibration frequency to which it is exposed. This resonant response to the vibration will cause symptoms ranging from simple motion sickness to severe discomfort, organ failure or tissue degeneration.

Lower back pain

The most pronounced and common effect is lower back pain. This can be linked to the vibration acting on the musculo-skeletal system of the body, causing the degeneration of the small cartilage (intervertebral) discs, allowing tissues and nerves to be strained and pinched leading to various back and neck problems.

The tolerance limits of the body to vibration in a lorry cab.

How the bottom of the back is affected by vibration

Long periods of sitting while the spinal column is being aggravated by vibration exposure causes the nutrients needed for growth and repair to diffuse outwards. This causes irreparable damage at a cellular level and wear and reduced healing of discs and vertebra within the spinal column.

Muscle fatigue also occurs as the muscles try to react to the vibrational energy to maintain balance and protect and support the spinal column. But these are often too slow as the muscular and nervous system cannot react fast enough to the shocks and loads being applied to the body.

Other health effects that have been associated with whole-body vibration and especially the driving environment are haemorrhoids, high blood pressure, kidney disorders and even impotence – and other adverse reproductive effects in men and women.

Control of WBV influence

Vibration is a complex hazard that does not have one control measure that will solve all problems. However, it is not always necessary to spend great sums of money on evaluation of vibration exposures, when a good risk assessment exercise is carried out taking into account factors such as exposure periods, worker complaints and symptoms, medical records and ergonomic principles and design at the workplace or on the vehicle.

If a driver or worker has a genuine complaint – a forklift driver with lower back pain – then something should be done to try and rectify this. The money could be spent on control measures and include possible solutions such as “air-ride” suspended seats, suspended cabs, maintaining vehicle suspension systems, and inflating tyres to their proper pressure. Seats with arm rests, lumbar support, an adjustable seat back and an adjustable seat pan are also useful for correcting driving surfaces to reduce vibration at the source. All it takes is a true holistic approach using sound occupational health and safety principles (from: http://www.napit.org.uk/)

HAND ARM VIBRATION

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Vibration may be transmitted to the hands and arms by the use of hand held power tools, hand guided machinery, or by holding materials being processed by machines. Exposure is particularly common in agriculture, construction (particularly scabbling), mining, engineering, forestry, public utilities, and shipbuilding. It is estimated that about 1 million people in the United Kingdom are exposed to potentially harmful levels of hand arm vibration in their work, and as many as 300 000 may have developed adverse health effects as a result. The health effects of exposure to hand arm vibration have been recognised for many years and have been ascribed a variety of labels. There is now general consensus on the use of the term “hand arm vibration syndrome” to describe the vascular (sometimes also known as vibration white finger), neurological, and musculoskeletal symptoms that can result. Acute vibration exposure causes vasoconstriction of the blood vessels supplying the fingers and, if prolonged, it may damage the endothelium and stimulate smooth muscle proliferation so that the lumen of the vessels gradually narrows. Damage also occurs to the peripheral nerves, with acute oedema and chronic demyelination. Muscular weakness in the hand is common, carpal tunnel syndrome is recognised in some cases, and there is evidence to indicate that premature osteoarthrosis of the wrist and elbow may occur. The precise relation between these elements of the syndrome remains a matter for debate, but there is no doubt that the vascular and neurological components can occur separately. In the early stages of vibration injury the only symptom may be a tingling in the fingers, most noticeable at the end of the working day. This may be associated with a loss of sensation and periodic blanching of the tips of the fingers when exposed to cold. As the condition progresses the blanching extends to the root of the fingers, although the thumbs are rarely affected. In more severe cases there is considerable pain, with a loss of grip strength and dexterity, and attacks may occur even in warm surroundings. Rarely the condition can progress to the extent that circulation is permanently impaired and the fingers become cyanosed—exceptionally, cases of vibration induced gangrene have been reported.

CLINICAL PICTURE

The diagnosis of vibration syndrome has been done by the history takings, physical and laboratory examinations. First of all, we must learn whether a patient works with hand-held vibratory tools for a long-term. The complaints in the early stage include disorders of the peripheral nervous and circulatory systems, and of the muscle-skeletal system. Numbness and cold sense in the fingers and stiff shoulders in the arm occur first. The reduction in muscle strength may also be present. In the second half of stage 2, Raynaud’s phenomenon in the fingers happens even in a very hot bath (42-43°C) as well as in cold exposure. Palmar hyperhydrosis as a sign of the autonomic nerve disorders appears even wheo work is performed. Ulnar nerve paralysis or paresis occurs in some cases. Headache, insomnia, forgetfulness, irritability, depressive mood, tinnitus, and impotence appear as the stage progresses. These complaints should be due to the autonomic and central nervous system disorders, but actually, some of them may be considered to be “symptom-induced symptoms.” For example, when muscle pain is persistent, the patient will fall into a depressive mood (Fig. 1). The symptoms and signs in the syndrome include three major disorders: peripheral circulatory, nervous and muscular disorders, bone-joint system disorders, and the autonomic and central nervous disorders associated with hearing loss, nystagmus and vertigo. The mixed type with three major disorders is observed in 60 to 70% of the patients. Physical examinations reveal circulatory, nervous and muscle disorders in the fingers and arms. Impairment of sensory perception and tactile discrimination are present, of which extent in the body surface must be examined. Reduction in muscle strength may also be present. The time course of the peripheral complaints falls into two types. Type A begins with muscle-joint system disorders, and type B with numbness. The period between the beginning of chain saw operation and the occurrence of Raynaud’s phenomenon is not always related to the total hours of usage. However, the older the worker is at the beginning of the usage, the earlier the peripheral disorders occur.

 

 

Vibration induced gangrene

 

Diagnostics of vibration disease

The inspection of patient in a clinic must be begun with the purposeful questioning about the conditions of work, feature of his labour activity. 

At finding out of professional anamnesis it is necessary to take into account, how long the worker works on this plant or factory. It is necessary to find out, whether he had the contact with other occupational hazards.

Collecting the complaints of the patient of it is very important to pay attention to the characteristic signs of disease: albication of fingers of hands on a cold (its duration and localization); aching pains in extremities, paresthesias; chilling of hands and feet, muscle weakness, headaches, dizziness, bad sleep, crabbiness, pains in a heart and stomach.

Characterizing the state of CNS and presence of polyneurotic syndrome with the phenomena of angiospasm of peripheral vessels, which take basic place in the clinical picture of vibration disease, it is necessary to examine in detail the upper and lower extremities, paying attention to the colour of skin, configuration of fingers, expressed secretory disturbances, temperature of skin, state of perceptible sphere. It is necessary to examine internal organs. Foremost it touches the cardio-vascular system, detection of angiodistonic, angiospastic syndromes, and manifestation of neurocirculatory dystonia.

STOCKHOLM WORKSHOP SCALES VASCULAR COMPONENT

Stage

Grade

Description

0V

 

No attacks

1V

Mild

Occasional attacks affecting only the tips of one or more fingers

2V

Moderate

Occasional attacks affecting distal and middle (rarely also proximal) phalanges of one or more fingers

3V

Severe

Frequent attacks affecting all phalanges of most fingers

4V

Very severe

As in stage 3, with trophic changes in the fingertips

 

STOCKHOLM WORKSHOP SCALES SENSORINEURAL COMPONENT

Stage

Grade

Description

0

 

Vibration-exposed but no symptoms

1sn

Mild

Intermittent numbness with or without tingling

2sn

Moderate

Intermittent or persistent numbness, reduced sensory perception

3sn

Severe

Intermittent or persistent numbness, reduced tactile discrimination

and/or manipulative dexterity

 

 

A system for allocating a weighted numerical value to each phalange affected and calculating an overall score for finger blanching in each hand is used in the Griffin method. This system is a useful method in practice for monitoring progression or regression of symptoms in individual fingers. It does not take account of the frequency of attacks, which may be more relevant in assessing functional disability. Some attacks can lead to a variable degree of blanching.  In this case the worst distribution should be recorded. A total value for each hand can be arrived at by summing the digit scores. In the figure, the score for the left hand is 16 and that for the right hand is 4.

It is necessary to pay attention to the additional signs which indicate on propensity of vessels to the spasm or atony. Often the appearance of hands, without the results of capillaroscopy, enables to suspect the change of vascular tone of capillaries. Albication of hands is typical for I stage, purple-cyanotic color – for II – III stage of disease. Sometimes it is possible to expose the edema of hands, expressed hyperhidrosis and so called “lace” picture on hands, which is characterized that on the red-cyanotic background of palm’s surface there are plural pale points or spots. These are spastically modified capillaries which are surrounded by capillaries in a state of atony.

The diagnosis of vibration disease is proposed on the basis of the collected complaints, anamnesis of disease and life, study of professional route, sanitary and hygienic description work conditions.

