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36. Barometric Pressure Increased

36. Barometric Pressure Increased (2)

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36. Barometric Pressure Increased


Chapter Editor: T.J.R. Francis


Table of Contents



Working under Increased Barometric Pressure

Eric Kindwall


Decompression Disorders

Dees F. Gorman



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1. Instructions for compressed-air workers
2. Decompression illness: Revised classification

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37. Barometric Pressure Reduced

37. Barometric Pressure Reduced (4)

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37. Barometric Pressure Reduced

Chapter Editor:  Walter Dümmer

Table of Contents

Figures and Tables

Ventilatory Acclimatization to High Altitude
John T. Reeves and John V. Weil

Physiological Effects of Reduced Barometric Pressure
Kenneth I. Berger and William N. Rom

Health Considerations for Managing Work at High Altitudes
John B. West

Prevention of Occupational Hazards at High Altitudes
Walter Dümmer


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38. Biological Hazards

38. Biological Hazards (4)

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38. Biological Hazards

Chapter Editor: Zuheir Ibrahim Fakhri

Table of Contents


Workplace Biohazards
Zuheir I. Fakhri

Aquatic Animals
D. Zannini

Terrestrial Venomous Animals
J.A. Rioux and B. Juminer

Clinical Features of Snakebite
David A. Warrell


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1. Occupational settings with biological agents
2. Viruses, bacteria, fungi & plants in the workplace
3. Animals as a source of occupational hazards

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39. Disasters, Natural and Technological

39. Disasters, Natural and Technological (12)

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39. Disasters, Natural and Technological

Chapter Editor: Pier Alberto Bertazzi

Table of Contents

Tables and Figures

Disasters and Major Accidents
Pier Alberto Bertazzi

     ILO Convention concerning the Prevention of Major Industrial Accidents, 1993 (No. 174)

Disaster Preparedness
Peter J. Baxter

Post-Disaster Activities
Benedetto Terracini and Ursula Ackermann-Liebrich

Weather-Related Problems
Jean French

Avalanches: Hazards and Protective Measures
Gustav Poinstingl

Transportation of Hazardous Material: Chemical and Radioactive
Donald M. Campbell

Radiation Accidents
Pierre Verger and Denis Winter

     Case Study: What does dose mean?

Occupational Health and Safety Measures in Agricultural Areas Contaminated by Radionuclides: The Chernobyl Experience
Yuri Kundiev, Leonard Dobrovolsky and V.I. Chernyuk

Case Study: The Kader Toy Factory Fire
Casey Cavanaugh Grant

Impacts of Disasters: Lessons from a Medical Perspective
José Luis Zeballos






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1. Definitions of disaster types
2. 25-yr average # victims by type & region-natural trigger
3. 25-yr average # victims by type & region-non-natural trigger
4. 25-yr average # victims by type-natural trigger (1969-1993)
5. 25-yr average # victims by type-non-natural trigger (1969-1993)
6. Natural trigger from 1969 to 1993: Events over 25 years
7. Non-natural trigger from 1969 to 1993: Events over 25 years
8. Natural trigger: Number by global region & type in 1994
9. Non-natural trigger: Number by global region & type in 1994
10. Examples of industrial explosions
11. Examples of major fires
12. Examples of major toxic releases
13. Role of major hazard installations management in hazard control
14. Working methods for hazard assessment
15. EC Directive criteria for major hazard  installations
16. Priority chemicals used in identifying major hazard installations
17. Weather-related occupational risks
18. Typical radionuclides, with their radioactive half-lives
19. Comparison of different nuclear accidents
20. Contamination in Ukraine, Byelorussia & Russia after Chernobyl
21. Contamination strontium-90 after the Khyshtym accident (Urals 1957)
22. Radioactive sources that involved the general public
23. Main accidents involving industrial irradiators
24. Oak Ridge (US) radiation accident registry (worldwide, 1944-88)
25. Pattern of occupational exposure to ionizing radiation worldwide
26. Deterministic effects: thresholds for selected organs
27. Patients with acute irradiation syndrome (AIS) after Chernobyl
28. Epidemiological cancer studies of high dose external irradiation
29. Thyroid cancers in children in Belarus, Ukraine & Russia, 1981-94
30. International scale of nuclear incidents
31. Generic protective measures for general population
32. Criteria for contamination zones
33. Major disasters in Latin America & the Caribbean, 1970-93
34. Losses due to six natural disasters
35. Hospitals & hospital beds damaged/ destroyed by 3 major disasters
36. Victims in 2 hospitals collapsed by the 1985 earthquake in Mexico
37. Hospital beds lost resulting from the March 1985 Chilean earthquake
38. Risk factors for earthquake damage to hospital infrastructure



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40. Electricity

40. Electricity (3)

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40. Electricity

Chapter Editor:  Dominique Folliot



Table of Contents 

Figures and Tables

Electricity—Physiological Effects
Dominique Folliot

Static Electricity
Claude Menguy

Prevention And Standards
Renzo Comini


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1. Estimates of the rate of electrocution-1988
2. Basic relationships in electrostatics-Collection of equations
3. Electron affinities of selected polymers
4. Typical lower flammability limits
5. Specific charge associated with selected industrial operations
6. Examples of equipment sensitive to electrostatic discharges


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41. Fire

41. Fire (6)

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41. Fire

Chapter Editor:  Casey C. Grant


Table of Contents 

Figures and Tables

Basic Concepts
Dougal Drysdale

Sources of Fire Hazards
Tamás Bánky

Fire Prevention Measures
Peter F. Johnson

Passive Fire Protection Measures
Yngve Anderberg

Active Fire Protection Measures
Gary Taylor

Organizing for Fire Protection
S. Dheri


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1. Lower & upper flammability limits in air
2. Flashpoints & firepoints of liquid & solid fuels
3. Ignition sources
4. Comparison of concentrations of different gases required for inerting


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42. Heat and Cold

42. Heat and Cold (12)

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42. Heat and Cold

Chapter Editor:  Jean-Jacques Vogt


Table of Contents 

Figures and Tables

Physiological Responses to the Thermal Environment
W. Larry Kenney

Effects of Heat Stress and Work in the Heat
Bodil Nielsen

Heat Disorders
Tokuo Ogawa

Prevention of Heat Stress
Sarah A. Nunneley

The Physical Basis of Work in Heat
Jacques Malchaire

Assessment of Heat Stress and Heat Stress Indices
Kenneth C. Parsons

     Case Study: Heat Indices: Formulae and Definitions

Heat Exchange through Clothing
Wouter A. Lotens

     Formulae and Definitions

Cold Environments and Cold Work
Ingvar Holmér, Per-Ola Granberg and Goran Dahlstrom

Prevention of Cold Stress in Extreme Outdoor Conditions
Jacques Bittel and Gustave Savourey

Cold Indices and Standards
Ingvar Holmér


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1. Electrolyte concentration in blood plasma & sweat
2. Heat Stress Index & Allowable Exposure Times: calculations
3. Interpretation of Heat Stress Index values
4. Reference values for criteria of thermal stress & strain
5. Model using heart rate to assess heat stress
6. WBGT reference values
7. Working practices for hot environments
8. Calculation of the SWreq index & assessment method: equations
9. Description of terms used in ISO 7933 (1989b)
10. WBGT values for four work phases
11. Basic data for the analytical assessment using ISO 7933
12. Analytical assessment using ISO 7933
13. Air temperatures of various cold occupational environments
14. Duration of uncompensated cold stress & associated reactions
15. Indication of anticipated effects of mild & severe cold exposure
16. Body tissue temperature & human physical performance
17. Human responses to cooling: Indicative reactions to hypothermia
18. Health recommendations for personnel exposed to cold stress
19. Conditioning programmes for workers exposed to cold
20. Prevention & alleviation of cold stress: strategies
21. Strategies & measures related to specific factors & equipment
22. General adaptational mechanisms to cold
23. Number of days when water temperature is below 15 ºC
24. Air temperatures of various cold occupational environments
25. Schematic classification of cold work
26. Classification of levels of metabolic rate
27. Examples of basic insulation values of clothing
28. Classification of thermal resistance to cooling of handwear
29. Classification of contact thermal resistance of handwear
30. Wind Chill Index, temperature & freezing time of exposed flesh
31. Cooling power of wind on exposed flesh


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43. Hours of Work

43. Hours of Work (1)

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43. Hours of Work

Chapter Editor:  Peter Knauth


Table of Contents 

Hours of Work
Peter Knauth


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1. Time intervals from beginning shiftwork until three illnesses
2. Shiftwork & incidence of cardiovascular disorders


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44. Indoor Air Quality

44. Indoor Air Quality (8)

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44. Indoor Air Quality

Chapter Editor:  Xavier Guardino Solá


Table of Contents 

Figures and Tables

Indoor Air Quality: Introduction
Xavier Guardino Solá

Nature and Sources of Indoor Chemical Contaminants
Derrick Crump

María José Berenguer

Tobacco Smoke
Dietrich Hoffmann and Ernst L. Wynder

Smoking Regulations
Xavier Guardino Solá

Measuring and Assessing Chemical Pollutants
M. Gracia Rosell Farrás

Biological Contamination
Brian Flannigan

Regulations, Recommendations, Guidelines and Standards
María José Berenguer


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1. Classification of indoor organic pollutants
2. Formaldehyde emission from a variety of materials
3. Ttl. volatile organic comp’ds concs, wall/floor coverings
4. Consumer prods & other sources of volatile organic comp’ds
5. Major types & concentrations in the urban United Kingdom
6. Field measurements of nitrogen oxides & carbon monoxide
7. Toxic & tumorigenic agents in cigarette sidestream smoke
8. Toxic & tumorigenic agents from tobacco smoke
9. Urinary cotinine in non-smokers
10. Methodology for taking samples
11. Detection methods for gases in indoor air
12. Methods used for the analysis of chemical pollutants
13. Lower detection limits for some gases
14. Types of fungus which can cause rhinitis and/or asthma
15. Micro-organisms and extrinsic allergic alveolitis
16. Micro-organisms in nonindustrial indoor air & dust
17. Standards of air quality established by the US EPA
18. WHO guidelines for non-cancer and non-odour annoyance
19. WHO guideline values based on sensory effects or annoyance
20. Reference values for radon of three organizations


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47. Noise

47. Noise (5)

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47. Noise

Chapter Editor:  Alice H. Suter


Table of Contents 

Figures and Tables

The Nature and Effects of Noise
Alice H. Suter

Noise Measurement and Exposure Evaluation
Eduard I. Denisov and German A. Suvorov

Engineering Noise Control
Dennis P. Driscoll

Hearing Conservation Programmes
Larry H. Royster and Julia Doswell Royster

Standards and Regulations
Alice H. Suter


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1. Permissible exposure limits (PEL)for noise exposure, by nation


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48. Radiation: Ionizing

48. Radiation: Ionizing (6)

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48. Radiation: Ionizing

Chapter Editor:  Robert N. Cherry, Jr.


Table of Contents

Robert N. Cherry, Jr.

Radiation Biology and Biological Effects
Arthur C. Upton

Sources of Ionizing Radiation
Robert N. Cherry, Jr.

Workplace Design for Radiation Safety
Gordon M. Lodde

Radiation Safety
Robert N. Cherry, Jr.

Planning for and Management of Radiation Accidents
Sydney W. Porter, Jr.

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Tuesday, 15 February 2011 19:36

Working Under Increased Barometric Pressure

Written by

The atmosphere normally consists of 20.93% oxygen. The human body is naturally adapted to breathe atmospheric oxygen at a pressure of approximately 160 torr at sea level. At this pressure, haemoglobin, the molecule which carries oxygen to the tissue, is approximately 98% saturated. Higher pressures of oxygen cause little important increase in oxyhaemoglobin, since its concentration is virtually 100% to begin with. However, significant amounts of unburnt oxygen may pass into physical solution in the blood plasma as the pressure rises. Fortunately, the body can tolerate a fairly wide range of oxygen pressures without appreciable harm, at least in the short term. Longer term exposures may lead to oxygen toxicity problems.

When a job requires breathing compressed air, as in diving or caisson work, oxygen deficiency (hypoxia) is rarely a problem, as the body will be exposed to an increasing amount of oxygen as the absolute pressure rises. Doubling the pressure will double the number of molecules inhaled per breath while breathing compressed air. Thus the amount of oxygen breathed is effectively equal to 42%. In other words, a worker breathing air at a pressure of 2 atmospheres absolute (ATA), or 10 m beneath the sea, will breathe an amount of oxygen equal to breathing 42% oxygen by mask on the surface.

Oxygen toxicity

On the earth’s surface, human beings can safely continuously breathe 100% oxygen for between 24 and 36 hours. After that, pulmonary oxygen toxicity ensues (the Lorrain-Smith effect). The symptoms of lung toxicity consist of substernal chest pain; dry, non-productive cough; a drop in the vital capacity; loss of surfactant production. A condition known as patchy atelectasis is seen on x-ray examination, and with continued exposure microhaemorrhages and ultimately production of permanent fibrosis in the lung will develop. All stages of oxygen toxicity through the microhaemorrhage state are reversible, but once fibrosis sets in, the scarring process becomes irreversible. When 100% oxygen is breathed at 2 ATA, (a pressure of 10 m of sea water), the early symptoms of oxygen toxicity become manifest after about six hours. It should be noted that interspersing short, five-minute periods of air breathing every 20 to 25 minutes can double the length of time required for symptoms of oxygen toxicity to appear.

Oxygen can be breathed at pressures below 0.6 ATA without ill effect. For example, a worker can tolerate 0.6 atmosphere oxygen breathed continuously for two weeks without any loss of vital capacity. The measurement of vital capacity appears to be the most sensitive indicator of early oxygen toxicity. Divers working at great depths may breathe gas mixtures containing up to 0.6 atmospheres oxygen with the rest of the breathing medium consisting  of  helium  and/or  nitrogen.  Six  tenths  of  an atmosphere corresponds to breathing 60% oxygen at 1 ATA or at sea level.

At pressures greater than 2 ATA, pulmonary oxygen toxicity no longer becomes the primary concern, as oxygen can cause seizures secondary to cerebral oxygen toxicity. Neurotoxicity was first described by Paul Bert in 1878 and is known as the Paul Bert effect. If a person were to breathe 100% oxygen at a pressure of 3 ATA for much longer than three continuous hours, he or she will very likely suffer a grand mal seizure. Despite over 50 years of active research as to the mechanism of oxygen toxicity of the brain and lung, this response is still not completely understood. Certain factors are known, however, to enhance toxicity and to lower the seizure threshold. Exercise, CO2 retention, use of steroids, presence of fever, chilling, ingestion of amphetamines, hyperthyroidism and fear can have an oxygen tolerance effect. An experimental subject lying quietly in a dry chamber at pressure has much greater tolerance than a diver who is working actively in cold water underneath an enemy ship, for example. A military diver may experience cold, hard exercise, probable CO2 build-up using a closed-circuit oxygen rig, and fear, and may experience a seizure within 10-15 minutes working at a depth of only 12 m, whereas a patient lying quietly in a dry chamber may easily tolerate 90 minutes at a pressure of 20 m without great danger of seizure. Exercising divers may be exposed to partial pressure of oxygen up to 1.6 ATA for short periods up to 30 minutes, which corresponds to breathing 100% oxygen at a depth of 6 m. It is important to note that one should never expose anyone to 100% oxygen at a pressure greater than 3 ATA, nor for a time longer than 90 minutes at that pressure, even with a subject quietly recumbent.