The typical additional signs of vascular disorders which confirm a diagnosis are: asymmetry of arterial pressure, symptom of “white spot”, Pile’s symptom, test on reactive hyperemia, test of Boholyepov, cold test.

1.    Symptom of “white spot”. You ask a patient to clench firmly the fist of hand and through 5 sec quickly unclench it. In a norm the white spots which appeared have to vanish in 5 sec. If spots do not disappear quickly – the test is positive.

2.    Pile’s symptom. A pulse is found on both radial arteries, and then by rapid motion lift up the hands of patient. Thus a pulse can vanish on a few seconds. Such test is positive.

3.    Test on reactive hyperemia. You impose a cuff on a shoulder and pump a pressure 180 – 200 mm of column of mercury. Then ask to lift hands up, in 2 min. to put hands down, take cuff off and write down time of hand’s reddening. In a norm the reddening begins in 1,5 – 2 sec. and passes in 15 sec. Lengthening of this time testifies to the spasm of vessels, and shortening – about their atony.

4.    Test of Boholyepov. A patient stretches both hands with the unbended fingers ahead. At that you pay attention on colouring of skin, state of veins and capillary net of nail bed of fingers. Then a patient lifts a right hand up, and put down a left on 30 sec. After it, returns hands in previous position. We look after the change of vein and capillary circulation of blood. Normally, the changes of blood filling are normalized in 30 sec. At insufficiency of circulation of blood, pallor or cyanosis, which arose up disappear slower, than the more expressed is a disorder of peripheral circulation of blood.

          5. Cold test. The hands of explored are dipped into a cold water (+10°С) on 5 min. At albication of fingers the test is considered positive. Pay attention on prevalence and intensity of the process, mark the time of renewal of skin temperature after cooling. Normally it does not exceed 20 min. At patients with vibration disease there is an acute deceleration of renewal of skin temperature.

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Capillaroscope

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Diagnostic of sensory during vibration disease

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Atrophy of muscles during vibration diseases

Medical treatment

Medical treatment of vibration disease must be realized in complex with the account of clinical symptomatology. Application of vasorelaxants, ganglionic blockers and physiotherapy methods is effective.

During VD conditioned by the influence of local vibration, which flows mainly with neurovascular disorders and pangs, are recommended the ganglionic blockers (Gexameton, Benzogexoniy) with the small doses of central anticholinergic drugs (Difacil, Aminazin, Amizil) and vasorelaxants (Nicotinic acid, No-shpa, Novocaine).

Difacil (spasmolytin) – 1% solution (s-n) in 10 ml i/m (intramuscularly) every other day, in the course there are 4 – 5 injection with an interruption 2 -3 days. In general it needs 2 – 3 courses. Difacil can be alternated with Novocaine 0,5% s-n i/v (intravenously) in 5 – 10 ml every other day during 10 days.  Also they apply Aminazin, Amizil,  Galidor,  No-shpa during 10 – 12 days.  From antiadrenergic Melildof (Dopegit) is recommended.

Are indicated paravertebral blocks of 0,25% s-n of Difacil 40 ml and 0,25% s-n of Novocaine 40-50 ml, or 0,25% s-n of Lidocaine.

For medical treatment of asthenoneurotic syndrome indicate sedative (valerian, motherwort, Novopasit) and tonics, and also biogenic stimulators (aloe, glutamic acid, fibs, plazmol, ginseng tincture, vitreous body, eleuterococ).

For the removal of pain syndrome: Analgin, nonsteroid antiphlogistics (Ibuprofen, Voltaren, Indometacin, mefenamic acid, Butadion).

For the improvement of circulation (peripheral, coronal and cerebral) of blood indicate the medicines which extend coronal vessels and improve the cerebral circulation of blood: Devincan, Vincapan, Apresin, Paverin hydrochloride, Aprofen,  Cinarizin, Piracetam, Cavinton.

  For the increase of the tone of parasympathetic nervous system, reduction of disturbances at vegetative-sensory polyneuropathy prescribe: Prozerin, Oxazil,  Galantamin.

For the improvement of microcirculation are indicated: ATF, Parmidin, Riboxin, anabolic hormones – Retabolin, Perabol.

With the purpose of improvement of protein metabolism prescribe: Unitol, Penicilamid.

A good effect has application of medicines which normalize vein tone: Venoruton, vein vasodilators – nitrates  (Nitrosorbit, Nitroglycerine), arterial vasodilators – Apresin, antagonists of calcium – Nifedipin, Corinfar, Adalat.

From tonics is effective introduction of 40% s-n of glucose, calcium gluconate, calcium chloride, preparations of bromine, caffeine.

At VD a vitamin metabolism is violated, especially due to the deficit of vitamins of group B and C. Because of it prescribe: ascorbic acid, vitamins B1, B12, B6.  They can cause a sensitizing of organism; therefore in such cases desensitizers are prescribed: Dimedrol, Pipolfen, Suprastin, Diazolin, Fencarol, Tavegin.

At susceptibility to angiospasms a vitamin PP, which has vasorelaxants effect, is indicated.

Physiotherapy methods include: electrophoresis with 5% s-n of Novocaine or 2% s-n of Benzogecsoniy on the hands or collar area. At polyneurotic syndromes apply high-frequency electrotherapy (UHV) on collar area – 15 procedures. General ultraviolet irradiation by small and suberithematic doses – 10 sessions.

A good effect is observed at application of acupuncture.  At the lesion of locomotor system are indicated: marsh, paraffin, ozocerite applications at a temperature  +40 – +45°, and also balneotherapy with application of hydrogen sulfide, radon, oxygen baths at a temperature  +37°, during 10 – 15 minutes. Also remedial gymnastics, massage of hands and collar areas are indicated.

  Ill people are sent to sanatorium-and-spa treatment in health resorts: Yalta, Yevpatoriya, Odessa, Khmelnic, Berdyansk.

 

 

Prophylaxis

In the prophylaxis of vibration disease reduction of the harmful influence of vibration on the organism of worker is most essential, and consequently a creation of new instruments and equipment, which would generate vibration within the limits of possible norm. An important measure is introduction to construction of mechanisms and instruments, devices which lower or extinguish the vibration.

A great importance for warning of vibration disease has the correct organization of labour.

Periodic medical examinations, the basic task of which consists in warning of the negative influence of professional factors on the organism of workers, early recognition and detection of vibration disease, belong to the prophylactic measures.

The contra-indications to the employment on the work  related  with influence of vibration are the chronic diseases of the peripheral nervous system, obliterating endarteritis, Raynaud’s disease, disease of locomotor system, marked asthenic states, expressed vegetative dysfunction, vagopaties with susceptibility to angiospasms, stenocardia, hypertensive disease of ІІ -III stages, disease of endocrine glands with stable disturbance (saccharine diabetes), stomach and duodenal ulcer, neuritis, polyneuritis, stable hearing loss of any etiology, otosclerosis, chronic diseases of female breeding organs.

Periodic medical examinations are realized not rarer once in 12 months with participation of internist, neurologist, otolaryngologist. At the inspection it is necessary to realize capillaroscopy, measuring of skin temperature, cold test, to explore a vibration, pain sensitiveness, if necessary radiography of hands, spine.

Описание: Описание: http://bspgloves.com/UploadFiles/201211125134886457.jpg

These gloves are padded with a layer of vibration dampening polymer. Specially compounded,formed-chloroprene coated, seamless-lined gloves. Good for protection from repetitive impact and work with pneumatic vibrating tools. Ergonomic design offers both comfort and flexibility.

From: http://bspgloves.com/pic_show.asp?id=109

REDUCING HAND-ARM VIBRATION THROUGH USE OF BETTER PROTECTIVE EQUIPMENT AND LOW-VIBRATION POWER HAND TOOLS

The Navy Clothing and Textile Research Facility supported an evaluation by the National Institutes for Occupational Safety and Health (NIOSH), to identify commercially available antivibration (AV) gloves and to measure their effectiveness at reducing exposure to vibration commonly generated by powered hand-tools. The study determined the most effective gloves for reducing exposure to various frequencies of vibration and found that several gloves marketed as having vibration-reducing qualities were not highly effective. Study results were communicated to the General Services Administration and Defense Logistics Agency to ensure that only the most effective products are marketed by the Federal Government. The research project also developed guidance for a simpler and more efficient way of evaluating the effectiveness of gloves used to reduce transmitted hand-arm vibration.  This project was part of a larger collaboration between DOD, GSA, DLA and NIOSH to improve the availability of low vibration power hand tools and certified (third-party tested) anti-vibration gloves within the Federal supply system and increase awareness of hand-arm vibration issues and control measures.

A Study of Anti-Vibration Gloves

One available method of reducing the risk of HAVs to workers who operate the types of tools and machinery described above is through the use of Anti-Vibration Gloves. Gloves may be advertised as “anti-vibration” (AV) without demonstrating a specific level of vibration attenuation because of the lack of regulatory criteria.  In fact, there are several models of gloves which are marketed as “AV” gloves but which do not meet the requirements of the applicable American National Standards Institute/International Organization for Standardization (ANSI/ISO) standards for anti-vibration gloves.  ANSI S2.73/ISO 10819, which is advisory in the US, specifies that anti-vibration gloves must provide full finger protection and provide a specific level of vibration reduction, measured at specified test frequencies by an independent

laboratory.  The Naval Safety Center Safety Liaison Office initiated a collaborative review of glove products described by their manufactures as “anti-vibration gloves” and “low vibration” hand-tools with many different subject matter experts including researchers from NIOSH.

RISK MANAGEMENT

Assessment of risk is based on the type of vibrating equipment employed and its pattern of use. In the United Kingdom the action level for introducing preventative measures is if exposure regularly exceeds an A(8) of 2.8m/s2 (dominant axis). It is important to recognise that this is not a “safe” level: some individuals are likely to develop hand arm vibrations with prolonged use even if this threshold is not exceeded. A new European Vibration Directive has recently been adapted (to be transferred into UK law in 2005), which sets a limit value on exposure of 5 m/s2 (sum of three axes) and an action value of 2.5m/s2 (sum of three axes). Manufacturers of vibrating tools may be able to provide useful data on levels under standard conditions, but care must be taken because actual levels in field use can differ substantially from those generated in a controlled environment. Similarly, field measurements can vary widely depending on mode of use and the materials being worked. In practice it is therefore usual to institute a preventive programme wherever there is prolonged use of tools likely to be hazardous. Prevention programmes aim to eliminate or substitute the hazardous process where possible. Where this is not possible, the procurement of low vibration machinery, fitting of vibration reducing adaptations (such as vibration reducing handles), regular maintenance and re-engineering of processes to avoid the need for prolonged tight gripping of high vibration parts will reduce exposure. Keeping the hands and body warm helps to maintain a good blood supply to the fingers and thereby reduces the risk of injury. Vibration reducing gloves are available but their efficacy is limited. A key element in a preventive programme is the provision of training and information about the hazard and the means of reducing risk.

HEALTH SURVEILLANCE

Health surveillance aims to identify those who develop early symptoms so that progression can be avoided and it is appropriate if exposure levels are likely to trigger a prevention programme. Pre-employment screening is helpful in identifying  individuals with conditions such as Raynaud’s disease that are a contraindication to work with vibrating tools, in establishing baseline measurements, and in educating workers about measures to minimise risk—not least the avoidance of smoking. It is good practice to repeat the assessment for newly exposed workers to identify those who may be particularly susceptible. Thereafter, annual review is recommended, with any symptoms being reported to a designated person as soon as they occur. Assessment should comprise a structured history and relevant clinical examination that will identify early hand arm vibration syndrome and assist with differential diagnosis, as a number of constitutional conditions give rise to similar symptoms. Guidelines from the UK Health and Safety Executive (see Further reading) give a sample questionnaire and guidance on tests that may be helpful for examination. Various methods of grading signs and symptoms have been devised and those of Taylor and Pelmear, and Griffin have been widely used. However, the most commonly used system of classification for hand arm vibration syndrome is currently the Stockholm Workshop scale, which grades the vascular and sensorineural components by severity. This scale, and the speed of progression along it, can helpfully be used to guide the management of affected workers. No effective treatment is available for this condition: management relies on adjustments to work, and limitation of vibration exposure. Cessation of vibration exposure may well compromise an individual’s continuing employment, and great care is therefore required before making any such recommendation. A number of additional test measurements (detailed Lindsell CJ and Griffin  MJ, 1988) can be carried out by specialist centres to help confirm the degree of incapacity, and referral should be considered in such circumstances.

CASE REPORT

A 54-year-old miner presented with a 2–3 year history of cold intolerance and blanching in his toes. The worker denied symptoms of HAVS. The worker had been employed in the mining industry for 35 years: initially as a furnace man for 17 years and then as an underground miner operating drills and roof bolters for 18 years. The worker retired 3 months prior to assess ment. Roof bolters are used to drill holes and place bolts to support the mine roof. These machines expose workers to foot-transmitted continuous vibration while drilling and bolting because the console is mounted on the machine and the platform upon which the worker stands vibrates when the machine is in operation. The worker estimated that he operated roof bolters 4 h/day, 3 days/week, during the 4 years immediately preceding assessment. The worker reported additional occupational exposure to foot-transmitted vibration from scissor lifts and load-haul-dump vehicles. History taking identified no non-occupational sources of foot-transmitted vibration exposure. Past medical history included hypertension (not pharmacologically treated) and hypercholesterolemia. He was anex-smoker (35-pack-year history), who had stopped smoking 6 years previously. He had a history of wrist fracture, but denied other trauma to the hands, fingers, feet or toes. There was no history of frostbite to the fingers or toes and he had no personal or family history of primary Raynaud’s disease, connective tissue disease, diabetes mellitus, gout, arthritis, neurological problems or thyroid disease. His only medication at the time of assessment was rosuvastatin.

Physical examination showed a blood pressure of 160/90. Cardiac examination was normal. Adson’s and Allen’s tests were normal. There were no trophic changes in the fingers or toes. Neurological and musculoskeletal examinations of both the upper and lower extremities were normal. Blood tests for systemic causes of secondary Raynaud’s phenomenon, including complete blood count, erythrocyte sedimentation rate, thyroid-stimulating hormone, cryoglobulins, rheumatoid factor, antinuclear antibody and serum immunoelectrophoresis, were normal. Doppler investigation was negative for peripheral vascular disease in the upper and lower extremities. Cold provocation plethysmography [4], nerve conduction studies and current perception threshold tests were all normal in the hands. Digital plethysmography for the toes showed normal toe waveforms at room temperature with moderate dampening of all toe waveforms post-cold

stress. The worker was diagnosed with Raynaud’s phenomenon of occupational origin in the feet. He was advised to avoid cold exposure as much as possible, to dress warmly whenever exposed to cold ambient conditions and to minimize vibration exposure to the feet. A trial with a calcium-blocking agent was suggested for treatment of his vasospastic symptoms. At 4 months follow-up, the worker had not yet tried pharmacological treatment and described no significant change in his condition, hypothesis, although it does suggest that local vascular pathology secondary to direct vibration exposure may be the principal pathophysiological mechanism in some cases.

 

 

II. OCCUPATIONAL DISEASES BOUND WITH ATMOSPHERIC PRESSURE CHANGES

Altitude sickness

Описание: Описание: https://encrypted-tbn2.gstatic.com/images?q=tbn:ANd9GcSsrJN4R32R4q5YNQMev0431Ud_aln-DtOV6Sq4ZSC1IH9M7F5XpQ

The altitude sickness is a disease that results from a considerable and fast decrease of partial pressure of oxygen (ð02) in ambient gas medium. In 1918 Schneider had offered to aggregate pathologic conditions that arise in time of flight and climb up an altitude in a unified nosological unit that have received a title of altitude sickness. It originates in pilots, and also in people, who work on high-level regions.

Описание: Описание: Definition of High Altitude

 Etiology and pathogenesis. Main cause of altitude sickness originating is an acute oxygen deficiency. Oxygen deficiency development is predetermined by reduction of barometric pressure with obligatory fall ðO2 in air or decrease of oxygen contain in air or in man-made gas medium of hermetically sealed rooms. The first situation can arise during high-altitude flights on flight vehicles with cabins of open type or after lesion of airtightness of cabins of a closed type; the second one is owing to failure of systems that regenerate air in hermetically sealed cabins and rooms. Adaptive reactions directed on improvements of oxygen transportation to cells, and pathological reactions conditioned by oxygen deficit, are closely interweaved in pathogenesis of altitude sickness. It can be considered in such sequence. Deficit of oxygen in environment results in decrease of partial pressure in alveolar air and arterial blood. Lowering of partial pressure in arterial blood causes in turn and irritation of chemoceptors of reflexogenic vascular zones (sinocarotid and aortal). Amplification of impulses of chemoceptors is the beginning of many reflex adaptive reactions that determine increase of a minute volume of blood, stimulation of hypophysisadrenal system and above-vesiculate formations of brain, including cerebral cortex. Development of hyperventilation results in acapnia originating. It plays a certain part in pathogenesis of altitude sickness, and therefore it can be a cause of lesions of blood circulation and breathing regulations. Changes in activity of central nervous system that are showed in view of sensory and motor lesions arise due to considerable deficit of oxygen in arterial blood on the background of adaptation reactions. At those structures that are the most sensitive to oxygen deficiency in blood suffer first of all: photoceptors of eyes’ cellular tissue, cortex of cerebral hemispheres, cerebellum.