There is considerable individual variation in susceptibility to seizure between individuals and, surprisingly, within the same individual, from day to day. For this reason, “oxygen tolerance” tests are essentially meaningless. Giving seizure-suppressing drugs, such as phenobarbital or phenytoin, will prevent oxygen seizures but do nothing to mitigate permanent brain or spinal cord damage if pressure or time limits are exceeded.

Carbon monoxide

Carbon monoxide can be a serious contaminant of the diver’s or caisson worker’s breathing air. The most common sources are internal combustion engines, used to power compressors, or other operating machinery in the vicinity of the compressors. Care should be taken to be sure that compressor air intakes are well clear of any sources of engine exhaust. Diesel engines usually produce little carbon monoxide but do produce large quantities of oxides of nitrogen, which can produce serious toxicity to the lung. In the United States, the current federal standard for carbon monoxide levels in inspired air is 35 parts per million (ppm) for an 8-hour working day. For example, at the surface even 50 ppm would not produce detectable harm, but at a depth of 50 m it would be compressed and produce the effect of 300 ppm. This concentration can produce a level of up to 40% carboxyhaemoglobin over a period of time. The actual analysed parts per million must be multiplied by the number of atmospheres at which it is delivered to the worker.

Divers and compressed-air workers should become aware of the early symptoms of carbon monoxide poisoning, which include headache, nausea, dizziness and weakness. It is important to ensure that the compressor intake be always located upwind from the compressor engine exhaust pipe. This relationship must be continually checked as the wind changes or the vessels position shifts.

For many years it was widely assumed that carbon monoxide would combine with the body’s haemoglobin to produce carboxyhaemoglobin, causing its lethal effect by blocking transport of oxygen to the tissues. More recent work shows that although this effect does cause tissue hypoxia, it is not in itself fatal. The most serious damage occurs at the cellular level due to direct toxicity of the carbon monoxide molecule. Lipid peroxidation of cell membranes, which can only be terminated by hyperbaric oxygen treatment, appears to be the main cause of death and long-term sequelae.

Carbon dioxide

Carbon dioxide is a normal product of metabolism and is eliminated from the lungs through the normal process of respiration. Various types of breathing apparatus, however, can impair its elimination or cause high levels to build up in the diver’s inspired air.

From a practical point of view, carbon dioxide can exert deleterious effects on the body in three ways. First, in very high concentrations (above 3%), it can cause judgmental errors, which at first may amount to inappropriate euphoria, followed by depression if the exposure is prolonged. This, of course, can have serious consequences for a diver under water who wants to maintain good judgement to remain safe. As the concentration climbs, CO2 will eventually produce unconsciousness when levels rise much above 8%. A second effect of carbon dioxide is to exacerbate or worsen nitrogen narcosis (see below). At partial pressures of above 40 mm Hg, carbon dioxide begins to have this effect (Bennett and Elliot 1993). At high PO2‘s, such as one is exposed to in diving, the respiratory drive due to high CO2 is attenuated and it is possible under certain conditions for divers who tend to retain CO2 to increase their levels of carbon dioxide sufficient to render them unconscious. The final problem with carbon dioxide under pressure is that, if the subject is breathing 100% oxygen at pressures greater than 2 ATA, the risk for seizures is greatly enhanced as carbon dioxide levels rise. Submarine crews have easily tolerated breathing 1.5% CO2 for two months at a time with no functional ill effect, a concentration that is thirty times the normal concentration found in atmospheric air. Five thousand ppm, or ten times the level found in normal fresh air, is considered safe for the purposes of industrial limits. However, even 0.5% CO2 added to 100% oxygen mix will predispose a person to seizures when breathed at increased pressure.


Nitrogen is an inert gas with regard to normal human metabolism. It does not enter into any form of chemical combination with compounds or chemicals within the body. However, it is responsible for severe impairment in a diver’s mental functioning when breathed under high pressure.

Nitrogen behaves as an aliphatic anaesthetic as atmospheric pressure increases, which results in the concentration of nitrogen also increasing. Nitrogen fits well into the Meyer-Overton hypothesis which states that any aliphatic anaesthetic will exhibit anaesthetic potency in direct proportion to its oil-water solubility ratio. Nitrogen, which is five times more soluble in fat than in water, produces an anaesthetic effect precisely at the predicted ratio.

In actual practice, diving to depths of 50 m can be accomplished with compressed-air, although the effects of nitrogen narcosis first become evident between 30 and 50 m. Most divers, however, can function adequately within these parameters. Deeper than 50 m, helium/oxygen mixtures are commonly used to avoid the effects of nitrogen narcosis. Air diving has been done to depths of slightly over 90 m, but at these extreme pressures, the divers were barely able to function and could hardly remember what tasks they had been sent down to accomplish. As noted earlier, any excess CO2 build-up further worsens the effect of nitrogen. Because ventilatory mechanics are affected by the density of gas at great pressures, there is an automatic CO2 build-up in the lung because of changes in laminar flow within the bronchioles and the diminution of the respiratory drive. Thus, air diving deeper than 50 m can be extremely dangerous.

Nitrogen exerts its effect by its simple physical presence dissolved in neural tissue. It causes a slight swelling of the neuronal cell membrane, which makes it more permeable to sodium and potassium ions. It is felt that interference with the normal depolarization/repolarization process is responsible for clinical symptoms of nitrogen narcosis.


Decompression tables

A decompression table sets out the schedule, based on depth and time of exposure, for decompressing a person who has been exposed to hyperbaric conditions. Some general statements can be made about decompression procedures. No decompression table can be guaranteed to avoid decompression illness (DCI) for everyone, and indeed as described below, many problems have been noted with some tables currently in use. It must be remembered that bubbles are produced during every normal decompression, no matter how slow. For this reason, although it can be stated that the longer the decompression the less the likelihood of DCI, at the extreme of least likelihood, DCI becomes an essentially random event.


Habituation, or acclimatization, occurs in divers and compressed-air workers, and renders them less susceptible to DCI after repeated exposures. Acclimatization can be produced after about a week of daily exposure, but it is lost after an absence from work of between 5 days to a week or by a sudden increase in pressure. Unfortunately  construction  companies  have  relied  on  acclimatization to make work possible with what are viewed as grossly inadequate decompression tables. To maximize the utility of acclimatization, new workers are often started at midshift to allow them to habituate without getting DCI. For example, the present Japanese Table 1 for compressed-air workers utilizes the split shift, with a morning and afternoon exposure to compressed air with a surface interval of one hour between exposures. Decompression from the first exposure is about 30% of that required by the US Navy and the decompression from the second exposure is only 4% of that required by the Navy. Nevertheless, habituation makes this departure from physiologic decompression possible. Workers with even ordinary susceptibility to decompression illness self-select themselves out of compressed-air work.

The mechanism of habituation or acclimatization is not understood. However, even if the worker is not experiencing pain, damage to brain, bone, or tissue may be taking place. Up to four times as many changes are visible on MRIs taken of the brains of compressed-air workers compared to age-matched controls that have been studied (Fueredi, Czarnecki and Kindwall 1991). These probably reflect lacunar infarcts.

Diving decompression

Most modern decompression schedules for divers and caisson workers are based on mathematical models akin to those developed originally by J.S. Haldane in 1908 when he made some empirical observations on permissible decompression parameters. Haldane observed that a pressure reduction of one half could be tolerated in goats without producing symptoms. Using this as a starting point, he then, for mathematical convenience, conceived of five different tissues in the body loading and unloading nitrogen at varying rates based on the classical half time equation. His staged decompression tables were then designed to avoid exceeding a 2:1 ratio in any of the tissues. Over the years, Haldane’s model has been modified empirically in attempts to make it fit what divers were observed to tolerate. However, all mathematical models for the loading and elimination of gases are flawed, since there are no decompression tables which remain as safe or become safer as time and depth are increased.

Probably the most reliable decompression tables currently available for air diving are those of the Canadian Navy, known as the DCIEM tables (Defence and Civil Institute of Environmental Medicine). These tables were tested thoroughly by non-habituated divers over a wide range of conditions and produce a very low rate of decompression illness. Other decompression schedules which have been well tested in the field are the French National Standards, originally developed by Comex, the French diving company.

The US Navy Air Decompression tables are unreliable, especially when pushed to their limits. In actual use, US Navy Master Divers routinely decompress for a depth 3 m (10 ft) deeper and/or one exposure time segment longer than required for the actual dive to avoid problems. The Exceptional Exposure Air Decompression Tables are particularly unreliable, having produced decompression illness on 17% to 33% of all the test dives. In general, the US Navy’s decompression stops are probably too shallow.

Tunnelling and caisson decompression

None of the air decompression tables which call for air breathing during decompression, currently in wide use, appear to be safe for tunnel workers. In the United States, the current federal decompression schedules (US Bureau of Labor Statuties 1971), enforced by the Occupational Safety and Health Administration (OSHA), have been shown to produce DCI in one or more workers on 42% of the working days while being used at pressures between 1.29 and 2.11 bar. At pressures over 2.45 bar, they have been shown to produce a 33% incidence of aseptic necrosis of the bone (dysbaric osteonecrosis). The British Blackpool Tables are also flawed. During the building of the Hong Kong subway, 83% of the workers using these tables complained of symptoms of DCI. They have also been shown to produce an incidence of dysbaric osteonecrosis of up to 8% at relatively modest pressures.

The new German oxygen decompression tables devised by Faesecke in 1992 have been used with good success in a tunnel under the Kiel Canal. The new French oxygen tables also appear to be excellent by inspection but have not yet been used on a large project.

Using a computer which examined 15 years of data from successful and unsuccessful commercial dives, Kindwall and Edel devised compressed-air caisson decompression tables for the US National Institute for Occupational Safety and Health in 1983 (Kindwall, Edel and Melton 1983) using an empirical approach which avoided most of the pitfalls of mathematical modelling. Modelling was used only to interpolate between real data points. The research upon which these tables was based found that when air was breathed during decompression, the schedule in the tables did not produce DCI. However, the times used were prohibitively long and therefore impractical for the construction industry. When an oxygen variant of the table was computed, however, it was found that decompression time could be shortened to times similar to, or even shorter than, the current OSHA-enforced air decompression tables cited above. These new tables were subsequently tested by non-habituated subjects of varying ages at pressures ranging from 0.95 bar to 3.13 bar in 0.13 bar increments. Average work levels were simulated by weight lifting and treadmill walking during exposure. Exposure times were as long as possible, in keeping with the combined work time and decompression time fitting into an eight-hour work day. These are the only schedules which will be used in actual practice for shift work. No DCI was reported during these tests and bone scan and x ray failed to reveal any dysbaric osteonecrosis. To date, these are the only laboratory-tested decompression schedules in existence for compressed-air workers.

Decompression of hyperbaric chamber personnel

US Navy air decompression schedules were designed to produce a DCI incidence of less than 5%. This is satisfactory for operational diving, but much too high to be acceptable for hyperbaric workers who work in clinical settings. Decompression schedules for hyperbaric chamber attendants can be based on naval air decompression schedules, but since exposures are so frequent and thus are usually at the limits of the table, they must be liberally lengthened and oxygen should be substituted for compressed-air breathing during decompression. As a prudent measure, it is recommended that a two-minute stop be made while breathing oxygen, at least three metres deeper than called for by the decompression schedule chosen. For example, while the US Navy requires a three-minute decompression stop at three metres, breathing air, after a 101 minute exposure at 2.5 ATA, an acceptable decompression schedule for a hyperbaric chamber attendant undergoing the same exposure would be a two-minute stop at 6 m breathing oxygen, followed by ten minutes at 3 m breathing oxygen. When these schedules, modified as above, are used in practice, DCI in an inside attendant is an extreme rarity (Kindwall 1994a).

In addition to providing a fivefold larger “oxygen window” for nitrogen elimination, oxygen breathing offers other advantages. Raising the PO2 in venous blood has been demonstrated to lessen blood sludging, reduce the stickiness of white cells, reduce the no-reflow phenomenon, render red cells more flexible in passing through capillaries and counteract the vast decrease in deformability and filterability of white cells which have been exposed to compressed air.

Needless to say, all workers using oxygen decompression must be thoroughly trained and apprised of the fire danger. The environment of the decompression chamber must be kept free of combustibles and ignition sources, an overboard dump system must be used to convey exhaled oxygen out of the chamber and redundant oxygen monitors with a high oxygen alarm must be provided. The alarm should sound if oxygen in the chamber atmosphere exceeds 23%.

Working with compressed air or treating clinical patients under hyperbaric conditions sometimes can accomplish work or effect remission in disease that would otherwise be impossible. When rules for the safe use of these modalities are observed, workers need not be at significant risk for dysbaric injury.

Caisson Work and Tunnelling

From time to time in the construction industry it is necessary to excavate or tunnel through ground which is either fully saturated with water, lying below the local water table, or following a course completely under water, such as a river or lake bottom. A time-tested method for managing this situation has been to apply compressed air to the working area to force water out of the ground, drying it sufficiently so that it can be mined. This principle has been applied to both caissons used for bridge pier construction and soft ground tunnelling (Kindwall 1994b).


A caisson is simply a large, inverted box, made to the dimensions of the bridge foundation, which typically is built in a dry dock and then floated into place, where it is carefully positioned. It is then flooded and lowered until it touches bottom, after which it is driven down further by adding weight as the bridge pier itself is constructed. The purpose of the caisson is to provide a method for cutting through soft ground to land the bridge pier on solid rock or a good geologic weight-bearing stratum. When all sides of the caisson have been embedded in the mud, compressed air is applied to the interior of the caisson and water is forced out, leaving a muck floor which can be excavated by men working within the caisson. The edges of the caisson consist of a wedge-shaped cutting shoe, made of steel, which continues to descend as earth is removed beneath the descending caisson and weight is applied from above as the bridge tower is constructed. When bed rock is reached, the working chamber is filled with concrete, becoming the permanent base for the bridge foundation.

Caissons have been used for nearly 150 years and have been successful in the construction of foundations as deep as 31.4 m below mean high water, as on Bridge Pier No. 3 of the Auckland, New Zealand, Harbour Bridge in 1958.

Design of the caisson usually provides for an access shaft for workers, who can descend either by ladder or by a mechanical lift and a separate shaft for buckets to remove the spoil. The shafts are provided with hermetically sealed hatches at either end which enable the caisson pressure to remain the same while workers or materials exit or enter. The top hatch of the muck shaft is provided with a pressure sealed gland through which the hoist cable for the muck bucket can slide. Before the top hatch is opened, the lower hatch is shut. Hatch interlocks may be necessary for safety, depending on design. Pressure must be equal on both sides of any hatch before it can be opened. Since the walls of the caisson are generally made of steel or concrete, there is little or no leakage from the chamber while under pressure except under the edges. The pressure is raised incrementally to a pressure just slightly greater than is necessary to balance off sea pressure at the edge of the cutting shoe.

People working in the pressurized caisson are exposed to compressed air and may experience many of the same physiologic problems that face deep-sea divers. These include decompression illness, barotrauma of the ears, sinus cavities and lungs and if decompression schedules are inadequate, the long-term risk of aseptic necrosis of the bone (dysbaric osteonecrosis).

It is important that a ventilation rate be established to carry away CO2 and gases emanating from the muck floor (especially methane) and whatever fumes may be produced from welding or cutting operations in the working chamber. A rule of thumb is that six cubic metres of free air per minute must be provided for each worker in the caisson. Allowance must also be made for air which is lost when the muck lock and man lock are used for the passage of personnel and materials. As the water is forced down to a level exactly even with the cutting shoe, ventilation air is required as the excess bubbles out under the edges. A second air supply, equal in capacity to the first, with an independent power source, should be available for emergency use in case of compressor or power failure. In many areas this is required by law.

Sometimes if the ground being mined is homogeneous and consists of sand, blow pipes can be erected to the surface. The pressure in the caisson will then extract the sand from the working chamber when the end of the blow pipe is located in a sump and the excavated sand is shovelled into the sump. If coarse gravel, rock, or boulders are encountered, these have to be broken up and removed in conventional muck buckets.

If the caisson should fail to sink despite the added weight on top, it may sometimes be necessary to withdraw the workers from the caisson and reduce the air pressure in the working chamber to allow the caisson to fall. Concrete must be placed or water admitted to the wells within the pier structure surrounding the air shafts above the caisson to reduce the stress on the diaphragm at the top of the working chamber. When just beginning a caisson operation, safety cribs or supports should be kept in the working chamber to prevent the caisson from suddenly dropping and crushing the workers. Practical considerations limit the depth to which air-filled caissons can be driven when men are used to hand mine the muck. A pressure of 3.4 kg/cm2 gauge (3.4 bar or 35 m of fresh water) is about the maximum tolerable limit because of decompression considerations for the workers.

An automated caisson excavating system has been developed by the Japanese wherein a remotely operated hydraulically powered backhoe shovel, which can reach all corners of the caisson, is used for excavation. The backhoe, under television control from the surface, drops the excavated muck into buckets which are hoisted remotely from the caisson. Using this system, the caisson can proceed down to almost unlimited pressures. The only time that workers need enter the working chamber is to repair the excavating machinery or to remove or demolish large obstacles which appear below the cutting shoe of the caisson and which cannot be removed by the remote-controlled backhoe. In such cases, workers enter for short periods much as divers and can breathe either air or mixed gas at higher pressures to avoid nitrogen narcosis.

When people have worked long shifts under compressed-air at pressures greater than 0.8 kg/cm2 (0.8 bar), they must decompress in stages. This can be accomplished either by attaching a large decompression chamber to the top of the man shaft into the caisson or, if space requirements are such at the top that this is impossible, by attaching “blister locks” to the man shaft. These are small chambers which can accommodate only a few workers at a time in a standing position. Preliminary decompression is taken in these blister locks, where the time spent is relatively short. Then, with considerable excess gas remaining in their bodies, the workers rapidly decompress to the surface and quickly move to a standard decompression chamber, sometimes located on an adjacent barge, where they are repressurized for subsequent slow decompression. In compressed-air work, this process is known as “decanting” and was fairly common in England and elsewhere, but is prohibited in the United States. The object is to return workers to pressure within five minutes, before bubbles can grow sufficiently in size to cause symptoms. However, this is inherently dangerous because of the difficulties of moving a large gang of workers from one chamber to another. If one worker has trouble clearing his ears during repressurization, the whole shift is placed in jeopardy. There is a much safer procedure, called “surface decompression”, for divers, where only one or two are decompressed at the same time. Despite every precaution on the Auckland Harbour Bridge project, as many as eight minutes occasionally elapsed before bridge workers could be put back under pressure.

Compressed air tunnelling

Tunnels are becoming increasingly important as the population grows, both for the purposes of sewage disposal and for unobstructed traffic arteries and rail service beneath large urban centres. Often, these tunnels must be driven through soft ground considerably below the local water table. Under rivers and lakes, there may be no other way to ensure the safety of the workers than to put compressed air on the tunnel. This technique, using a hydraulically driven shield at the face with compressed air to hold back the water, is known as the plenum process. Under large buildings in a crowded city, compressed air may be necessary to prevent surface subsidence. When this occurs, large buildings can develop cracks in their foundations, sidewalks and streets may drop and pipes and other utilities can be damaged.

To apply pressure to a tunnel, bulkheads are erected across the tunnel to provide the pressure boundary. On smaller tunnels, less than three metres in diameter, a single or combination lock is used to provide access for workers and materials and removal of the excavated ground. Removable track sections are provided by the doors so that they may be operated without interference from the muck-train rails. Numerous penetrations are provided in these bulkheads for the passage of high-pressure air for the tools, low-pressure air for pressurizing the tunnel, fire mains, pressure gauge lines, communications lines, electrical power lines for lighting and machinery and suction lines for ventilation and removal of water in the invert. These are often termed blow lines or “mop lines”. The low-pressure air supply pipe, which is 15-35 cm in diameter, depending on the size of the tunnel, should extend to the working face in order to ensure good ventilation for the workers. A second low-pressure air pipe of equal size should also extend through both bulkheads, terminating just inside the inner bulkhead, to provide air in the event of rupture or break in the primary air supply. These pipes should be fitted with flapper valves which will close automatically to prevent depressurization of the tunnel if the supply pipe is broken. The volume of air required to efficiently ventilate the tunnel and keep CO2 levels low will vary greatly depending on the porosity of the ground and how close the finished concrete lining has been brought to the shield. Sometimes micro-organisms in the soil produce large amounts of CO2. Obviously, under such conditions, more air will be required. Another useful property of compressed air is that it tends to force explosive gases such as methane away from the walls and out of the tunnel. This holds true when mining areas where spilled solvents such as petrol or degreasers have saturated the ground.

A rule of thumb developed by Richardson and Mayo (1960) is that the volume of air required usually can be calculated by multiplying the area of the working face in square metres by six and adding six cubic metres per man. This gives the number of cubic metres of free air required per minute. If this figure is used, it will cover most practical contingencies.

The fire main must also extend through to the face and be provided with hose connections every sixty metres for use in case of fire. Thirty metres of rotproof hose should be attached to the water-filled fire main outlets.

In very large tunnels, over about four metres in diameter, two locks should be provided, one termed the muck lock, for passing muck trains, and the man lock, usually positioned above the muck lock, for the workers. On large projects, the man lock is often made of three compartments so that engineers, electricians and others can lock in and out past a work shift undergoing decompression. These large man locks are usually built external to the main concrete bulkhead so they do not have to resist the external compressive force of the tunnel pressure when open to the outside air.

On very large subaqueous tunnels a safety screen is erected, spanning the upper half of the tunnel, to afford some protection should the tunnel suddenly flood secondary to a blow-out while tunnelling under a river or lake. The safety screen is usually placed as close as practicable to the face, avoiding the excavating machinery. A flying gangway or hanging walkway is used between the screen and the locks, the gangway dropping down to pass at least a metre below the lower edge of the screen. This will allow the workers egress to the man lock in the event of sudden flooding. The safety screen can also be used to trap light gases which may be explosive and a mop line can be attached through the screen and coupled to a suction or blow line. With the valve cracked, this will help to purge any light gases from the working environment. Because the safety screen extends nearly down to the centre of the tunnel, the smallest tunnel it can be employed on is about 3.6 m. It should be noted that workers must be warned to keep clear of the open end of the mop line, as serious accidents can be caused if clothing is sucked into the pipe.

Table 1 is a list of instructions which should be given to compressed-air workers before they first enter the compressed-air environment.

It is the responsibility of the retained physician or occupational health professional for the tunnel project to ensure that air purity standards are maintained and that all safety measures are in effect. Adherence to established decompression schedules by periodically examining the pressure recording graphs from the tunnel and man locks must also be carefully monitored.

Table 1. Instructions for compressed-air workers

  • Never “short” yourself on the decompression times prescribed by your employer and the official decompression code in use. The time saved is not worth the risk of decompression illness (DCI), a potentially fatal or crippling disease.
  • Do not sit in a cramped position during decompression. To do so allows nitrogen bubbles to gather and concentrate in the joints, thereby contributing to the risk of DCI. Because you are still eliminating nitrogen from your body after you go home, you should refrain from sleeping or resting in a cramped position after work, as well.
  • Warm water should be used for showers and baths up to six hours after decompressing; very hot water can actually bring on or aggravate a case of decompression illness.
  • Severe fatigue, lack of sleep and heavy drinking the night before can also help bring on decompression illness. Drinking alcohol and taking aspirin should never be used as a “treatment” for pains of decompression illness.
  • Fever and illness, such as bad colds, increase the risk of decompression illness. Strains and sprains in muscles and joints are also “favourite” places for DCI to begin.
  • When stricken by decompression illness away from the job site, immediately contact the company’s physician or one knowledgeable in treating this disease. Wear your identifying bracelet or badge at all times.
  • Leave smoking materials in the changing shack. Hydraulic oil is flammable and should a fire start in the closed environment of the tunnel, it could cause extensive damage and a shutdown of the job, which would lay you off work. Also, because the air is thicker in the tunnel due to compression, heat is conducted down cigarettes so that they become too hot to hold as they get shorter.
  • Do not bring thermos bottles in your lunch box unless you loosen the stopper during compression; if you do not do this, the stopper will be forced deep into the thermos bottle. During decompression, the stopper must also be loosened so that the bottle does not explode. Very fragile glass thermos bottles might implode when pressure is applied, even if the stopper is loose.
  • When the air lock door has been closed and pressure is applied, you will notice that the air in the air lock gets warm. This is called the “heat of compression” and is normal. Once the pressure stops changing, the heat will dissipate and the temperature will return to normal. During compression, the first thing you will notice is a fullness of your ears. Unless you “clear your ears” by swallowing, yawning, or holding your nose and trying to “blow the air out through your ears”, you will experience ear pain during compression. If you cannot clear your ears, notify the shift foreman immediately so that compression can be halted. Otherwise you may break your eardrums or develop a severe ear squeeze. Once you have reached maximum pressure, there will be no further problems with your ears for the remainder of the shift.
  • Should you experience buzzing in your ears, ringing in your ears, or deafness following compression which persists for more than a few hours, you must report to the compressed-air physician for evaluation. Under extremely severe but rare conditions, a portion of the middle ear structure other than the eardrum may be affected if you have had a great deal of difficulty clearing your ears and in that case this must be surgically corrected within two or three days to avoid permanent difficulty.
  • If you have a cold or an attack of hay fever, it is best not to try compressing in the air lock until you are over it. Colds tend to make it difficult or impossible for you to equalize your ears or sinuses.


Hyperbaric chamber workers

Hyperbaric oxygen therapy is becoming more common in all areas of the world, with some 2,100 hyperbaric chamber facilities now functioning. Many of these chambers are multiplace units, which are compressed with compressed air to pressures ranging from 1 to 5 kg/cm2 gauge. Patients are given 100% oxygen to breathe, at pressures up to 2 kg/cm2 gauge. At pressures greater than that they may breathe mixed gas for treatment of decompression illness. The chamber attendants, however, typically breathe compressed air and so their exposure in the chamber is similar to that experienced by a diver or compressed-air worker.

Typically the chamber attendant working inside a multiplace chamber is a nurse, respiratory therapist, former diver, or hyperbaric technician. The physical requirements for such workers are similar to those for caisson workers. It is important to remember, however, that a number of chamber attendants working in the hyperbaric field are female. Women are no more likely to suffer ill effects from compressed-air work than men, with the exception of the question of pregnancy. Nitrogen is carried across the placenta when a pregnant woman is exposed to compressed air and this is transferred to the foetus. Whenever decompression takes place, nitrogen bubbles form in the venous system. These are silent bubbles and, when small, do no harm, as they are removed efficiently by the pulmonary filter. The wisdom, however, of having these bubbles appear in a developing foetus is doubtful. What studies have been done indicate that foetal damage may occur under such circumstances. One survey suggested that birth defects are more common in the children of women who have engaged in scuba diving while pregnant. Exposure of pregnant women to hyperbaric chamber conditions should be avoided and appropriate policies consistent with both medical and legal considerations must be developed. For this reason, female workers should be precautioned about the risks during pregnancy and appropriate personnel job assignment and health education programmes should be instituted in order that pregnant women not be exposed to hyperbaric chamber conditions.

It should be pointed out, however, that patients who are pregnant may be treated in the hyperbaric chamber, as they breathe 100% oxygen and are therefore not subject to nitrogen embolization. Previous concerns that the foetus would be at increased risk for retrolental fibroplasia or retinopathy of the newborn have proven to be unfounded in large clinical trials. Another condition, premature closure of the patent ductus arteriosus, has also not been found to be related to the exposure.

Other Hazards

Physical injuries


In general, divers are prone to the same types of physical injury that any worker is liable to sustain when working in heavy construction. Breaking cables, failing loads, crush injuries from machines, turning cranes and so on, can be commonplace. However, in the underwater environment, the diver is prone to certain types of unique injury that are not found elsewhere.

Suction/entrapment injury is something especially to be guarded against. Working in or near an opening in a ship’s hull, a caisson which has a lower water level on the side opposite the diver, or a dam can be causative of this type of mishap. Divers often refer to this type of situation as being trapped by “heavy water”.

To avoid dangerous situations where the diver’s arm, leg, or whole body may be sucked into an opening such as a tunnel or pipe, strict precautions must be taken to tag out pipe valves and flood gates on dams so that they cannot be opened while the diver is in the water near them. The same is true of pumps and piping within ships that the diver is working on.

Injury can include oedema and hypoxia of an entrapped limb sufficient to cause muscle necrosis, permanent nerve damage, or even loss of the entire limb, or it may occasion gross crushing of a portion of the body or the whole body so as to cause death from simple massive trauma. Entrapment in cold water for a long period of time may cause the diver to die of exposure. If the diver is using scuba gear, he may run out of air and drown before his release can be effected, unless additional scuba tanks can be provided.

Propeller injuries are straightforward and must be guarded against by tagging out a ship’s main propulsion machinery while the diver is in the water. It must be remembered, however, that steam turbine-powered ships, when in port, are continuously turning over their screws very slowly, using their jacking gear to avoid cooling and distortion of the turbine blades. Thus the diver, when working on such a blade (trying to clear it from entangled cables, for example), must be aware that the turning blade must be avoided as it approaches a narrow spot close to the hull.