Описание: Описание: http://www.mrmeier.com/wp-content/uploads/2012/08/geolino01.jpg

Clinic. Two basic forms of altitude sickness are marked out: collapse and unconscious. The collapse form of altitude sickness originates practically at 3 % of able-bodied people in 5 – 30 minutes after altitude-chamber ascent on an altitude of 5000 m. It originates in 25 % cases for persons with functional failure of cardiovascular system regulation, and at 10-15 % cases for a practically able-bodied people after ascent on the altitude of 6000 – 7000 m. At that a general weakness, feeling of fever in all body or only in a head occurs, vision changes, air deficiency is felt, giddiness and loss of consciousness come up. Exterior of ill person, his/her behavior changes: paleness of face dermal cover comes up, sweating increases, features of face are sharpened, and it takes a suffering view. Motion activity is increased at first, and then delayed; a pose becomes constrained, a look is long, fixing on separate subjects. Attitude to surroundings becomes indifferent. Consciousness remains saved for continuous time, but all instructions of doctor are performed slowly and as if reluctantly. If a sufferer will not be supplied with a normal oxygen feed, his/her) condition can sharply worsen – a loss of consciousness will be set in. Frequency of cardiac contractions becomes less often, arterial pressure is reduced, and that testifies a development of collapse form of altitude sickness. Unconscious form often arises without any precursors. Ill person does not feel unpleasant sensations, loses feeling of adequate attitude to external situation and own condition, the loss of consciousness comes suddenly. In some cases attacks of clonic cramps precede to consciousness loss. Loss of consciousness at this form of altitude sickness refers to group of homeostatic unconsciousnesses, as its cause is hypoxemia – considerable decrease of blood saturation with oxygen. At that a cerebral blood circulation in some time after loss of consciousness remains on a rather high level, therefore a renewal of normal supply of organism with oxygen results in recovery of consciousness and disappearance of all symptoms of altitude sickness within 10-20 seconds.

LAKE LOUISE CRITERIA FOR ALTITUDE ILLNESS

(from: Sutton JR, Coates G, Houston CS. Hypoxia and Mountain Medicine. Burlington, Vt.: Queen City Printers; 1992;  High Altitude Medicine Guide. The Lake Louise consensus on the definition of altitude illness. http://www.high-altitude-medicine.com/AMS-LakeLouise.html. Accessed August 24, 2010)

ATTITUDE MOUNTAINE SICKNESS

Based on the Lake Louise AMS Questionnaire

Name________________________    Age ____   Sex____  Date ____________

History of acute mountain sickness, high-altitude cerebral edema, or high-altitude pulmonary edema?________________________________________

Medications:___________________________________________________

Ascent Profile:__________________________________________________

Treatment:____________________________________________________

 

Time   ____  ____  ____  ____  ____

Altitude   ____  ____  ____  ____  ____

Symptoms:

1.Headache:

No headache 0   ____  ____  ____  ____  ____

Mild headache 1   ____  ____  ____  ____  ____

Moderate headache 2   ____  ____  ____  ____  ____

Severe, incapacitating 3   ____  ____  ____  ____  ____

2. Gastrointestinal symptoms:

No GI symptoms 0   ____  ____  ____  ____  ____

Poor appetite or nausea 1   ____  ____  ____  ____  ____

Moderate nausea or vomiting 2   ____  ____  ____  ____  ____

Severe N&V, incapacitating 3   ____  ____  ____  ____  ____

3.Fatigue/weak:

Not tired or weak 0   ____  ____  ____  ____  ____

Mild fatigue/weakness 1   ____  ____  ____  ____  ____

Moderate fatigue/weakness 2   ____  ____  ____  ____  ____

Severe F/W, incapacitating 3   ____  ____  ____  ____  ____

4.Dizzy/lightheaded:

Not dizzy 0   ____  ____  ____  ____  ____

Mild dizziness 1   ____  ____  ____  ____  ____

Moderate dizziness 2   ____  ____  ____  ____  ____

Severe, incapacitating 3   ____  ____  ____  ____  ____

5.Difficulty sleeping:

Slept well as usual 0   ____  ____  ____  ____  ____

Did not sleep as well as usual 1   ____  ____  ____  ____  ____

Woke many times, poor night's sleep 2   ____  ____  ____  ____  ____

Could not sleep at all 3   ____  ____  ____  ____  ____

Symptom Score:

____  ____  ____  ____  ____

Clinical Assessment:

6.Change in mental status:

No change 0   ____  ____  ____  ____  ____

Lethargy/lassitude 1   ____  ____  ____  ____  ____

Disoriented/confused 2   ____  ____  ____  ____  ____

Stupor/semiconsciousness 3   ____  ____  ____  ____  ____

7.Ataxia(heel to toe walking):

No ataxia 0   ____  ____  ____  ____  ____

Maneuvers to maintain balance 1   ____  ____  ____  ____  ____

Steps off line 2   ____  ____  ____  ____  ____

Falls down 3   ____  ____  ____  ____  ____

Can't stand 4   ____  ____  ____  ____  ____

8.Peripheral edema:

No edema 0   ____  ____  ____  ____  ____

One location 1   ____  ____  ____  ____  ____

Two or more locations 2   ____  ____  ____  ____  ____

Clinical Assessment Score:

____  ____  ____  ____  ____

Total Score:                                                        ____  ____  ____  ____  ____

Source: American Family Physician, Volume 82, Number 9, November 1, 2010, www.aafp.org/afp

 

Altitude illness is a general term referring to the three problems that can occur on ascent to altitude: Acute Mountain Sickness (AMS), High Altitude Cerebral Edema (HACE), and High Altitude Pulmonary Edema (HAPE).

AMS and HACE are considered a spectrum of the same altitude illness. The small amount of swelling in the brain that contributes to mild AMS becomes significant swelling and progresses to severe headache, confusion, lethargy, lack of coordination, irritability, vomiting, seizures, coma, and eventually death if untreated. A person with HACE may look like a confused, disoriented drunk person, fumbling with clothing, unable to walk a straight line, and with slurred speech.

Описание: Описание: http://www.altitudemedicine.org/public/images/HACE_top.jpg

HAPE (High Altitude Pulmonary Edema) is an accumulation of fluid in the air sacs of the lungs, due to leaky capillaries. It severely inhibits exchange of oxygen in the lungs, and can result in death . HAPE symptoms start gradually within the first 2-4 days at altitude. The earliest symptoms are shortness of breath with exercise, with decreased exercise performance. As more fluid accumulates in the lungs, symptoms progress to severe shortness of breath even at rest, a persistent cough sometimes with blood, chest tightness or congestion, and severe weakness. Untreated patients progress to unconsciousness, coma, and death.

Criteria for diagnosing HAPE are a combination of symptoms and physical exam findings. At least two of the following symptoms: shortness of breath at rest, cough, weakness and decreased exercise performance, chest tightness or congestion; AND at least two of the following signs on physical exam: fast heart rate, fast breathing, crackles or wheezing heard in the lungs, or low oxygen measured by a device called a pulse oximeter or signs of low oxygen such as dusky or bluish appearance of the skin. Chest X-ray in a HAPE patient confirms fluid in the lungs.

Treatment. It is necessary to transfer a sufferer with altitude sickness to breathing by oxygen or mixture of oxygen with 3-5 % contents of carbon dioxide; it is the only reliable method of this disease treatment. The oxygen therapy for fast and full recovery of health in light cases is sufficient. Except for the oxygen therapy it is necessary to use a medicinal therapy at high-gravity forms of altitude sickness, if a sufferer is unconscious during continuous time or if a loss of consciousness arises multiply times and is accompanied by attacks of cramps, vomiting. Citramonum, caffeine, camphor, cordiaminum, strophanthin, lobeline or cytitonum are prescribed with this purpose. Drugs with dehydrational properties (mannitol, dextrane, and glucose) are recommended for a preventive measures and elimination of posthypoxic brain hypostasis.

Heat exchange. It is necessary to take into consideratioature of changes and feature of work at solution of problems, connected with capacity for work. Experiencing of light forms of altitude sickness that has not resulted a health condition ionperishable negative changes later on is not contraindication to work on a profession. Expressed and nonperishable changes result in disablement. Medical social commission of experts determine a degree of decrease of capacity for work, solve a problem concerning necessity of person transfer to disablement, give recommendations concerning a training for a new profession with allowance for degree of manifestations of occurred changes.

The most accepted method of preventing acute mountain sickness and high-altitude cerebral edema is to ascend slowly. However many climbers have difficulty following this advice. The general rule of thumb for persons at altitudes higher than 9,800 ft (3,000 m) is not to sleep more than 1,000 to 2,000 ft (300 to 600 m) above the previous night’s elevation. Acetazolamide, a carbonic anhydrase inhibitor, may be used as prophylaxis; it should be started at least one day before climbing and continued until acclimatization at the highest sleeping elevation, Although a systematic review in 2001 found that lower dosages are not effective, more recent studies support the use of 125 mg twice daily for prophylaxis. Adverse effects may include paresthesias (common),mild diuresis, and an aversion to carbonated beverages because of the inhibition of salivary carbonic anhydrase. Acetazolamideis contraindicated in persons with sulfa allergies. Dexamethasone is also effective for prophylaxis and treatment of acute mountain sickness as a second-line agent, but it does not assist in acclimatization and therefore may lead to rebound acute mountain sickness when it is discontinued. A small study showed that low-dose theophylline is also beneficial for prevention of acute mountain sickness.