Whole-body squeeze is a unique injury which can occur to deep sea divers using the classical copper helmet mated to the flexible rubberized suit. If there is no check valve or non-return valve where the air pipe connects to the helmet, cutting the air line at the surface will cause an immediate relative vacuum within the helmet, which can draw the entire body into the helmet. The effects of this can be instant and devastating. For example, at a depth of 10 m, about 12 tons of force is exerted on the soft part of the diver’s dress. This force will drive his body into the helmet if pressurization of the helmet is lost. A similar effect may be produced if the diver fails unexpectedly and fails to turn on compensating air. This can produce severe injury or death if it occurs near the surface, as a 10-metre fall from the surface will halve the volume of the dress. A similar fall occurring between 40 and 50 m will change the suit volume only about 17%. These volume changes are in accordance with Boyle’s Law.

Caisson and tunnel workers

Tunnel workers are subject to the usual types of accidents seen in heavy construction, with the additional problem of a higher incidence of falls and injuries from cave-ins. It must be stressed that an injured compressed-air worker who may have broken ribs should be suspected of having a pneumothorax until proven otherwise and therefore great care must be taken in decompressing such a patient. If a pneumothorax is present, it must be relieved at pressure in the working chamber before decompression is attempted.


Noise damage to compressed-air workers may be severe, as air motors, pneumatic hammers and drills are never properly equipped with silencers. Noise levels in caissons and tunnels have been measured at over 125 dB. These levels are physically painful, as well as causative of permanent damage to the inner ear. Echo within the confines of a tunnel or caisson exacerbates the problem.

Many compressed-air workers balk at wearing ear protection, saying that blocking the sound of an approaching muck train would be dangerous. There is little foundation for this belief, as hearing protection at best only attenuates sound but does not eliminate it. Furthermore, not only is a moving muck train not “silent” to a protected worker, but it also gives other cues such as moving shadows and vibration in the ground. A real concern is complete hermetic occlusion of the auditory meatus provided by a tightly fitting ear muff or protector. If air is not admitted to the external auditory canal during compression, external ear squeeze may result as the ear drum is forced outward by air entering the middle ear via the Eustachian tube. The usual sound protective ear muff is usually not completely air tight, however. During compression, which lasts only a tiny fraction of the total shift time, the muff can be slightly loosened should pressure equalization prove a problem. Formed fibre ear plugs which can be moulded to fit in the external canal provide some protection and are not air tight.

The goal is to avoid a time weighted average noise level of higher than 85 dBA. All compressed-air workers should have pre-employment base line audiograms so that auditory losses which may result from the high-noise environment can be monitored.

Hyperbaric chambers and decompression locks can be equipped with efficient silencers on the air supply pipe entering the chamber. It is important that this be insisted on, as otherwise the workers will be considerably bothered by the ventilation noise and may neglect to ventilate the chamber adequately. A continuous vent can be maintained with a silenced air supply producing no more than 75dB, about the noise level in an average office.


Fire is always of great concern in compressed-air tunnel work and in clinical hyperbaric chamber operations. One can be lulled into a false sense of security when working in a steel-walled caisson which has a steel roof and a floor consisting only of unburnable wet muck. However, even in these circumstances, an electrical fire can burn insulation, which will prove highly toxic and can kill or incapacitate a work crew very quickly. In tunnels which are driven using wooden lagging before the concrete is poured, the danger is even greater. In some tunnels, hydraulic oil and straw used for caulking can furnish additional fuel.

Fire under hyperbaric conditions is always more intense because there is more oxygen available to support combustion. A rise from 21% to 28% in the oxygen percentage will double the burning rate. As the pressure is increased, the amount of oxygen available to burn increases The increase is equal to the percentage of oxygen available multiplied by the number of atmospheres in absolute terms. For example, at a pressure of 4 ATA (equal to 30 m of sea water), the effective oxygen percentage would be 84% in compressed-air. However, it must be remembered that even though burning is very much accelerated under such conditions, it is not the same as the speed of burning in 84% oxygen at one atmosphere. The reason for this is that the nitrogen present in the atmosphere has a certain quenching effect. Acetylene cannot be used at pressures over one bar because of its explosive properties. However, other torch gases and oxygen can be used for cutting steel. This has been done safely at pressures up to 3 bar. Under such circumstances, however, scrupulous care must be exercised and someone must stand by with a fire hose to immediately quench any fire which might start, should an errant spark come in contact with something combustible.

Fire requires three components to be present: fuel, oxygen and an ignition source. If any one of these three factors is absent, fire will not occur. Under hyperbaric conditions, it is almost impossible to remove oxygen unless the piece of equipment in question can be inserted into the environment by filling it or surrounding it with nitrogen. If fuel cannot be removed, an ignition source must be avoided. In clinical hyperbaric work, meticulous care is taken to prevent the oxygen percentage in the multiplace chamber from rising above 23%. In addition, all electrical equipment within the chamber must be intrinsically safe, with no possibility of producing an arc. Personnel in the chamber should wear cotton clothing which has been treated with flame retardant. A water-deluge system must be in place, as well as a hand-held fire hose independently actuated. If a fire occurs in a multiplace clinical hyperbaric chamber, there is no immediate escape and so the fire must be fought with a hand-held hose and with the deluge system.

In monoplace chambers pressurized with 100% oxygen, a fire will be instantly fatal to any occupant. The human body itself supports combustion in 100% oxygen, especially at pressure. For this reason, plain cotton clothing is worn by the patient in the monoplace chamber to avoid static sparks which could be produced by synthetic materials. There is no need to fireproof this clothing, however, as if a fire should occur, the clothing would afford no protection. The only method for avoiding fires in the monoplace oxygen-filled chamber is to completely avoid any source of ignition.

When dealing with high pressure oxygen, at pressures over 10 kg/cm2 gauge, adiabatic heating must be recognized as a possible source of ignition. If oxygen at a pressure of 150 kg/cm2 is suddenly admitted to a manifold via a quick-opening ball valve, the oxygen may “diesel” if even a tiny amount of dirt is present. This can produce a violent explosion. Such accidents have occurred and for this reason, quick-opening ball valves should never be used in high pressure oxygen systems.



Tuesday, 15 February 2011 19:40

Decompression Disorders

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A wide range of workers are subject to decompression (a reduction in ambient pressure) as part of their working routine. These include divers who themselves are drawn from a wide range of occupations, caisson workers, tunnellers, hyperbaric chamber workers (usually nurses), aviators and astronauts. Decompression of these individuals can and does precipitate a variety of decompression disorders. While most of the disorders are well understood, others are not and in some instances, and despite treatment, injured workers can become disabled. The decompression disorders are the subject of active research.

Mechanism of Decompression Injury

Principles of gas uptake and release

Decompression may injure the hyperbaric worker via one of two primary mechanisms. The first is the consequence of inert gas uptake during the hyperbaric exposure and bubble formation in tissues during and after the subsequent decompression. It is generally assumed that the metabolic gases, oxygen and carbon dioxide, do not contribute to bubble formation. This is almost certainly a false assumption, but the consequent error is small and such an assumption will be made here.

During the compression (increase in ambient pressure) of the worker and throughout their time under pressure, inspired and arterial inert gas tensions will be increased relative to those experienced at normal atmospheric pressure—the inert gas(es) will then be taken up into tissues until an equilibrium of inspired, arterial and tissue inert gas tensions is established. Equilibrium times will vary from less than 30 minutes to more than a day depending upon the type of tissue and gas involved, and, in particular, will vary according to:

  • the blood supply to the tissue
  • the solubility of the inert gas in blood and in the tissue
  • the diffusion of the inert gas through blood and into the tissue
  • the temperature of the tissue
  • the local tissue work-loads
  • the local tissue carbon dioxide tension.


The subsequent decompression of the hyperbaric worker to normal atmospheric pressure will clearly reverse this process, gas will be released from tissues and will eventually be expired. The rate of this release is determined by the factors listed above, except, for as yet poorly understood reasons, it appears to be slower than the uptake. Gas elimination will be slower still if bubbles form. The factors that influence the formation of bubbles are well established qualitatively, but not quantitatively. For a bubble to form the bubble energy must be sufficient to overcome ambient pressure, surface tension pressure and elastic tissue pressures. The disparity between theoretical predictions (of surface tension and critical bubble volumes for bubble growth) and actual observation of bubble formation is explained variously by arguing that bubbles form in tissue (blood vessel) surface defects and/or on the basis of small short-lived bubbles (nuclei) that are continually formed in the body (e.g., between tissue planes or in areas of cavitation). The conditions that must exist before gas comes out of solution are also poorly defined—although it is likely that bubbles form whenever tissue gas tensions exceed ambient pressure. Once formed, bubbles provoke injury (see below) and become increasingly stable as a consequence of coalescence and recruitment of surfactants to the bubble surface. It may be possible for bubbles to form without decompression by changing the inert gas that the hyperbaric worker is breathing. This effect is probably small and those workers that have had a sudden onset of a decompression illness after a change in inspired inert gas almost certainly already had “stable” bubbles in their tissues.

It follows that to introduce a safe working practice a decompression programme (schedule) should be employed to avoid bubble formation. This will require modelling of the following:

  • the uptake of the inert gas(es) during the compression and the hyperbaric exposure
  • the elimination of the inert gas(es) during and after the decompression
  • the conditions for bubble formation.


It is reasonable to state that to date no completely satisfactory model of decompression kinetics and dynamics has been produced and that hyperbaric workers now rely on programmes that have been established essentially by trial and error.

Effect of Boyle’s Law on barotrauma

The second primary mechanism by which decompression can cause injury is the process of barotrauma. The barotraumata can arise from compression or decompression. In compression barotrauma, the air spaces in the body that are surrounded by soft tissue, and hence are subject to increasing ambient pressure (Pascal’s principle), will be reduced in volume (as reasonably predicted by Boyles’ law: doubling of ambient pressure will cause gas volumes to be halved). The compressed gas is displaced by fluid in a predictable sequence:

  • The elastic tissues move (tympanic membrane, round and oval windows, mask material, clothing, rib cage, diaphragm).
  • Blood is pooled in the high compliance vessels (essentially veins).
  • Once the limits of compliance of blood vessels are reached, there is an extravasation of fluid (oedema) and then blood (haemorrhage) into the surrounding soft tissues.
  • Once the limits of compliance of the surrounding soft tissues are reached, there is a shift of fluid and then blood into the air space itself.


This sequence can be interrupted at any time by an ingress of additional gas into the space (e.g., into the middle ear on performing a valsalva manoeuvre) and will stop when gas volume and tissue pressure are in equilibrium.

The process is reversed during decompression and gas volumes will increase, and if not vented to atmosphere will cause local trauma. In the lung this trauma may arise from either over-distension or from shearing between adjacent areas of lung that have significantly different compliance and hence expand at different rates.

Pathogenesis of Decompression Disorders

The decompression illnesses can be divided into the barotraumata, tissue bubble and intravascular bubble categories.


During compression, any gas space may become involved in barotrauma and this is especially common in the ears. While damage to the external ear requires occlusion of the external ear canal (by plugs, a hood, or impacted wax), the tympanic membrane and middle ear is frequently damaged. This injury is more likely if the worker has upper respiratory tract pathology that causes eustachian tube dysfunction. The possible consequences are middle ear congestion (as described above) and/or tympanic membrane rupture. Ear pain and a conductive deafness are likely. Vertigo may result from an ingress of cold water into the middle ear through a ruptured tympanic membrane. Such vertigo is transient. More commonly, vertigo (and possibly also a sensorineural deafness) will result from inner ear barotrauma. During compression, inner ear damage often results from a forceful valsalva manoeuvre (that will cause a fluid wave to be transmitted to the inner ear via the cochlea duct). The inner ear damage is usually within the inner ear—round and oval window rupture is less common.

The paranasal sinuses often are similarly involved and usually because of a blocked ostium. In addition to local and referred pain, epistaxis is common and cranial nerves may be “compressed”. It is noteworthy that the facial nerve may be likewise affected by middle ear barotrauma in individuals with a perforate auditory nerve canal. Other areas that may be affected by compressive barotrauma, but less commonly, are the lungs, teeth, gut, diving mask, dry-suits and other equipment such as buoyancy compensating devices.

Decompressive barotraumata are less common than compressive barotraumata, but tend to have a more adverse outcome. The two areas primarily affected are the lungs and inner ear. The typical pathological lesion of pulmonary barotrauma has yet to be described. The mechanism has been variously ascribed to the over-inflation of alveoli either to “open up pores” or mechanically to disrupt the alveolus, or as the consequence of shearing of lung tissue due to local differential lung expansion. Maximum stress is likely at the base of alveoli and, given that many underwater workers often breathe with small tidal excursions at or near total lung capacity, the risk of barotrauma is increased in this group as lung compliance is lowest at these volumes. Gas release from damaged lung may track through the interstitium to the hilum of the lungs, mediastinum and perhaps into the subcutaneous tissues of the head and neck. This interstitial gas may cause dyspnoea, substernal pain and coughing which may be productive of a little bloodstained sputum. Gas in the head and neck is self-evident and may occasionally impair phonation. Cardiac compression is extremely rare. Gas from a barotraumatised lung may also escape into the pleural space (to cause a pneumothorax) or into the pulmonary veins (to eventually become arterial gas emboli). In general, such gas most commonly either escapes into the interstitium and pleural space or into the pulmonary veins. Concurrent obvious damage to the lung and arterial gas embolism are (fortunately) uncommon.

Autochthonous tissue bubbles

If, during decompression, a gas phase forms, this is usually, initially, in tissues. These tissue bubbles may induce tissue dysfunction via a variety of mechanisms—some of these are mechanical and others are biochemical.

In poorly compliant tissues, such as long bones, the spinal cord and tendons, bubbles may compress arteries, veins, lymphatics and sensory cells. Elsewhere, tissue bubbles may cause mechanical disruption of cells or, at a microscopic level, of myelin sheaths. The solubility of nitrogen in myelin may explain the frequent involvement of the nervous system in decompression illness amongst workers who have been breathing either air or an oxygen-nitrogen gas mixture. Bubbles in tissues may also induce a biochemical “foreign-body” response. This provokes an inflammatory response and may explain the observation that a common presentation of decompression illness is an influenza-like illness. The significance of the inflammatory response is demonstrated in animals such as rabbits, where inhibition of the response prevents the onset of decompression illness. The major features of the inflammatory response include a coagulopathy (this is particularly important in animals, but less so in humans) and the release of kinins. These chemicals cause pain and also an extravasation of fluid. Haemoconcentration also results from the direct effect of bubbles on blood vessels. The end result is a significant compromise of the microcirculation and, in general, measurement of the haematocrit correlates well with the severity of the illness. Correction of this haemoconcentration has a predictably significant benefit on outcome.

Intravascular bubbles

Venous bubbles may either form de-novo as gas comes out of solution or they may be released from tissues. These venous bubbles travel with blood flow to the lungs to be trapped in the pulmonary vasculature. The pulmonary circulation is a highly effective filter of bubbles because of the relatively low pulmonary artery pressure. In contrast, few bubbles are trapped for long periods in the systemic circulation because of the significantly greater systemic arterial pressure. The gas in bubbles trapped in the lung diffuses into the pulmonary air spaces from where it is exhaled. While these bubbles are trapped, however, they may cause adverse effects by either provoking an imbalance of lung perfusion and ventilation or by increasing pulmonary artery pressure and consequently right heart and central venous pressure. The increased right heart pressure can cause “right to left” shunting of blood through pulmonary shunts or intra-cardiac “anatomical defects” such that bubbles bypass the lung “filter” to become arterial gas emboli. Increases in venous pressure will impair venous return from tissues, thereby impairing the clearance of inert gas from the spinal cord; venous haemorrhagic infarction may result. Venous bubbles also react with blood vessels and blood constituents. An effect on blood vessels is to strip the surfactant lining from endothelial cells and hence to increase vascular permeability, which may be further compromised by the physical dislocation of endothelial cells. However, even in the absence of such damage, endothelial cells increase the concentration of glycoprotein receptors for polymorphonuclear leukocytes on their cell surface. This, together with a direct stimulation of white blood cells by bubbles, causes leucocyte binding to endothelial cells (reducing flow) and subsequent infiltration into and through the blood vessels (diapedesis). The infiltrating polymorphonuclear leukocytes cause future tissue injury by release of cytotoxins, oxygen free radicals and phospholipases. In blood, bubbles will not only cause the activation and accumulation of polymorphonuclear leukocytes, but also the activation of platelets, coagulation and complement, and the formation of fat emboli. While these effects have relatively minor importance in the highly compliant venous circulation, similar effects in the arteries can reduce blood flow to ischaemic levels.

Arterial bubbles (gas emboli) can arise from:

  • pulmonary barotrauma causing the release of bubbles into the pulmonary veins
  • bubbles  being  “forced”  through  the  pulmonary  arterioles (this process is enhanced by oxygen toxicity and by those bronchodilators that  are  also  vasodilators  such as  aminophylline)
  • bubbles bypassing the lung filter through a right to left vascular channel (e.g., patent foramen ovale).


Once in the pulmonary veins, bubbles return to the left atrium, left ventricle, and then are pumped into the aorta. Bubbles in the arterial circulation will distribute according to buoyancy and blood flow in large vessels, but elsewhere with blood flow alone. This explains the predominant embolism of the brain and, in particular, the middle cerebral artery. The majority of bubbles that enter the arterial circulation will pass through into the systemic capillaries and into the veins to return to the right side of the heart (usually to be trapped in the lungs). During this transit these bubbles may cause a temporary interruption of function. If the bubbles remain trapped in the systemic circulation or are not redistributed within five to ten minutes, then this loss of function may persist. If bubbles embolise the brain stem circulation, then the event may be lethal. Fortunately, the majority of bubbles will be redistributed within minutes of first arrival in the brain and a recovery of function is usual. However, during this transit the bubbles will cause the same vascular (blood vessels and blood) reactions as described above in venous blood and veins. Consequently, a significant and progressive decline in cerebral blood flow may occur, which may reach the levels at which normal function cannot be sustained. The hyperbaric worker will, at this time, suffer a relapse or deterioration in function. In general, about two-thirds of hyperbaric workers who suffer cerebral arterial gas embolism will spontaneously recover and about one-third of these will subsequently relapse.

Clinical Presentation of Decompression Disorders

Time of onset

Occasionally, the onset of decompression illness is during the decompression. This is most commonly seen in the barotraumata of ascent, particularly involving the lungs. However, the onset of the majority of decompression illnesses occurs after decompression is complete. Decompression illnesses due to the formation of bubbles in tissues and in blood vessels usually become evident within minutes or hours after decompression. The natural history of many of these decompression illnesses is for the spontaneous resolution of symptoms. However, some will only resolve spontaneously incompletely and there is a need for treatment. There is substantial evidence that the earlier the treatment the better the outcome. The natural history of treated decompression illnesses is variable. In some cases, residual problems are seen to resolve over the following 6-12 months, while in others symptoms appear not to resolve.

Clinical manifestations

A common presentation of decompression illness is an influenza-like condition. Other frequent complaints are various sensory disorders, local pain, particularly in the limbs; and other neurologic manifestations, which may involve higher functions, special senses and motor weariness (less commonly the skin and lymphatic systems may be involved). In some groups of hyperbaric workers, the most common presentation of decompression illness is pain. This may be a discrete pain about a specific joint or joints, back pain or referred pain (when the pain is often located in the same limb as are overt neurologic deficits), or less commonly, in an acute decompression illness, vague migratory aches and pains may be noticed. Indeed, it is reasonable to state that the manifestations of the decompression illnesses are protean. Any illness in a hyperbaric worker that occurs up to 24-48 hours after a decompression should be assumed to be related to that decompression until proven otherwise.


Until recently, the decompression illnesses were classified into:

  • the barotraumata
  • cerebral arterial gas embolism
  • decompression sickness.


Decompression sickness was further subdivided into Type 1 (pain, itch, swelling and skin rashes), Type 2 (all other manifestations) and Type 3 (manifestations of both cerebral arterial gas embolism and decompression sickness) categories. This classification system arose from an analysis of the outcome of caisson workers using new decompression schedules. However, this system has had to be replaced both because it is neither discriminatory nor prognostic and because there is a low concordance in diagnosis between experienced physicians. The new classification of the decompression illnesses recognises the difficulty in distinguishing between cerebral arterial gas embolism and cerebral decompression sickness and similarly the difficulty in distinguishing Type 1 from Type 2 and Type 3 decompression sickness. All decompression illnesses are now classified as such—decompression illness, as described in table 1. This term is prefaced with a description of the nature of the illness, the progression of symptoms and a list of the organ systems in which the symptoms are manifest (no assumptions are made about the underlying pathology). For example, a diver may have acute progressive neurological decompression illness. The complete classification of the decompression illness includes a comment on the presence or absence of barotrauma and the likely inert gas loading. These latter terms are relevant to both treatment and likely fitness to return to work.


Table 1. Revised classification system of the decompression illnesses











Spontaneously resolving


Decompression illness

+ or -




Evidence of barotrauma













First Aid Management


Rescue and resuscitation

Some hyperbaric workers develop a decompression illness and require to be rescued. This is particularly true for divers. This rescue may require their recovery to a stage or diving bell, or a rescue from underwater. Specific rescue techniques must be established and practised if they are to be successful. In general, divers should be rescued from the ocean in a horizontal posture (to avoid possibly lethal falls in cardiac output as the diver is re-subjected to gravity—during any dive there is a progressive loss of blood volume consequent to displacement of blood from the peripheries into the chest) and consequent diuresis and this posture should be maintained until the diver is, if necessary, in a recompression chamber.

The resuscitation of an injured diver should follow the same regimen as used in resuscitations elsewhere. Of specific note is that the resuscitation of a hypothermic individual should continue at least until the individual is rewarmed. There is no convincing evidence that resuscitation of an injured diver in the water is effective. In general, the divers’ best interests are usually served by early rescue ashore, or to a diving bell/platform.

Oxygen and fluid resuscitation

A hyperbaric worker with a decompression illness should be laid flat, to minimize the chances of bubbles distributing to the brain, but not placed in a head-down posture which probably adversely affects the outcome. The diver should be given 100% oxygen to breathe; this will require either a demand valve in a conscious diver or a sealing mask, high flow rates of oxygen and a reservoir system. If oxygen administration is to be prolonged, then airbreaks should be given to ameliorate or retard the development of pulmonary oxygen toxicity. Any diver with decompression illness should be re-hydrated. There is probably no place for oral fluids in the acute resuscitation of a severely injured worker. In general, it is difficult to administer oral fluids to someone lying flat. Oral fluids will require the administration of oxygen to be interrupted and then usually have negligible immediate effect on the blood volume. Finally, since subsequent hyperbaric oxygen treatment may cause a convulsion, it is not desirable to have any stomach contents. Ideally then, fluid resuscitation should be by the intravenous route. There is no evidence of any advantage of colloid over crystalloid solutions and the fluid of choice is probably normal saline. Solutions containing lactate should not be given to a cold diver and dextrose solutions should not be given to anyone with a brain injury (as aggravation of the injury is possible). It is essential that an accurate fluid balance be maintained as this is probably the best guide to the successful resuscitation of a hyperbaric worker with decompression illness. Bladder involvement is sufficiently common that early recourse to bladder catheterization is warranted in the absence of urinary output.

There are no drugs that are of proven benefit in the treatment of the decompression illnesses. However, there is growing support for lignocaine and this is under clinical trial. The role of lignocaine is thought to be both as a membrane stabiliser and as an inhibitor of the polymorphonuclear leukocyte accumulation and blood vessel adherence that is provoked by bubbles. It is noteworthy that one of the probable roles of hyperbaric oxygen is also to inhibit the accumulation of and adherence to blood vessels of leucocytes. Finally, there is no evidence that any benefit is derived from the use of platelet inhibitors such as aspirin or other anticoagulants. Indeed, as haemorrhage into the central nervous system is associated with severe neurological decompression illness, such medication may be contra-indicated.


Retrieval of a hyperbaric worker with decompression illness to a therapeutic recompression facility should occur as soon as is possible, but must not involve any further decompression. The maximum altitude to which such a worker should be decompressed during aeromedical evacuation is 300 m above sea level. During this retrieval, the first aid and adjuvant care described above should be provided.

Recompression Treatment


The definitive treatment of most of the decompression illnesses is recompression in a chamber. The exception to this statement are the barotraumata that do not cause arterial gas embolism. The majority of aural barotrauma victims require serial audiology, nasal decongestants, analgesics and, if inner ear barotrauma is suspected, strict bed rest. It is possible however that hyperbaric oxygen (plus stellate ganglion blockade) may be an effective treatment of this latter group of patients. The other barotraumata that often require treatment are those of the lung—most of those respond well to 100% oxygen at atmospheric pressure. Occasionally, chest cannulation may be needed for a pneumothorax. For other patients, early recompression is indicated.


An increase in ambient pressure will make bubbles smaller and hence less stable (by increasing surface tension pressure). These smaller bubbles will also have a greater surface area to volume for resolution by diffusion and their mechanical disruptive and compressive effects on tissue will be reduced. It is also possible that there is a threshold bubble volume that will stimulate a “foreign-body” reaction. By reducing bubble size, this effect may be reduced. Finally, reducing the volume (length) of columns of gas that are trapped in the systemic circulation will promote their redistribution to the veins. The other outcome of most recompressions is an increase in the inspired (PiO2) and arterial oxygen tension (PaO2). This will relieve hypoxia, lower interstitial fluid pressure, inhibit the activation and accumulation of polymorphonuclear leukocytes that is usually provoked by bubbles, and lower the haematocrit and hence blood viscosity.


The ideal pressure at which to treat decompression illness is not established, although the conventional first choice is 2.8 bar absolute (60 fsw; 282 kPa), with further compression to 4 and 6 bar absolute pressure if the response of symptoms and signs is poor. Experiments in animals suggest that 2 bars absolute pressure is as effective a treatment pressure as greater compressions.


Similarly, the ideal gas to be breathed during the therapeutic recompression of these injured workers is not established. Oxygen-helium mixtures may be more effective in the shrinkage of air bubbles than either air or 100% oxygen and are the subject of ongoing research. The ideal PiO2 is thought, from in vivo research, to be about 2 bar absolute pressure although it is well established, in head injured patients, that the ideal tension is lower at 1.5 bars absolute. The dose relationship with regard to oxygen and inhibition of bubble-provoked polymorphonuclear leukocyte accumulation has not yet been established.

Adjuvant care

The treatment of an injured hyperbaric worker in a recompression chamber must not be allowed to compromise his/her need for adjuvant care such as ventilation, rehydration and monitoring. To be a definitive treatment facility, a recompression chamber must have a working interface with the equipment routinely used in critical care medical units.

Follow-up treatment and investigations

Persistent and relapsing symptoms and signs of decompression illness are common and most injured workers will require repeated recompressions. These should continue until the injury is and remains corrected or at least until two successive treatments have failed to produce any sustained benefit. The basis of ongoing investigation is careful clinical neurological examination (including mental status), as available imaging or provocative investigative techniques have either an associated excessive false positive rate (EEG, bone radio-isotope scans, SPECT scans) or an associated excessive false negative rate (CT, MRI, PET, evoked response studies). One year after an episode of decompression illness, the worker should be x-rayed to determine if there is any dysbaric osteonecrosis (aseptic necrosis) of their long bones.


The outcome after recompression therapy of decompression illness depends entirely upon the group being studied. Most hyperbaric workers (e.g., military and oil-field divers) respond well to treatment and significant residual deficits are uncommon. In contrast, many recreational divers treated for decompression illness have a subsequent poor outcome. The reasons for this difference in outcome are not established. Common sequelae of decompression illness are in order of decreasing frequency: depressed mood; problems in short-term memory; sensory symptoms such as numbness; difficulties with micturition and sexual dysfunction; and vague aches and pains.

Return to hyperbaric work

Fortunately, most hyperbaric workers are able to return to hyperbaric work after an episode of decompression illness. This should be delayed for at least a month (to allow a return to normal of the disordered physiology) and must be discouraged if the worker suffered pulmonary barotrauma or has a history of recurrent or severe inner ear barotrauma. A return to work should also be contingent upon:

  • the severity of the decompression illness being commensurate with the extent of the hyperbaric exposure/decompression stress
  • a good response to treatment
  • no evidence of sequelae.



Tuesday, 15 February 2011 19:44

Ventilatory Acclimatization to High Altitude

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People are increasingly working at high altitudes. Mining operations, recreational facilities, modes of transportation, agricultural pursuits and military campaigns are often at high altitude, and all of these require human physical and mental activity. All such activity involves increased requirements for oxygen. A problem is that as one ascends higher and higher above sea level, both the total air pressure (the barometric pressure, PB) and the amount of oxygen in the ambient air (that portion of total pressure due to oxygen, PO2) progressively fall. As a result, the amount of work we can accomplish progressively decreases. These principles affect the workplace. For example, a tunnel in Colorado was found to require 25% more time to complete at an altitude of 11,000 ft than comparable work at sea level, and altitude effects were implicated in the delay. Not only is there increased muscular fatigue, but also, deterioration of mental function. Memory, computation, decision making and judgement all become impaired. Scientists doing calculations at the Mona Loa Observatory at an altitude above 4,000 m on the island of Hawaii have found they require more time to perform their calculations and they make more mistakes than at sea level. Because of the increasing scope, magnitude, variety and distribution of human activities on this planet, more people are working at high altitude, and effects of altitude become an occupational issue.

Fundamentally important to occupational performance at altitude is maintaining the oxygen supply to the tissues. We (and other animals) have defences against low oxygen states (hypoxia). Chief among these is an increase in breathing (ventilation), which begins when the oxygen pressure in the arterial blood (PaO2) decreases (hypoxemia), is present for all altitudes above sea level, is progressive with altitude and is our most effective defence against low oxygen in the environment. The process whereby breathing increases at high altitude is called ventilatory acclimatization. The importance of the process can be seen in figure 1, which shows that the oxygen pressure in the arterial blood is higher in acclimatized subjects than in unacclimatized subjects. Further, the importance of acclimatization in maintaining the arterial oxygen pressure increases progressively with increasing altitude. Indeed, the unacclimatized person is unlikely to survive above an altitude of 20,000 ft, whereas acclimatized persons have been able to climb to the summit of Mount Everest (29,029 ft, 8,848 m) without artificial sources of oxygen.