Treatment of high-altitude cerebral edema starts with immediate descent, if possible. Descent of 1,000 ft (300 m) may be all that is required. If descent is not possible (e.g., because of weather conditions), supplemental oxygen should be administered, and the patient should be placed in a portable hyperbaric oxygen chamber until descent is possible. Portable hyperbaric chambers are fairly lightweight and are typically carried by high-altitude rescue teams. They may be used on major expeditions, and are often available at rescue stations. Dexamethasone should also be given until descent is possible and until symptoms have resolved.

Ginkgo has been studied for prophylaxis and treatment of acute mountain sickness and high-altitude cerebral edema, but results are varied, and it is not recommended. Although descent and treatment are not required for persons with mild acute mountain sickness, persons with moderate to severe sickness should be treated as if they have early high-altitude cerebral edema. (Source: American Family Physician, Volume 82, Number 9, November 1, 2010, www.aafp.org/afp)

Medications for the Prevention and Treatment of Altitude Illness

(Source: American Family Physician, Volume 82, Number 9, November 1, 2010, www.aafp.org/afp; Hackett PH, Rennie D, Levine HD. The incidence, importance, and prophylaxis of acute mountain sickness. Lancet. 1976;2(7996):1149-1155, Hackett PH, Roach RC. High-altitude illness. N Engl J Med. 2001;345(2):107-114; van Patot MC, Leadbetter G III, Keyes LE, Maakestad KM, Olson S, Hackett PH. Prophylactic low-dose acetazolamide reduces the incidence and severity of acute mountain sickness. High Alt Med Biol. 2008;9(4): 289-293; Dumont L, Mardirosoff C, Tramèr MR. Efficacy and harm of pharmacological prevention of acute mountain sickness: quantitative systematic review.  BMJ. 2000;321(7256):267-272)

High-Altitude Pulmonary Edema

The pathophysiology of high-altitude pulmonary edema is not completely understood, but the primary mechanism is thought to be exaggerated hypoxic pulmonary vasoconstriction that causes increased pulmonary capillary pressure. Elevated pulmonary capillary pressure leads to mechanical disruption of the pulmonary capillaries and subsequent extravasation of fluid into the interstitial and alveolar spaces without inflammation. Limited availability of nitric oxide may increase pulmonary arterial pressure, and impaired sodium and water transportation within the lung may also contribute to the pathophysiology.

INCIDENCE AND RISK FACTORS

The incidence of high-altitude pulmonary edema in unacclimatized mountaineers at 15,000 ft (4,600 m) is approximately 4 percent. As with acute mountain sickness and high-altitude cerebral edema, risk factors for the development of high-altitude pulmonary edema include individual susceptibility, history of altitude illness, rapid ascent, altitude attained, and strenuous physical exertion. Acute mountain sickness is not a prerequisite for the development of high-altitude pulmonary edema.

DIAGNOSIS

High-altitude pulmonary edema often develops overnight, approximately one to four days after rapid ascent to altitudes above 8,000 ft (2,400 m). Affected persons may initially report fatigue, weakness, dyspnea, decreased exercise tolerance, and delayed recovery from exertion. Physical signs include frothy sputum with associated cough, cyanosis, rales, reduced oxygen saturation, tachypnea, and tachycardia. When high-altitude pulmonary edema is clinically suspected, decreased oxygen saturation (as measured by portable pulse oximetry, which is generally available at support camps) may confirm the diagnosis. If available, chest radiographs may show asymmetric patchy infiltrates in variable locations.

PREVENTION AND TREATMENT

High-altitude pulmonary edema is the leading cause of death from altitude illness, but it is avoidable with careful ascent and reversible with early recognition and treatment. Small randomized trials have shown that when started one day before ascent, prophylactic dexamethasone, nifedipine (Procardia), salmeterol (Serevent), and phosphodiesterase-5 inhibitors (tadalafil [Cialis], sildenafil [Viagra]) reduce the incidence of high-altitude pulmonary edema in persons with a history of the condition, whereas acetazolamide does not. No comparative studies have shown one type of prophylactic agent to be superior to another. Case reports consistently show that supplemental oxygen, relative rest, and descent lead to improvement in persons with high-altitude pulmonary edema. Immediate descent is the treatment of choice. Supplemental oxygen may be administered if available, and simulated descent by placing the patient in a portable hyperbaric chamber may be helpful temporarily. When descent is not possible, limited evidence suggests that treatment with acetazolamide, bed rest, nifedipine, supplemental oxygen, salmeterol, or phosphodiesterase-5 inhibitors may improve oxygen saturation and pulmonary edema. There is no strong evidence that medications improve outcomes or facilitate resolution of high-altitude pulmonary edema better than descent alone.

Other High-Altitude Medical Conditions

A dry cough in the absence of other symptoms of high-altitude pulmonary edema is common at high altitudes, and can be severe enough to cause extreme discomfort or rib fractures. The cause of high-altitude bronchitis and cough is likely multifactorial, consisting of a combination of irritation of the respiratory cilia and mucosa, rhinorrhea resulting in mouth breathing, bronchoconstriction, respiratory tract infection, and minimal amounts of pulmonary edema. Breathing through a face mask or sucking on candy is recommended to alleviate cough. Peripheral edema, which rarely signals significant disease, is also associated with high altitudes. It is usually transient, resolves with descent, and can be controlled with diuretics, if needed. High-altitude retinopathy is a common, typically benign condition that is thought to be caused by increased retinal blood flow in response to hypoxic conditions at altitudes above 16,400 ft (5,000 m). Although usually asymptomatic, it may be associated with other altitude-related illnesses and may predict acute mountain sickness and high-altitude cerebral and pulmonary edema. Ultraviolet keratitis (snow blindness), which results from corneal epithelial injury from ultraviolet radiation exposure, is another common condition at high altitudes, and may be disabling. Wearing ultraviolet-protectant sunglasses with large lenses and side shields is recommended when traveling in snowy conditions at high altitudes. Treatment is aimed at decreasing pain and preventing infection while the corneal epithelium heals. Medications include nonsteroidal anti-inflammatory drugs and other analgesics, ophthalmic antibiotics, and topical cycloplegics. Ophthalmic nonsteroidal anti-inflammatory drugs are effective analgesics for corneal abrasions and do not interfere with the healing process. Contact lenses, if used, should be removed, and the affected eye is often patched. Climbers who have undergone radial keratotomy are at risk of severe and sudden refractive shift; however, persons who have had photorefractive keratectomy do not seem to be at risk.

How to treat HACE (High Altitude Cerebral Edema)?

§   A person with HACE MUST go down to a lower altitude. Oxygen therapy should be started if available

§   Dexamethasone, a steroid medication can improve HACE symptoms.

§   If a person cannot descend due to weather or other conditions, then hyperbaric therapy with a Gamow bag or other hyperbaric bag should be initiated, if available.

Acute Altitude Exposure and Chronic Illness

Chronic medical conditions may worsen as elevation increases and arterial oxygen saturation decreases. Therefore, certain conditions (e.g., pulmonary hypertension, severe chronic obstructive pulmonary disease, uncontrolled congestive heart failure) are contraindications to high altitudes. With the exception of chronic obstructive pulmonary disease, these conditions do not increase the risk of acute mountain sickness. Changes in barometric pressure also affect persons with pre-existing hypertension, coronary artery disease, and arrhythmias. Despite the additional stress that high altitudes pose to the cardiovascular system, activity restriction is not justified in patients with stable coronary artery disease. Acute mountain sickness, high-altitude cerebral edema, and high-altitude pulmonary edema can exacerbate cardiovascular instability; informing patients about the warning signs of these conditions is important. Proper acclimatization and appropriate prophylaxis are advised. Patients with sickle cell disease are at increased risk of splenic infarct and complications of sickle cell crisis at altitudes of 4,900 ft (1,500 m) or greater. Treatment of sickle cell crisis does not differ with elevation, and supplemental oxygen should be readily available. Diabetes mellitus, especially type 1 diabetes, presents a unique challenge to the physician counseling a patient traveling to a high altitude. Although there is no increased risk of altitude illness in climbers with diabetes, they must be aware of the potential for glycemic management issues that can be complicated by being in a remote—and often very cold—environment. Glucose meters may not function properly at high altitudes or in cold environments.

Chronic Conditions Affected by Altitude Exposure

(Source: American Family Physician, Volume 82, Number 9, November 1, 2010, www.aafp.org/afp; Basnyat B, Murdoch DR. High-altitude illness.  Lancet. 2003;361(9373):1967-1974; Hackett PH, Roach RC. High-altitude illness.  N Engl J Med. 2001;345(2):107-114; Mader TH, Blanton CL, Gilbert BN, et al. Refractive changes during 72-hour exposure to high altitude after refractive surgery. Ophthalmology. 1996;103(8):1188-1195; Green RL, Huntsman RG, Serjeant GR. The sickle-cell and altitude. Br Med J. 1971;4(5787):593-595)

 

Altitude Sickness Prevention

Altitude sickness is preventable. The body needs time to adjust to high altitude. Physical conditioning has no bearing on this.

·            For people who do not know the rate at which their bodies adjust to high altitude, the following preventive measures are recommended.

o   If traveling by air to a ski area above 8,250 feet (2,500 meters), incorporate a layover of 1-2 days at an intermediate altitude.

o   Avoid physical exertion for the first 24 hours.

o   Drink plenty of fluids, and avoid alcoholic beverages.

o   Consume a high-carbohydrate diet.

o   If mountain climbing or hiking, ascend gradually once past 8,000 feet (2,400 meters) above sea level

o   Increase the sleeping altitude by no more than 1,000 feet (300 meters) per 24 hours. The mountaineer’s rule is “climb high, sleep low.” This means that on layover days, a climber can ascend to a higher elevation during the day and return to a lower sleeping elevation at night. This helps to hasten acclimatization.

·            The doctor may prescribe acetazolamide (Diamox) to prevent acute altitude sickness. This medication speeds acclimatization.

·            If rapid ascent is unavoidable, as in rescue missions, or if a person is prone to developing HAPE, the doctor may also prescribe nifedipine (Procardia). Nifedipine is normally used to treat high blood pressure.

·            Prevention of high altitude cerebral edema (HACE) is the same as for acute altitude sickness.

 

HIGH ALTITUDE PULMONARY EDEMA: A CASE REPORT

Wei-Ber Liao, Hui-CHung Yang, Mei-CHaan Ku, JYi-JYH Hung

From the

Department of Emergency Medicine, Department of Internal Medicine, Department of Medicine Imaging, Saint Mary’s Hospital, Luodong

Address reprint requests and correspondence: Dr. Wei-Ber Liao

Department of Emergency Medicine, Saint Mary’s Hospital, Luodong

160 Chongcheng South Road, Luodong Township, Yilan County 265, Taiwan (R.O.C.)

Tel: (03)9544106 ext 7001   Fax: (03)9575653

E-mail: [email protected]

A 46 year old man was mountain climbing with his colleagues for 4 days, averaging 600 to 800 meters per day. They reached the summit at 3742 meters on the 4th day, but after 20 minutes, high winds forced them to descend to a mountain cabin at 2600 meters where they stayed overnight. That night, he became dyspneic and coughed out yellowish fluid, unrelieved by intake of ginger soup. The following morning he was too weak to move and was carried down to 2000 meters by his companions. Emergency Medical Technician (EMT) personnel arrived after two hours and he was carried  down the trail and taken to the emergency room (ER) of our hospital. On initial assessment by EMT personnel at 2000 meters, his pulse was 92 beats per minute (bpm), respiratory rate was 21 /min and blood pressure was 178/125 mmHg, and he was noted to be febrile. Upon arrival in the ER, he was tachypneic with a respiratory rate of 38/min, pulse of 115 bpm , and blood pressure of 241/202 mmHg, His body temperature was 39.9 and coarse rales were heard over both lung fields. Pertinent past history revealed that this patient had two previous episodes of high altitude sickness. Meanwhile, his chest radiograph revealed massive left lung infiltration (Fig. 1A), prompting immediate admission to the intensive care unit (ICU).

In the ICU, he was immediately intubated (Fig. 1B) and light amber fluid was obtained. His SpO2 dropped from an initial 91% to 70%. Manual ventilation with a bag valve mask raised the SpO2 back to 90% afterwhich he was connected to a ventilator. His initial arterial blood gas (ABG) resul ts were pH: 7.384, PCO2: 29.9 mmHg, PO2: 52.8 mmHg, HCO3-: 17.5 mEq/L, SBE: -6.6 mEq/L, and SO2%: 88.9; Other tests conducted included complete blood count with differential which showed leucocytosis WBC: 23,270/μL with 90.4% segments; RBC: 6.32 × 106/μL, Hgb: 19.5 g/dl, Hct: 57.4%. while other biochemistry tests included CRP: 7.00 mg/dl. Glucose 198 mg/dl, GOT 37 IU/L, Bil T/D: 1.5/0.2 mg/dl, NH3: 53 umol/L, Alb: 3.5 g/dl, BUN: 27 mg/dl, Cr 1.2 mg/dl, Na: 143 mEq/L, K: 3.9 mEq/L, and Ca: 7.7 mg/dl. His initial electrocardiogram (EKG) showed persistent RV-strain (Fig. 2A). A cardiac B-mode echocardiogram showed a flattened interventricular septum (D-shaped left ventricle) with normal left ventricular function. PiCCO parameters were as follows:

The patient had persistent high grade fever >39 so antimicrobial therapy with Moxifloxacin (Avelox) 400 mg once a day was started but later shifted to Piperacillin/Tazobactam (Tazocin) 4.5 g every 8 hours, Amikacin(Amikin) 250 mg every 12 hours and Doxycycline 100 mg once a day on his third hospital day (HD). Doxycycline was continued until he was discharged. He was also given Furosemide (Lasix) 40 mg intravenously every 8 h), Acetazolamide (Diamox) 250 mg every 6 hours. On his 2nd hospital day, (HD), chest radiograph showed slight resolution of the butterfly appearance (Fig. 1C) .On his 3rd HD, Furosemide (20 mg/amp) was tapered to 1 amp every 8 hours, Oral Acetazolamide (Diamox) 250 mg/tab 1 tablet twice a day & Dobutamine 250 mg were also added thus he was successfully extubated bringing about improvement in his clinical condition. (Fig. 1D).Normal findings found radiographically on his 4th HD while ABG results were pH: 7.46, PCO2: 23.5 mmHg, PO2: 86.3 mmHg, HCO3-: 16.9 mEq/L, SBE: -7.2 mEq/L, A-aDO2: 34.4 mm Hg, and SpO2%: 97.2. Furosemide was discontinued while Acetazolamide was tapered to 250 mg every 12 hours. Hypertension was treated with Nifedipine(Adalat) 5 mg every 8 hours. On his 5th HD, the EKG showed S1Q3T3 with an Incomplete right bundle branch pattern (Fig. 2B) and no pulmonary embolus seen on computerized chest tomography. Serum chloride level   was found to be  100 mEq/L and was corrected with 250 cc normal saline . ABGs on his 6th HD  were pH: 7.445, PCO2: 32.4 mmHg, PO2: 109.7 mmHg, SpO2%: 98.4%, HCO3-: 22.5 mEq/L, and SBE: -1.8 mEq/L. He was clinically stable until his discharge on the 8th HD. Complete blood count at discharge were WBC: 22,540/μL, segmenters: 91.0%; RBC: 4.95 x 106/μL,  and Hemoglobin: 15.1 g/dl. and CRP < 0.5 mg/dl. Two weeks later, on his out patient follow-up complete blood count results  were  WBC: 6.05x 103/μL, segmenters: 72.2%; RBC: 4.05 x106/μL, and Hemoglobin: 12.7 g/dl.

Fig. 1  A.  Left hilar area shows a more severe patchy infiltrations than the right side with massive alveolar infiltration extending to the periphery. There is no noticeable Kerley B line over the costophrenic angle nor any visible vessels along the outer third of the lungs. These findings are consistent with non-cardiogenic pulmonary edema. Fig. 1  B.  Four hours after intubation, there is increased density over the left hilar area and infiltration  in the right upper lung. Fig. 1  C.  On the second day after intubation, the butterfly appearance is less severe. Fig. 1  D.  The first day after extubation, the butterfly appearance has resolved

Fig. 2  A.  Electrocardiogram (ECG) on admission shows tachycardia, poor R wave progression over the precordial leads, clockwise rotation, left axis deviation and low voltage over the limb leads.

Fig. 2  B.  ECG on the 5th ICU day shows  sinus rhythm with a S1Q3T3 pattern, incomplete right bundle branch block and a flattened T wave.

Discussion

Severe high altitude sickness  starts at an altitude above 2,100 meters because arterial blood oxygen saturation drops to less than 90% at this height (majority of cases occur at heights between 2400 to 3600 meters). Variable factors such as speed of ascent, the final altitude, rest time in between climbs and individual susceptibility affect its occurrence. Despite taking a Chinese herbal drug (Hung jin tian) as prophylaxis before climbing, he still suffered from HAPE. A previous history of high altitude sickness predicts its recurrence.