Figure 1. Ventilatory acclimatization



The stimulus for the increase in ventilation at high altitude largely and almost exclusively arises in a tissue which monitors the oxygen pressure in the arterial blood and is contained within an organ called the carotid body, about the size of a pinhead, located at a branch point in each of the two carotid arteries, at the level of the angle of the jaw. When the arterial oxygen pressure falls, nerve-like cells (chemoreceptor cells) in the carotid body sense this decrease and increase their firing rate along the 9th cranial nerve, which carries the impulses directly to the respiratory control centre in the brain stem. When the respiratory centre receives increased numbers of impulses, it stimulates an increase in the frequency and depth of breathing via complex nerve pathways, which activate the diaphragm and the muscles of the chest wall. The result is an increased amount of air ventilated by the lungs, figure 2, which in turn acts to restore the arterial oxygen pressure. If a subject breathes oxygen or air enriched with oxygen, the reverse happens. That is, the chemoreceptor cells decrease their firing rate, which decreases the nerve traffic to the respiratory centre, and breathing decreases. These small organs on each side of the neck are very sensitive to small changes in oxygen pressure in the blood. Also, they are almost entirely responsible for maintaining the body’s oxygen level, for when both of them are damaged or removed, ventilation no longer increases when blood oxygen levels fall. Thus an important factor controlling breathing is the arterial oxygen pressure; a decrease in oxygen level leads to an increase in breathing, and an increase in oxygen level leads to a decrease in breathing. In each case the result is, in effect, the body’s effort to maintain blood oxygen levels constant.

Figure 2. Sequence of events in acclimatization


Time course (factors opposing the increase in ventilation at altitude)

Oxygen is required for the sustained production of energy, and when oxygen supply to tissues is reduced (hypoxia), tissue function may become depressed. Of all organs, the brain is most sensitive to lack of oxygen, and, as noted above, centres within the central nervous system are important in the control of breathing. When we breathe a low-oxygen mixture, the initial response is an increase in ventilation, but after 10 minutes or so the increase is blunted to some extent. While the cause for this blunting is not known, its suggested cause is depression of some central neural function related to the ventilation pathway, and has been called hypoxic ventilatory depression. Such depression has been observed shortly after ascent to high altitude. The depression is transient, lasting only a few hours, possibly because there is some tissue adaptation within the central nervous system.

Nevertheless, some increase in ventilation usually begins immediately on going to high altitude, although time is required before maximum ventilation is achieved. On arrival at altitude, increased carotid body activity attempts to increase ventilation, and thereby to raise the arterial oxygen pressure back to the sea level value. However, this presents the body with a dilemma. An increase in breathing causes an increased excretion of carbon dioxide (CO2) in the exhaled air. When CO2 is in body tissues, it creates an acid aqueous solution, and when it is lost in exhaled air, the body fluids, including blood, become more alkaline, thus altering the acid-base balance in the body. The dilemma is that ventilation is regulated not only to keep oxygen pressure constant, but also for acid-base balance. CO2 regulates breathing in the opposite direction from oxygen. Thus when the CO2 pressure (i.e., the degree of acidity somewhere within the respiratory centre) rises, ventilation rises, and when it falls, ventilation falls. On arrival at high altitude, any increase in ventilation caused by the low oxygen environment will lead to a fall in CO2 pressure, which causes alkalosis and acts to oppose the increased ventilation (figure 2). Therefore, the dilemma on arrival is that the body cannot maintain constancy in both oxygen pressure and acid-base balance. Human beings require many hours and even days to regain proper balance.

One method for rebalancing is for the kidneys to increase alkaline bicarbonate excretion in the urine, which compensates for the respiratory loss of acidity, thus helping to restore the body’s acid-base balance toward the sea-level values. The renal excretion of bicarbonate is a relatively slow process. For example, on going from sea level to 4,300 m (14,110 ft), acclimatization requires from seven to ten days (figure 3). This action of the kidneys, which reduces the alkaline inhibition of ventilation, was once thought to be the major reason for the slow increase in ventilation following ascent, but more recent research assigns a dominant role to a progressive increase in the sensitivity of the hypoxic sensing ability of the carotid bodies during the early hours to days following ascent to altitude. This is the interval of ventilatory acclimatization. The acclimatization process allows, in effect, ventilation to rise in response to low arterial oxygen pressure even though the CO2 pressure is falling. As the ventilation rises and CO2 pressure falls with acclimatization at altitude, there is a resultant and concomitant rise in oxygen pressure within the lung alveoli and the arterial blood.

Figure 3. Time course of ventilatory acclimatization for sea level  subjects taken to 4,300 m altitude


Because of the possibility of transient hypoxic ventilatory depression at altitude, and because acclimatization is a process which begins only upon entering a low oxygen environment, the minimal arterial oxygen pressure occurs upon arrival at altitude. Thereafter, the arterial oxygen pressure rises relatively rapidly for the initial days and thereafter increases more slowly, as in figure 3. Because the hypoxia is worse soon after arrival, the lethargy and symptoms which accompany altitude exposure are also worse during the first hours and days. With acclimatization, a restored sense of well-being usually develops.

The time required for acclimatization increases with increasing altitude, consistent with the concept that greater increase in ventilation and acid-base adjustments require longer intervals for renal compensation to occur. Thus while acclimatization may require three to five days for a sea-level native to acclimatize at 3,000 m, for altitudes above 6,000 to 8,000 m, complete acclimatization, even if it is possible, may require six weeks or more (figure 4). When the altitude-acclimatized person returns to sea level, the process reverses. That is, the arterial oxygen pressure now rises to the sea-level value and ventilation falls. Now there is less CO2 exhaled, and CO2 pressure rises in the blood and in the respiratory centre. The acid-base balance is altered toward the acid side, and the kidneys must retain bicarbonate to restore balance. Although the time required for the loss of acclimatization is not as well understood, it seems to require approximately as long an interval as the acclimatization process itself. If so, then return from altitude, hypothetically, gives a mirror image of altitude ascent, with one important exception: arterial oxygen pressures immediately become normal on descent.






Figure 4. Effects of altitude on barometric pressure and inspired PO2


Variability among individuals

As might be expected, individuals vary with regard to time required for, and magnitude of, ventilatory acclimatization to a given altitude. One very important reason is the large variation between individuals in the ventilatory response to hypoxia. For example, at sea level, if one holds the CO2 pressure constant, so that it does not confound the ventilatory response to low oxygen, some normal persons show little or no increase in ventilation, while others show a very large (up to fivefold) increase. The ventilatory response to breathing low-oxygen mixtures seems to be an inherent characteristic of an individual, because family members behave more alike than do persons who are not related. Those persons who have poor ventilatory responses to low oxygen at sea level, as expected, also seem to have smaller ventilatory responses over time at high altitude. There may be other factors causing inter-individual variability in acclimatization, such as variability in the magnitude of ventilatory depression, in the function of the respiratory centre, in sensitivity to acid-base changes, and in renal handling of bicarbonate, but these have not been evaluated.


Poor sleep quality, particularly before there is ventilatory acclimatization, is not only a common complaint, but also a factor that will impair occupational efficiency. Many things interfere with the act of breathing., including emotions, physical activity, eating and the degree of wakefulness. Ventilation decreases during sleep, and the capacity for breathing to be stimulated by low oxygen or high CO2 also decreases. Respiratory rate and depth of breathing both decrease. Further, at high altitude, where there are fewer oxygen molecules in the air, the amount of oxygen stored in the lung alveoli between breaths is less. Thus if breathing ceases for a few seconds (called apnoea, which is a common event at high altitude), the arterial oxygen pressure falls more rapidly than at sea level, where, in essence, the reservoir for oxygen is greater.

Periodic cessation of breathing is almost universal during the first few nights following ascent to high altitude. This is a reflection of the respiratory dilemma of altitude, described earlier, working in cyclic fashion: hypoxic stimulation increases ventilation, which in turn lowers carbon dioxide levels, inhibits breathing, and increases hypoxic stimulation, which again stimulates ventilation. Usually there is an apnoeic period of 15 to 30 seconds, followed by several very large breaths, which often briefly awakens the subject, after which there is another apnoea. The arterial oxygen pressure sometimes falls to alarming levels as a result of the apnoeic periods. There may be frequent awakenings, and even when total sleep time is normal its fragmentation impairs sleep quality such that there is the impression of having had a restless or sleepless night. Giving oxygen eliminates the cycling of hypoxic stimulation, and alkalotic inhibition abolishes the periodic breathing and restores normal sleep.

Middle-aged males in particular also are at risk for another cause of apnoea, namely intermittent obstruction of the upper airway, the common cause of snoring. While intermittent obstruction at the back of the nasal passages usually causes only annoying noise at sea level, at high altitude, where there is a smaller reservoir of oxygen in the lungs, such obstruction may lead to severely low levels of arterial oxygen pressure and poor sleep quality.

Intermittent Exposure

There are work situations, particularly in the Andes of South America, that require a worker to spend several days at altitudes above 3,000 to 4,000 m, and then to spend several days at home, at sea level. The particular work schedules (how many days are to be spent at altitude, say four to 14, and how many days, say three to seven, at sea level) are usually determined by the economics of the workplace more than by health considerations. However, a factor to be considered in the economics is the interval required both for acclimatization and loss of acclimatization to the altitude in question. Particular attention should be placed on the worker’s sense of well-being and performance on the job on arrival and the first day or two thereafter, regarding fatigue, time required to perform routine and non-routine functions, and errors made. Also strategies should be considered to minimize the time required for acclimatization at altitude, and to improve function during the waking hours.



The major effects of high altitude on humans relate to the changes in barometric pressure (PB) and its consequential changes in the ambient pressure of oxygen (O2). Barometric pressure decreases with increasing altitude in a logarithmic fashion and can be estimated by the following equation:

where a = altitude, expressed in metres. In addition, the relationship of barometric pressure to altitude is influenced by other factors such as distance from the equator and season. West and Lahiri (1984) found that direct measurements of barometric pressure near the equator and at the summit of Mt. Everest (8,848 m) were greater than predictions based on the International Civil Aviation Organization Standard Atmosphere. Weather and temperature also affect the relationship between barometric pressure and altitude to the extent that a low-pressure weather system can reduce pressure, making sojourners to high altitude “physiologically higher”. Since the inspired partial pressure of oxygen (PO2) remains constant at approximately 20.93% of barometric pressure, the most important determinant of inspired PO2 at any altitude is the barometric pressure. Thus, inspired oxygen decreases with increasing altitude due to decreased barometric pressure, as shown in figure 1.

Figure 1. Effects of altitude on barometric pressure and inspired PO2


Temperature and ultraviolet radiation also change at high altitudes. Temperature decreases with increasing altitude at a rate of approximately 6.5 °C per 1,000 m. Ultraviolet radiation increases approximately 4% per 300 m due to decreased cloudiness, dust, and water vapour. In addition, as much as 75% of ultraviolet radiation can be reflected back by snow, further increasing exposure at high altitude. Survival in high altitude environments is dependent on adaptation to and/or protection from each of these elements.











While rapid ascent to high altitudes often results in death, slow ascent by mountaineers can be successful when accompanied by compensatory physiological adaptation measures. Acclimatization to high altitudes is geared towards maintaining an adequate supply of oxygen to meet metabolic demands despite the decreasing inspired PO2. In order to achieve this goal, changes occur in all organ systems involved with oxygen uptake into the body, distribution of O2 to the necessary organs, and O2 unloading to the tissues.

Discussion of oxygen uptake and distribution requires understanding the determinants of oxygen content in the blood. As air enters the alveolus, the inspired PO2 decreases to a new level (called the alveolar PO2) because of two factors: increased partial pressure of water vapour from humidification of inspired air, and increased partial pressure of carbon dioxide (PCO2) from CO2 excretion. From the alveolus, oxygen diffuses across the alveolar capillary membrane into the blood as a result of a gradient between alveolar PO2 and blood PO2. The majority of oxygen found in blood is bound to haemoglobin (oxyhaemoglobin). Thus, oxygen content is directly related to both the haemoglobin concentration in the blood and the percentage of O2 binding sites on haemoglobin that are saturated with oxygen (oxyhaemoglobin saturation). Therefore, understanding the relationship between arterial PO2 and oxyhaemoglobin saturation is essential for understanding the determinants of oxygen content in the blood. Figure 2 illustrates the oxyhaemoglobin dissociation curve. With increasing altitude, inspired PO2 decreases and, therefore, arterial PO2 and oxyhaemoglobin saturation decreases. In normal subjects, altitudes greater than 3,000 m are associated with sufficiently decreased arterial PO2 that oxyhaemoglobin saturation falls below 90%, on the steep portion of the oxyhaemoglobin dissociation curve. Further increases in altitude will predictably result in significant desaturation in the absence of compensatory mechanisms.

Figure 2. Oxyhaemoglobin dissociation curve


The ventilatory adaptations that occur in high-altitude environments protect the arterial partial pressure of oxygen against the effects of decreasing ambient oxygen levels, and can be divided into acute, subacute and chronic changes. Acute ascent to high altitude results in a fall in the inspired PO2 which in turn leads to a decrease in the arterial PO2 (hypoxia). In order to minimize the effects of decreased inspired PO2 on arterial oxyhaemoglobin saturation, the hypoxia that occurs at high altitude triggers an increase in ventilation, mediated through the carotid body (hypoxic ventilatory response–HVR). Hyperventilation increases carbon dioxide excretion and subsequently the arterial and then the alveolar partial pressure of carbon dioxide (PCO2) falls. The fall in alveolar PCO2 allows alveolar PO2 to rise, and consequently, arterial PO2 and arterial O2 content increases. However, the increased carbon dioxide excretion also causes a decrease in blood hydrogen ion concentration ([H+]) leading to the development of alkalosis. The ensuing alkalosis inhibits the hypoxic ventilatory response. Thus, on acute ascent to high altitude there is an abrupt increase in ventilation that is modulated by the development of an alkalosis in the blood.

Over the next several days at high altitude, further changes in ventilation occur, commonly referred to as ventilatory acclimatization. Ventilation continues to increase over the next several weeks. This further increase in ventilation occurs as the kidney compensates for the acute alkalosis by excretion of bicarbonate ions, with a resultant rise in blood [H+]. It was initially believed that renal compensation for the alkalosis removed the inhibitory influence of alkalosis on the hypoxic ventilatory response, thereby allowing the full potential of the HVR to be reached. However, measurements of blood pH revealed that the alkalosis persists despite the increase in ventilation. Other postulated mechanisms include: (1) cerebrospinal fluid (CSF) pH surrounding the respiratory control centre in the medulla may have returned to normal despite the persistent serum alkalosis; (2) increased sensitivity of the carotid body to hypoxia; (3) increased response of the respiratory controller to CO2. Once ventilatory acclimatization has occurred, both hyperventilation and the increased HVR persist for several days after return to lower altitudes, despite resolution of hypoxia.