High altitude sickness develops because of hypoxic pulmonary vasoconstrict ion inducing further pulmonary hypertension and pulmonary edema. When pulmonary edema ensues, pulmonary artery pressure usually rises to levels greater than 20 mmHg which is 30% to 50% higher than that among those wi thout pulmonary edema. Meanwhile, myocardial blood flow reserve also decreases bringing about further RV strain.  This patient had persistent RV strain and S1Q3T3 with an ICRBBB pattern on EKG, although the EKG pattern returned to normal after one week. HAPE occurs because of hypoxic vasoconstriction of the pulmonary artery and permeability changes in pulmonary vessels leading to acute pulmonary edema. This was proven by the PiCCO values of this patient. When he had pulmonary edema, the patient’s PVPI of 4.7 was twice the normal value of 1.8, and the ELWI of 15 was also twice the normal value of 7. Changes in pulmonary permeability bring about fluid shift to the interstitial spaces of the lungs. Hemoconcentration follows as evident by a hemoglobin value over 15 g/dl bringing about inadequate delivery of oxygen to the hypothalamus thus inducing secondary hyperthermia due to thermoregulatory dysfunction. The patient’s body temperature was persistent ly elevated with leucocytosis (WBC >20,000/ul) making us doubt whether there was any underlying bacterial infection.  The CRP level decreased from 7.0 mg/dl on admission to < 0.5 mg/dl after one week. Two weeks later, his WBC count was 6,000/μL and hemoglobin was 12.7 g/dl at the OPD. We presumed his leucocytosis, erythrocytosis and high grade fever were due to hemoconcentration brought about by fluid shift secondary to increased pulmonary permeability.

Although acute mountain sickness does not have the conventional inflammatory response, it can mimic systemic inflammatory response syndrome since it complies with several of its diagnostic criteria such as temperature > 38 (39.9), heart rate > 90 beats/minute (92 beats/minute), respiratory rate > 20 breaths/minute (38 breaths/minute) and high WBC count >12,000/mm3 (WBC count 23,270/mm3). The initial response to acute pulmonary hypertension is increased pulmonary permeability leading to acute pulmonary edema, right ventricular strain, hemoconcentration and hyperthermia. A rising body temperature after rapid ascent to high altitude is an early sign of acute mountain sickness and is also associated with the severity of hypoxemia. This patient’s clinical presentation led us to a better understanding of HAPE and its treatment.

Source: J Emerg Crit Care Med. Vol. 21, No. 1, 2010

DECOMPRESSION SICKNESS

Описание: Описание: https://encrypted-tbn3.gstatic.com/images?q=tbn:ANd9GcR-P1QbmZVtgrnJWyTe8bs4MRbppvOB7HTJzSBlvniEoqF0quDT

Some technology processes are carried out under conditions of heightened atmospheric pressure. For example, a drifting of horizontal and vertical underground excavations through watered seams or fulfillment of work under water that is possible only under condition of water forcing out from an air working chamber using compressed air. Pneumatic work is performed in special units named torsion boxes and they are most widespread at building bridges and dams, foundations under various facilities, tunnels, undergrounds, in coal and mining industry and so on. Influence of heightened atmospheric pressure is testing with help of divers and scuba diving. The caisson disease is a pathological condition that develops owing to formation of gas bubbles in blood and tissues in case of decrease of external respiration (in a man on leaving caisson and emergence).

A risk factor is something that increases your chance of getting a disease or condition. The only risk factor for decompression sickness is a sudden reduction in pressure. This occurs as a result of:

§  Rising too quickly to the surface from deep sea scuba diving

§  A fast ascent into a high altitude from a low altitude

§  Sudden exit from a high pressure or hyperbaric chamber

§  Increased risk with increased depth of dive

§  Long duration of dive

§  Multiple dives in one day

§  Flying after diving

§  Diving in cold water

§  Fatigue

§  Exertion

§  Dehydration

§  Obesity

§  Increased age

Etiology and pathogenesis.

Decompression Sickness

Описание: Описание: Decompression Sickness

Photo illustrating Decompression Sickness

Decompression Sickness

Problems resulting from nitrogen leaving the body when ambient pressure is lowered i.e. coming up.

 From: http://www.gooddive.com/scuba-diving-glossary/decompression-sickness.htm

Caisson sickness is a consequence of transition of gases of blood and tissues from dissolved condition in free one – similar to gas – in case of decrease of environment atmospheric pressure. At that, gas bubbles are formed, they destroy normal blood circulation, stimulate nervous endings, deform and damage tissues of organism. Main part of general pressure of gases in lungs and consequently blood and tissues falls on a portion of nitrogen, a physiologically inert gas that does not take participation in gaseous exchanges. High partial pressure of nitrogen in lungs, its physiology and non-reactivity predetermine its basic role in formation of gas bubbles in case of decompression development. Term of dynamic balance recovery for various tissues of organism is unequal at change of nitrogen partial pressure in external and alveolar air. Blood, lymph and tissues, which perfuse well, are saturated faster and destroy it. Dynamic balance of gas becomes broken, tissues and liquid of organism become oversaturated with gases first of all by nitrogen at lowering of pressure of environment (when a worker leaves a caisson box, at ascent from depth onto surface). Process of excess nitrogen removal from tissues before arrangement of a new gas balance at sluggish decompression usually flows without formation of gas bubbles. Oversaturation of tissues with gases reaches a critical level in case of fast decompression. Conditions for bubbles formation in tissues and liquids are formed. There are two basic types of bubbles. The first on include bubbles located outside of vessels, formation and return development is determined by process of diffusion – exchange of gases between a bubble and medium that surrounds it. The bubbles located inside tissues, definitely refer to this type. They are capable to enlarge and press on tissues that surround them, causing their deformation, and that invokes sensation of pain in patients. Mechanism of development of sensations of muscular-articular decompression pain at patients has such characteristics.

Описание: Описание: Bone x-rays that show the effects of  rapid decompression on the body. Left=normal bone, right=bone with bubble.

Bone x-rays that show the effects of rapid decompression on the body. Left=normal bone, right=bone with bubble.

The second type involves gas bubbles, evolution of which is conditioned not only by processes of diffusion, but also by junction of one bubble with another or, to the contrary, by its splitting into even finer bubbles. They join one another, being formed in venous channel, that gives possibility for acute aeroembolism development in circulatory system.

 

Pathologic and anatomic picture. The most expressed and specific morphological manifestations in case of fast death from a high-gravity decompression disease are availability of numerous bubbles in venous system, a right half of heart overflowed and spread by gas bubbles, phenomenon of edema and emphysema of lungs, numerous zones of hemorrhages in various organs and tissues.


Описание: Описание: http://www.aafp.org/afp/2001/0601/afp20010601p2211-f1.jpg


FIGURE 1.

Experimental preparation of decompression illness (i.e., cerebral decompression sickness and arterial gas embolism) demonstrating the presence of bubbles passing within vasculature of the cortical subarachnoid space (arrow). Note the regions of surface hemorrhage (upper right) on surrounding gyri.

From http://www.aafp.org/afp/2001/0601/p2211.html

Clinic. Three degrees of gravity of a decompression sickness are marked out: mild, mean and high-gravity. Itch of skin, eruption, non-acute pain in muscles, bones, joints and along nerve trunk is characteristic for the mild degree. More often, continuous pain arises in one or several joints of extremities, in particular in knees, shoulders, and also in radiocarpal, elbow joints and ankles. The pain has no concrete localization. Most of all it is felt around of joint, being diffused to all directions from it. The pain, as a rule, strengthens at palpation of joint and bending of extremities. Joints and muscles experiencing the greatest physical loadings are involved in the process most often. Itch of skin is felt on a body or on proximal segments of extremities. It reminds itch of skin after a bite of an insect. Some portions of skin have mottled pattern due to skin vascular

embolism. Gas accumulation in hypodermic gives start to development of hypodermic emphysema. The disease of the mean degree of gravity is characterized by disease of an internal ear, gastrointestinal tract and organ of sight. First of all syndrome Menyera is formed as a result of gas bubbles origination in labyrinth of internal ear. Acute weakness, gravity and headaches are watched in a clinical picture. These signs integrates with a loss of consciousness, vomiting, buzzing in the ears, and decrease of hearing. Strong paleness of dermal covers, heightened hidrosis appears. Patients complain that all subjects are revolved before eyes; a minor turn of head strengthens agonizing sensations.

Livedo reticularis (cutis marmorata) due to decompression sickness in a recreational diver

This rash occurring after a dive is uncommon but almost pathognomonic of decompression sickness.