Further ventilatory changes occur after several years of living at high altitude. Measurements in high-altitude natives have shown a decreased HVR when compared to values obtained in acclimatized individuals, although not to levels seen in subjects at sea level. The mechanism for the decreased HVR is unknown, but may be related to hypertrophy of the carotid body and/or development of other adaptive mechanisms for preserving tissue oxygenation such as: increased capillary density; increased gas exchange capacity of the tissues; increased number and density of mitochondria; or increased vital capacity.

In addition to its effect on ventilation, hypoxia also induces constriction of the vascular smooth muscle in the pulmonary arteries (hypoxic vasoconstriction). The ensuing increase in pulmonary vascular resistance and pulmonary artery pressure redirects blood flow away from poorly ventilated alveoli with low alveolar PO2 and towards better ventilated alveoli. In this manner, pulmonary arterial perfusion is matched to lung units that are well ventilated, providing another mechanism for preserving arterial PO2.

Oxygen delivery to the tissues is further enhanced by adaptations in the cardiovascular and haematological systems. On initial ascent to high altitude, heart rate increases, resulting in an increase in cardiac output. Over several days, cardiac output falls due to decreased plasma volume, caused by an increased water loss that occurs at high altitudes. With more time, increased erythropoietin production leads to increased haemoglobin concentration, providing the blood with increased oxygen-carrying capacity. In addition to increasing levels of haemoglobin, changes in the avidity of oxygen binding to haemoglobin may also help maintain tissue oxygenation. A shift of the oxyhaemoglobin dissociation curve to the right may be expected because it would favour release of oxygen to the tissues. However, data obtained from the summit of Mt. Everest and from hypobaric chamber experiments simulating the summit suggest that the curve is shifted to the left (West and Lahiri 1984; West and Wagner 1980; West et al. 1983). Although a left shift would make oxygen unloading to the tissues more difficult, it may be advantageous at extreme altitudes because it would facilitate oxygen uptake in the lungs despite markedly reduced inspired PO2 (43 mmHg on the summit of Mt. Everest versus 149 mmHg at sea level).

The last link in the chain of oxygen supply to the tissues is cellular uptake and utilization of O2. Theoretically, there are two potential adaptations that can occur. First, minimization of the distance that oxygen has to travel on diffusion out of the blood vessel and into the intracellular site responsible for oxidative metabolism, the mitochondria. Second, biochemical alterations can occur that improve mitochondrial function. Minimization of diffusion distance has been suggested by studies that show either increased capillary density or increased mitochondrial density in muscle tissue. It is unclear whether these changes reflect either recruitment or development of capillaries and mitochondria, or are an artefact due to muscle atrophy. In either case, the distance between the capillaries and the mitochondria would be decreased, thereby facilitating oxygen diffusion. Biochemical alterations that may improve mitochondrial function include increased myoglobin levels. Myoglobin is an intracellular protein that binds oxygen at low tissue PO2 levels and facilitates oxygen diffusion into the mitochondria. Myoglobin concentration increases with training and correlates with muscle cell aerobic capacity. Although these adaptations are theoretically beneficial, conclusive evidence is lacking.

Early accounts of high altitude explorers describe changes in cerebral function. Decreased motor, sensory and cognitive abilities, including decreased ability to learn new tasks and difficulty expressing information verbally, have all been described. These deficits may lead to poor judgement and to irritability, further compounding the problems encountered in high-altitude environments. On return to sea level, these deficits improve with a variable time course; reports have indicated impaired memory and concentration lasting from days to months, and decreased finger-tapping speed for one year (Hornbein et al. 1989). Individuals with greater HVR are more susceptible to long-lasting deficits, possibly because the benefit of hyperventilation on arterial oxyhaemoglobin saturation may be offset by hypocapnia (decreased PCO2 in the blood), which causes constriction of the cerebral blood vessels leading to decreased cerebral blood flow.

The preceding discussion has been limited to resting conditions; exercise provides an additional stress as oxygen demand and consumption increases. The fall in ambient oxygen at high altitude causes a fall in maximal oxygen uptake and, therefore, maximal exercise. In addition, the decreased inspired PO2 at high altitudes severely impairs oxygen diffusion into the blood. This is illustrated in figure 3, which plots the time course of oxygen diffusion into the alveolar capillaries. At sea level, there is excess time for equilibration of end-capillary PO2 to alveolar PO2, whereas at the summit of Mt. Everest, full equilibration is not realized. This difference is due to the decreased ambient oxygen level at high altitudes leading to a decreased diffusion gradient between alveolar and venous PO2. With exercise, cardiac output and blood flow increase, thereby reducing transit time of blood cells across the alveolar capillary, further exacerbating the problem. From this discussion, it becomes apparent that the left shift in the O2 and haemoglobin dissociation curve with altitude is necessary as compensation for the decreased diffusion gradient for oxygen in the alveolus.

Figure 3. The calculated time course of oxygen tension in the alveolar capillary


Disturbed sleep is common among sojourners at high altitude. Periodic (Cheyne-Stokes) breathing is universal and characterized by periods of rapid respiratory rate (hyperpnoea) alternating with periods of absent respirations (apnoea) leading to hypoxia. Periodic breathing tends to be more pronounced in individuals with the greatest hypoxic ventilatory sensitivity. Accordingly, sojourners with lower HVR have less severe periodic breathing. However, sustained periods of hypoventilation are then seen, corresponding with sustained decreases in oxyhaemoglobin saturation. The mechanism for periodic breathing probably relates to increased HVR causing increased ventilation in response to hypoxia. The increased ventilation leads to increased blood pH (alkalosis), which in turn suppresses ventilation. As acclimatization progresses, periodic breathing improves. Treatment with acetazolamide reduces periodic breathing and improves arterial oxyhaemoglobin saturation during sleep. Caution should be used with medications and alcohol that suppress ventilation, as they may exacerbate the hypoxia seen during sleep.

Pathophysiological Effects of Reduced Barometric Pressure

The complexity of human physiological adaptation to high altitude provides numerous potential maladaptive responses. Although each syndrome will be described separately, there is considerable overlap between them. Illnesses such as acute hypoxia, acute mountain sickness, high-altitude pulmonary oedema, and high-altitude cerebral oedema most likely represent a spectrum of abnormalities that share a similar pathophysiology.


Hypoxia occurs with ascent to high altitudes because of the decreased barometric pressure and the resultant decrease in ambient oxygen. With rapid ascent, hypoxia occurs acutely, and the body does not have time to adjust. Mountaineers have generally been protected from the effects of acute hypoxia because of the time that elapses, and hence the acclimatization that occurs, during the climb. Acute hypoxia is problematic for both aviators and rescue personnel in high-altitude environments. Acute oxyhaemoglobin desaturation to values less than 40 to 60% leads to loss of consciousness. With less severe desaturation, individuals note headache, confusion, drowsiness and loss of coordination. Hypoxia also induces a state of euphoria which Tissandier, during his balloon flight in 1875, described as experiencing “inner joy”. With more severe desaturation, death occurs. Acute hypoxia responds rapidly and completely to either administration of oxygen or descent.

Acute mountain sickness

Acute mountain sickness (AMS) is the most common disorder in high-altitude environments and afflicts up to two-thirds of sojourners. The incidence of acute mountain sickness is dependent on multiple factors, including rate of ascent, length of exposure, degree of activity, and individual susceptibility. Identification of affected individuals is important in order to prevent progression to pulmonary or cerebral oedema. Identification of acute mountain sickness is made through recognition of characteristic signs and symptoms occurring in the appropriate setting. Most often, acute mountain sickness occurs within a few hours of a rapid ascent to altitudes greater than 2,500 m. The most common symptoms include headache that is more pronounced at night, loss of appetite that may be accompanied by nausea and vomiting, disturbed sleep, and fatigue. Individuals with AMS often complain of shortness of breath, cough and neurological symptoms such as memory deficits and auditory or visual disturbances. Findings on physical exam may be lacking, although fluid retention may be an early sign. The pathogenesis of acute mountain illness may relate to relative hypoventilation that would increase cerebral blood flow and intracranial pressure by increasing arterial PCO2 and decreasing arterial PO2. This mechanism may explain why persons with greater HVR are less likely to develop acute mountain sickness. The mechanism for fluid retention is not well understood, but may be related to abnormal plasma levels for proteins and/or hormones that regulate renal excretion of water; these regulators may respond to the increased activity of the sympathetic nervous system noted in patients with acute mountain sickness. The accumulation of water may in turn lead to the development of oedema or swelling of the interstitial spaces in the lungs. More severe cases may go on to develop pulmonary or cerebral oedema.

Prevention of acute mountain sickness can be accomplished through slow, graded ascent, allowing adequate time for acclimatization. This may be especially important for those individuals with greater susceptibility or a prior history of acute mountain sickness. In addition, administration of acetazolamide before or during ascent may help prevent and ameliorate symptoms of acute mountain sickness. Acetazolamide inhibits the action of carbonic anhydrase in the kidneys and leads to increased excretion of bicarbonate ions and water, producing an acidosis in the blood. The acidosis stimulates respiration, leading to increased arterial oxyhaemoglobin saturation and decreased periodic breathing during sleep. Through this mechanism, acetazolamide speeds the natural process of acclimatization.

Treatment of acute mountain sickness can be accomplished most effectively by descent. Further ascent to high altitudes is contra-indicated, as the disease may progress. When descent is not possible, oxygen may be administered. Alternatively, portable lightweight fabric hyperbaric chambers may be brought on expeditions to high-altitude environments. Hyperbaric bags are particularly valuable when oxygen is not available and descent is not possible. Several drugs are available that improve symptoms of acute mountain sickness, including acetazolamide and dexamethasone. The mechanism of action of dexamethasone is unclear, although it may act by decreasing oedema formation.

High-altitude pulmonary oedema

High-altitude pulmonary oedema affects approximately 0.5 to 2.0% of individuals who ascend to altitudes greater than 2,700 m and is the most common cause of death due to illnesses encountered at high altitudes. High-altitude pulmonary oedema develops from 6 to 96 hours after ascent. Risk factors for the development of high-altitude pulmonary oedema are similar to those for acute mountain sickness. Common early signs include symptoms of acute mountain sickness accompanied by decreased exercise tolerance, increased recovery time after exercise, shortness of breath on exertion, and persistent dry cough. As the condition worsens, the patient develops shortness of breath at rest, findings of audible congestion in the lungs, and cyanosis of the nail beds and lips. The pathogenesis of this disorder is uncertain but probably relates to increased microvascular pressure or increased permeability of the microvasculature leading to the development of pulmonary oedema. Although pulmonary hypertension may help explain the pathogenesis, elevation in the pulmonary artery pressure due to hypoxia has been observed in all individuals who ascend to high altitude, including those who do not develop pulmonary oedema. Nevertheless, susceptible individuals may possess uneven hypoxic constriction of the pul-monary arteries, leading to over-perfusion of the microvasculature in localized areas where hypoxic vasoconstriction was absent or diminished. The resulting increase in pressure and shear forces may damage the capillary membrane, leading to oedema formation. This mechanism explains the patchy nature of this disease and its appearance on x-ray examination of the lungs. As with acute mountain sickness, individuals with a lower HVR are more likely to develop high-altitude pulmonary oedema as they have lower oxyhaemoglobin saturations and, therefore, greater hypoxic pulmonary vasoconstriction.

Prevention of high-altitude pulmonary oedema is similar to prevention of acute mountain sickness and includes gradual ascent and use of acetazolamide. Recently, use of the smooth-muscle relaxing agent nifedipine has been shown to be of benefit in preventing disease in individuals with a prior history of high-altitude pulmonary oedema. Additionally, avoidance of exercise may have a preventive role, although it is probably limited to those individuals who already posses a subclinical degree of this disease.

Treatment of high-altitude pulmonary oedema is best accomplished by assisted evacuation to a lower altitude, keeping in mind that the victim needs to limit his or her exertion. After descent, improvement is rapid and additional treatment other than bed rest and oxygen are usually not necessary. When descent is not possible, oxygen therapy may be beneficial. Drug treatment has been attempted with multiple agents, most successfully with the diuretic furosemide and with morphine. Caution must be used with these drugs, as they can lead to dehydration, decreased blood pressure, and respiratory depression. Despite the effectiveness of descent as therapy, mortality remains at approximately 11%. This high mortality rate may reflect failure to diagnose the disease early in its course, or inability to descend coupled with lack of availability of other treatments.

High-altitude cerebral oedema

High-altitude cerebral oedema represents an extreme form of acute mountain sickness that has progressed to include generalized cerebral dysfunction. The incidence of cerebral oedema is unclear because it is difficult to differentiate a severe case of acute mountain sickness from a mild case of cerebral oedema. The pathogenesis of high-altitude cerebral oedema is an extension of the pathogenesis of acute mountain sickness; hypoventilation increases cerebral blood flow and intracranial pressure progressing to cerebral oedema. Early symptoms of cerebral oedema are identical to symptoms of acute mountain sickness. As the disease progresses, additional neurological symptoms are noted, including severe irritability and insomnia, ataxia, hallucinations, paralysis, seizures and eventually coma. Examination of the eyes commonly reveals swelling of the optic disc or papilloedema. Retinal haemorrhages are frequently noted. In addition, many cases of cerebral oedema have concurrent pulmonary oedema.

Treatment of high-altitude cerebral oedema is similar to treatment of other high-altitude disorders, with descent being the preferred therapy. Oxygen should be administered to maintain oxyhaemoglobin saturation greater that 90%. Oedema formation may be decreased with use of corticosteroids such as dexamethasone. Diuretic agents have also been utilized to decrease oedema, with uncertain efficacy. Comatose patients may require additional support with airway management. The response to treatment is variable, with neurological deficits and coma persisting for days to weeks after evacuation to lower altitudes. Preventative measures for cerebral oedema are identical to measures for other high-altitude syndromes.

Retinal haemorrhages

Retinal haemorrhages are extremely common, affecting up to 40% of individuals at 3,700 m and 56% at 5,350 m. Retinal haemorrhages are usually asymptomatic. They are most likely caused by increased retinal blood flow and vascular dilatation due to arterial hypoxia. Retinal haemorrhages are more common in individuals with headaches and can be precipitated by strenuous exercise. Unlike other high-altitude syndromes, retinal haemorrhages are not preventable by acetazolamide or furosemide therapy. Spontaneous resolution is usually seen within two weeks.

Chronic mountain sickness

Chronic mountain sickness (CMS) afflicts residents and long-term inhabitants of high altitude. The first description of chronic mountain sickness reflected Monge’s observations of Andean natives living at altitudes above 4,000 m. Chronic mountain sickness, or Monge’s disease, has since been described in most high-altitude dwellers except Sherpas. Males are more commonly affected than females. Chronic mountain sickness is characterized by plethora, cyanosis and elevated red blood cell mass leading to neurological symptoms that include headache, dizziness, lethargy and impaired memory. Victims of chronic mountain sickness may develop right heart failure, also called cor pulmonale, due to pulmonary hypertension and markedly reduced oxyhaemoglobin saturation. The pathogenesis of chronic mountain sickness is unclear. Measurements from affected individuals have revealed a decreased hypoxic ventilatory response, severe hypoxemia that is exacerbated during sleep, increased haemoglobin concentration and increased pulmonary artery pressure. Although a cause-and-effect relationship seems likely, evidence is lacking and often confusing.