Описание: Описание: Figure 3

From http://www.thelancet.com/journals/lancet/article/PIIS0140673610610859/images?imageId=gr3&sectionType=green&hasDownloadImagesLink=true

There is a possibility of consciousness loss. Gastrointestinal lesions are characterized with accumulation of gas in intestines, vessels of mesentery and are accompanied by arise of strong abdominal pain, often defecation. Palpation of abdomen is agonizing; it is strained. Visual acuity is reduced and accompanied by dilatation of pupils and oppression of their reaction on light. The high-gravity degree of caisson sickness is met today seldom. It is characterized by formation of emboluses in vessels of central nervous

system, heart and lungs. Patients complain on general weakness and weakness in legs, sharp coughs, strong pain in thorax, in particular at breathing, asphyxia. Clinical signs of oedema of lungs occur in due course. A significant amount of gas bubbles of different size that produce lesion of cardiovascular activity is accumulated in cavities of right heart and in vessels of lungs in case of originating of multiple aeroembolism. Thus paleness, strong weakness, often and surface breathing is marked in patients: arterial pressure drops. Pulse falls down, dermal covers gain cyanotic tint. Loss of consciousness can be set at expressed phenomena of hypoxia. Myocardial and lung infarction is probable. The cerebral lesions are conditioned by gas emboluses in brain. Weakness, headache arises after a short-lived latent period. Sensitiveness of one half of body disappears in light cases, and phenomena of paralysis arise in more gravity cases: speech is lost; signs of facial nerve paresis and paraparesis of lower extremities appear. It is accompanied by distress of urination and defecation.

The chronic decompression disease is determined. Two forms of it aremarked out: primary and secondary. The primary chronic decompression sickness develops slowly. Deforming osteoarthrosis is the main clinical manifestation of this form. The secondary chronic form represents a complex of pathological changes owing to experienced acute caisson sickness. Its main clinical symptom is aeropathic myelosis and Meniere’s syndrome. At chronic form of the disease, gas embolas are localized in different organs, mainly in bones. At first the clinical picture flows without symptoms both permanent pain symptom and lesion of function of extremities arise only at complication of the process by deforming osteoarthrosis. Head and proximal ending of diaphysis of thigh are violated at the first turn. After that, head and upper part of diaphysis of shoulder, then distal parts of thigh, proximal endings of shinbone, lower endings shoulder and radial bones are struck.

Diagnosis of caisson sickness is established on a basis of the characteristic complaints and clinical symptomatology that come up after decompression. Occurrence of dermal itch, pain sensations, Meniere’s syndrome, paralyses, sudden development of collapse – all this with allowance for the preceding decompression is a direct evidence of caisson sickness.

Treatment. Prehospital Care

·                 Extricate the patient from water and immobilize if trauma is suspected. Generally, in-water recompression is not believed to be a safe option. Problems with air supply, hypothermia, potential oxygen toxicity, dehydration, and the uncontrolled environment make it less than ideal and increase the risks of drowning. However, in remote areas without reasonable-distance HBO chamber support, this may be the only option.

·                 Administer 100% oxygen, intubate if necessary, and intravenously administer saline or lactated Ringer solution.

·                 The use of first aid oxygen has proven so beneficial that the Divers Alert Network (DAN) has made a major effort to place oxygen at dive locations, in particular those that are remote with lengthy transport times to the nearest hyperbaric chambers and to ensure that people are trained in its use. A study of the use of first aid oxygen found that the median time to its use after surfacing was 4 hours and 2.2 hours after the onset of DCS symptoms. Forty-seven percent of victims received the oxygen. Complete relief of symptoms was found in 14% of victims. Even more striking was that 51% of victims showed improvement. This was with the oxygen before HBO treatment. Even after a single HBO treatment, those that had received oxygen before the HBO dive, even if many hours earlier, had better outcomes.

·                 Aspirin is commonly considered and given in diving accidents for antiplatelet activity if the patient is not bleeding. However, there are no current data to support this practice.

·                 Thus far there is no substantive data showing a benefit for other adjunctive treatments, such as recompression with helium/oxygen and NSAIDS

·                 Perform cardiopulmonary resuscitation and advanced cardiac life support, if required, as well as needle decompression of the chest if tension pneumothorax is suspected.

·                 Do not put the patient into the Trendelenburg position. Placing the patient in a head-down posture used to be considered a standard treatment of diving injuries to prevent cerebral gas embolization. This practice should be abandoned. The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier. It also wastes time and complicates movement of the patient.

·                 Transport to the nearest ED and hyperbaric facility, if feasible, and try to keep all diving gear with the diver. Diving gear may provide clues as to why the diver had trouble (eg, faulty air regulator, hose leak, carbon monoxide contamination of compressed air).

Emergency Department Care

·                 Administer 100% oxygen to wash nitrogen out of the lungs and set up an increased diffusion gradient to increase nitrogen offloading from the body.

·                 Do not put the patient into the Trendelenburg position. Placing the patient in a head-down posture used to be considered a standard treatment of diving injuries to prevent cerebral gas embolization. This practice should be abandoned. The process actually increases intracranial pressure and exacerbates injury to the blood-brain barrier. It also wastes time and complicates movement of the patient.

·                 Perform intubation, aggressive resuscitation, and chest tube thoracostomy, if indicated.

·                 Administer intravenous fluids for rehydration until urinary output is 1-2 mL/h. Rehydration improves circulation and perfusion.

·                 Aspirin is commonly considered and given in diving accidents for antiplatelet activity if the patient is not bleeding. However, there are no current data to support this practice.

·                 Treat the patient for nausea, vomiting, pain, and headache.

·                 Contact the closest hyperbaric facility (or DAN for referral) to arrange transfer and try to keep all diving gear with the diver. The diving gear may provide clues as to why the diver had trouble (eg, faulty air regulator, hose leak, carbon monoxide contamination of the compressed air).

·                 Patients with type I or mild type II DCS can dramatically improve and have complete symptom resolution. This improvement should not dissuade the practitioner from HBO referral or transfer, as relapses have occurred with worse outcomes.

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Verification of the ability to work. The sick-leave is given for a period of treatment for 10 days at mild degree of illness. Patient can be temporarily given a work outside of heightened atmospheric pressure and other unfavorable factors operation with issue of a labor sick-leave in case if further treatment in out-patient conditions is necessary. Return the sufferer of caisson sickness of mean gravity to the same work is authorized after a period of temporary incapacity for work. Availability of complications in the form of firm organic changes on the part of organ of sight and gastrointestinal tract leads to a steady disablement with a rather large list of counterindicative kinds of labor activity.

The labor forecast at a high-gravity degree of a caisson illness is always unfavorable. It is necessary to send patients on commissioning for disablement degree definition and rehabilitational measures elaboration.

Preventive measures. The warning of decompression disease is envisioned, first of all, by observance of rules of work in caisson-box. So, the maximal pressure during their realization should not exceed 3.9 atm. A working day in a caisson box is divided on two parts with a rest between them not less than 9-10 hours outside of a caisson box. General number of working hours during a day, including time of locking and unlocking, is ranged from 6 h till 2 h 40 minutes depending on pressure in a caisson box. Breathing with oxygen, struggle against overcooling of workers is a preventive action against caisson sickness. An ambulatory or a medicine post with a day-night duty of medical staff is organized for the well-timed and qualified health services on each site of construction where the caisson work is realized. Isolation ward on the occasion of a decompression sickness, medical airlock can be at a medical center. Persons permitted to decompression and diving jobs should pass preliminary medical examination. Contraindications for admittance for these jobs is hypertensive disease, pulmonary tuberculosis, respiratory tract lesion of not tubercular etiology, peptic ulcer of ventricles and duodenum, illness of nephroses and urinary bladder, diabetes mellitus, and excessive stoutness. All people working in a caisson box are subject to weekly medical examination with participation of doctor – therapeutist and otolaryngologist.

 

REFERENCES

1.                          1. Davidson’s Principles and practice of medicine (21st revised ed.) / by Colledge N.R., Walker B.R., and Ralston S.H., eds. – Churchill Livingstone, 2010. – 1376 p.

2.                          Harrison’s principles of internal medicine (18th edition) / by Longo D.L., Kasper D.L., Jameson J.L. et al. (eds.). – McGraw-Hill Professional, 2012. – 4012 p.

3. The Merck Manual of Diagnosis and Therapy / Edited by Robert S. Porter., 19th Revised edition. London: Elsevier Health Sciences, 2011. – 3754 p.

4. Kostyuk I. and Kapustnyk V. Translated from the Ukrainian by Occupational Diseases: Manual. – Kharkiv: Osnova, 2005. – 400 p.

5. Second national report on human exposure to environmental chemicals. Atlanta: Centers for Disease Control and Prevention, 2003. (Accessed October 6, 2003, at http:// www.cdc.gov/exposurereport/.

6. ABC of occupational and environmental medicine. Second edition / edited by David Snashall. – 2003. – p. 177-223.

7. Kuziv P.P., Bodnar L. P., Pokynchereda V.V. Professional diseases. – Ternopil, 2003. – 296 p.

8. K. Park. Park’s textbook of preventive and social medicine. – India. – 2005. – 711p.

9. Kostyuk I. and Kapustnyk V. Translated from Ukrainian. Occupational Diseases: Manual.- Kharkiv: Osnova, 2004.- 400 p.

10.                      Web -sites:

a)                          http://emedicine.medscape.com/

b)                         http://meded.ucsd.edu/clinicalmed/introduction.htm

c) http://www.cdc.gov

 

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