Many symptoms of chronic mountain sickness can be ameliorated by descent to sea level. Relocation to sea level removes the hypoxic stimulus for red blood cell production and pulmonary vasoconstriction. Alternate treatments include: phlebotomy to reduce red blood cell mass, and low-flow oxygen during sleep to improve hypoxia. Therapy with medroxyprogesterone, a respiratory stimulant, has also been found to be effective. In one study, ten weeks of medroxyprogesterone therapy was followed by improved ventilation and hypoxia, and decreased red blood cell counts.

Other conditions

Patients with sickle cell disease are more likely to suffer from painful vaso-occlusive crisis at high altitude. Even moderate altitudes of 1,500 m have been known to precipitate crises, and altitudes of 1,925 m are associated with a 60% risk of crises. Patients with sickle cell disease residing at 3,050 m in Saudi Arabia have twice as many crises as patients residing at sea level. In addition, patients with sickle cell trait may develop splenic infarct syndrome on ascent to high altitude. Likely aetiologies for the increased risk of vaso-occlusive crisis include: dehydration, increased red blood cell count, and immobility. Treatment of vaso-occlusive crisis includes descent to sea level, oxygen and intravenous hydration.

Essentially no data exist describing the risk to pregnant patients on ascent to high altitudes. Although patients residing at high altitude have an increased risk of pregnancy-induced hypertension, no reports of increased foetal demise exist. Severe hypoxia may cause abnormalities in foetal heart rate; however, this occurs only at extreme altitudes or in the presence of high-altitude pulmonary oedema. Therefore, the greatest risk to the pregnant patient may relate to the remoteness of the area rather than to altitude-induced complications.



Large numbers of people work at high altitudes, particularly in the cities and villages of the South American Andes and the Tibetan plateau. The majority of these people are highlanders who have lived in the area for many years and perhaps several generations. Much of the work is agricultural in nature—for example, tending domesticated animals.

However, the focus of this article is different. Recently there has been a large increase in commercial activities at altitudes of 3,500 to 6,000 m. Examples include mines in Chile and Peru at altitudes of around 4,500 m. Some of these mines are very large, employing over 1,000 workers. Another example is the telescope facility at Mauna Kea, Hawaii, at an altitude of 4,200 m.

Traditionally, the high mines in the South American Andes, some of which date back to the Spanish colonial period, have been worked by indigenous people who have been at high altitude for generations. Recently however, increasing use is being made of workers from sea level. There are several reasons for this change. One is that there are not enough people in these remote areas to operate the mines. An equally important reason is that as the mines become increasingly automated, skilled people are required to operate large digging machines, loaders and trucks, and local people may not have the necessary skills. A third reason is the economics of developing these mines. Whereas previously whole towns were set up in the vicinity of the mine to accommodate the workers’ families, and necessary ancillary facilities such as schools and hospitals, it is now seen to be preferable to have the families live at sea level, and have the workers commute to the mines. This is not purely an economic issue. The quality of life at an altitude of 4,500 m is less than at lower altitudes (e.g., children grow more slowly). Therefore the decision to have the families remain at sea level while the workers commute to high altitude has a sound socio-economic basis.

The situation where a workforce moves from sea level to altitudes of approximately 4,500 m raises many medical issues, many of which are poorly understood at the present time. Certainly most people who travel from sea level to an altitude of 4,500 m develop some symptoms of acute mountain sickness initially. Tolerance to the altitude often improves after the first two or three days. However, the severe hypoxia of these altitudes has a number of deleterious effects on the body. Maximal work capacity is decreased, and people fatigue more rapidly. Mental efficiency is reduced and many people find it is much more difficult to concentrate. Sleep quality is often poor, with frequent arousals and periodic breathing (the breathing waxes and wanes three or four times every minute) with the result that that the arterial PO2 falls to low levels following the periods of apnoea or reduced breathing.

Tolerance to high altitude varies greatly between individuals, and it is often very difficult to predict who is going to be intolerant of high altitude. A substantial number of people who would like to work at an altitude of 4,500 m find that they are unable to do so, or that the quality life is so poor that they refuse to remain at that altitude. Topics such as the selection of workers who are likely to tolerate high altitude, and the scheduling of their work between high altitude and the period with their families at sea level, are relatively new and not well understood.

Pre-employment Examination

In addition to the usual type of pre-employment examination, special attention should be given to the cardio-pulmonary system, because working at high altitude makes great demands on the respiratory and cardiovascular systems. Medical conditions such as early chronic obstructive pulmonary disease and asthma will be much more disabling at high altitude because of the high levels of ventilation, and should be specifically looked for. A heavy cigarette smoker with symptoms of early bronchitis is likely to have difficulty tolerating high altitude. Forced spirometry should be measured in addition to the usual chest examination including chest radiograph. If possible, an exercise test should be carried out because any exercise intolerance will be exaggerated at high altitude.

The cardiovascular system should be carefully examined, including an exercise electrocardiogram if that is feasible. Blood counts should be made to exclude workers with unusual degrees of anaemia or polycythaemia.

Living at high altitude increases the psychological stress in many people, and a careful history should be taken to exclude prospective workers with previous behavioural problems. Many modern mines at high altitude are dry (no alcohol permitted). Gastro-intestinal symptoms are common in some people at high altitude, and workers who have a history of dyspepsia may do poorly.

Selection of Workers to Tolerate High Altitude

In addition to excluding workers with lung or heart disease who are likely to do poorly at high altitude, it would be very valuable if tests could be carried out to determine who is likely to tolerate altitude well. Unfortunately little is known at the present time about predictors of tolerance to high altitude, though considerable work is being done on this at the present time.

The best predictor of tolerance to high altitude is probably previous experience at high altitude. If someone has been able to work at an altitude of 4,500 m for several weeks without appreciable problems, it is very likely that he or she will be able to do this again. By the same token, somebody who tried to work at high altitude and found that he or she could not tolerate it, is very likely to have the same problem next time. Therefore in selecting workers, a great deal of emphasis should be placed on successful previous employment at high altitude. However, clearly this criterion cannot be used for all workers because otherwise no new people would enter the high-altitude working pool.

Another possible predictor is the magnitude of the ventilatory response to hypoxia. This can be measured at sea level by giving the prospective worker a low concentration of oxygen to breathe and measuring the increase in ventilation. There is some evidence that people who have a relatively weak hypoxic ventilatory response tolerate high altitude poorly. For example, Schoene (1982) showed that 14 high-altitude climbers had significantly higher hypoxic ventilatory responses than ten controls. Further measurements were made on the 1981 American Medical Research Expedition to Everest, where it was shown that the hypoxic ventilatory response measured before and on the Expedition correlated well with performance high on the mountain (Schoene, Lahiri and Hackett 1984). Masuyama, Kimura and Sugita (1986) reported that five climbers who reached 8,000 m in Kanchenjunga had a higher hypoxic ventilatory response than five climbers who did not.

However, this correlation is by no means universal. In a prospective study of 128 climbers going to high altitudes, a measure of hypoxic ventilatory response did not correlate with the height reached, whereas a measurement of maximal oxygen uptake at sea level did correlate (Richalet, Kerome and Bersch 1988). This study also suggested that the heart rate response to acute hypoxia might be a useful predictor of performance at high altitude. There have been other studies showing a poor correlation between hypoxic ventilatory response and performance at extreme altitude (Ward, Milledge and West 1995).

The problem with many of these studies is that the results are chiefly applicable to much higher altitudes than of interest here. Also there are many examples of climbers with moderate values of hypoxic ventilatory response who do well at high altitude. Nevertheless, an abnormally low hypoxic ventilatory response is probably a risk factor for tolerating even medium altitudes such as 4,500 m.

One way of measuring the hypoxic ventilatory response at sea level is to have the subject rebreathe into a bag which is initially filled with 24% oxygen, 7% carbon dioxide, and the balance nitrogen. During rebreathing the PCO2 is monitored and held constant by means of a variable bypass and carbon dioxide absorber. Rebreathing can be continued until the inspired PO2 falls to about 40 mmHg (5.3 kPa). The arterial oxygen saturation is measured continually with a pulse oximeter, and the ventilation plotted against the saturation (Rebuck and Campbell 1974). Another way of measuring the hypoxic ventilatory response is to determine the inspiratory pressure during a brief period of airway occlusion while the subject is breathing a low-oxygen mixture (Whitelaw, Derenne and Milic-Emili 1975).

Another possible predictor of tolerance to high altitude is work capacity during acute hypoxia at sea level. The rationale here is that someone who is not able to tolerate acute hypoxia is more likely to be intolerant of chronic hypoxia. There is little evidence for or against this hypothesis. Soviet physiologists used tolerance to acute hypoxia as one of the criteria for selection of climbers for their successful 1982 Everest expedition (Gazenko 1987). On the other hand, the changes that occur with acclimatization are so profound that it would not be surprising if exercise performance during acute hypoxia were poorly correlated with the ability to work during chronic hypoxia.

Another possible predictor is the increase in pulmonary artery pressure during acute hypoxia at sea level. This can be measured non-invasively in many people by Doppler ultrasound. The main rationale for this test is the known correlation between the development of high-altitude pulmonary oedema and the degree of hypoxic pulmonary vasoconstriction (Ward, Milledge and West 1995). However, since high-altitude pulmonary oedema is uncommon in people working at an altitude of 4,500 m, the practical value of this test is questionable.

The only way to determine whether these tests for the selection of workers have practical value is a prospective study where the results of the tests done at sea level are correlated with subsequent assessment of tolerance to high altitude. This raises the question of how high-altitude tolerance will be measured. The usual way of doing this is by questionnaires such as the Lake Louise questionnaire (Hackett and Oelz 1992). However, questionnaires may be unreliable in this population because workers perceive that if they admit to altitude intolerance, they might lose their jobs. It is true that there are objective measures of altitude intolerance such as quitting work, rales in the lungs as indications of subclinical pulmonary oedema, and mild ataxia as an indication of subclinical high-altitude cerebral oedema. However, these features will be seen only in people with severe altitude intolerance, and a prospective study based solely on such measurements would be very insensitive.

It should be emphasized that the value of these possible tests for determining tolerance to working at high altitude has not been established. However, the economic implications of taking on a substantial number of workers who are unable to perform satisfactorily at high altitude are such that it would be very valuable to have useful predictors. Studies are presently underway to determine whether some of these predictors are valuable and feasible. Measurements such as the hypoxic ventilatory response to hypoxia, and work capacity during acute hypoxia at sea level, are not particularly difficult. However, they need to be done by a professional laboratory, and the cost of these investigations can be justified only if the predictive value of the measurements is substantial.

Scheduling between High Altitude and Sea Level

Again, this article is addressed to the specific problems which occur when commercial activities such as mines at altitudes of about 4,500 m employ workers who commute from sea level where their families live. Scheduling is obviously not an issue where people live permanently at high altitude.

Designing the optimal schedule for moving between high altitude and sea level is a challenging problem, and as yet there is little scientific basis for the schedules that have been employed so far. These have been based mainly on social factors such as how long the workers are willing to spend at high altitude before seeing their families again.

The main medical rationale for spending several days at a time at high altitude is the advantage gained from acclimatization. Many people who develop symptoms of acute mountain sickness after going to high altitude feel much better after two to four days. Therefore rapid acclimatization is occurring over this period. In addition it is known that the ventilatory response to hypoxia takes seven to ten days to reach a steady state (Lahiri 1972; Dempsey and Forster 1982). This increase in ventilation is one of the most important features of the acclimatization process, and therefore it is reasonable to recommend that the working period at high altitude be at least ten days.

Other features of high-altitude acclimatization probably take much longer to develop. One example is polycythaemia, which takes several weeks to reach a steady state. However, it should be added that the physiological value of polycythaemia is much less certain than was thought at one time. Indeed, Winslow and Monge (1987) have shown that the severe degrees of polycythaemia which are sometimes seen in permanent dwellers at altitudes of about 4,500 m are counterproductive in that work capacity can sometimes be increased if the haematocrit is lowered by removing blood over several weeks.

Another important issue is the rate of deacclimatization. Ideally the workers should not lose all the acclimatization that they have developed at high altitude during their period with their families at sea level. Unfortunately, there has been little work on the rate of deacclimatization, although some measurements suggest that the rate of change of the ventilatory response during deacclimatization is slower than during acclimatization (Lahiri 1972).

Another practical issue is the time required to move workers from sea level to high altitude and back again. In a new mine at Collahuasi in north Chile, it takes only a few hours to reach the mine by bus from the coastal town of Iquique, where most of the families are expected to live. However, if the worker resides in Santiago, the trip could take over a day. Under these circumstances, a short working period of three or four days at high altitude would clearly be inefficient because of the time wasted in travelling.

Social factors also play a critical role in any scheduling that involves time away from the family. Even if there are medical and physiological reasons why an acclimatization period of 14 days is optimal, the fact that the workers are unwilling to leave their families for more than seven or ten days may be an overriding factor. Experience so far shows that a schedule of seven days at high altitude followed by seven days at sea level, or ten days at high altitude followed by the same period at sea level are probably the most acceptable schedules.

Note that with this type of schedule, the worker never fully acclimatizes to high altitude, nor fully deacclimatizes while at sea level. He therefore spends his time oscillating between the two extremes, never receiving the full benefit of either state. In addition, some workers complain of extreme tiredness when they return to sea level, and spend the first two or three days recovering. Possibly this is related to the poor quality of sleep which is often a feature of living at high altitude. These problems highlight our ignorance of the factors that determine the best schedules, and more work is clearly needed in this area.

Whatever schedule is used, it is highly advantageous if the workers can sleep at a lower altitude than the workplace. Naturally whether this is feasible depends on the topography of the region. A lower altitude for sleeping is not feasible if it takes several hours to reach it because this cuts too much off the working day. However, if there is a location several hundred metres lower which can be reached within, say, one hour, setting up sleeping quarters at this lower altitude will improve sleep quality, workers’ comfort and sense of well-being, and productivity.

Oxygen Enrichment of Room Air to Reduce the Hypoxia of High Altitude

The deleterious effects of high altitude are caused by the low partial pressure of oxygen in the air. In turn, this results from the fact that while the oxygen concentration is the same as at sea level, the barometric pressure is low. Unfortunately there is little that can be done at high altitude to counter this “climatic aggression”, as it was dubbed by Carlos Monge, the father of high-altitude medicine in Peru (Monge 1948).

One possibility is to increase the barometric pressure in a small area, and this is the principle of the Gamow bag, which is sometimes used for the emergency treatment of mountain sickness. However, pressurizing large spaces such as rooms is difficult from a technical point of view, and there are also medical problems associated with entering and leaving a room with increased pressure. An example is middle ear discomfort if the Eustachian tube is blocked.

The alternative is to raise the oxygen concentration in some parts of the work facility, and this is a relatively new development that shows great promise (West 1995). As pointed out earlier, even after a period of acclimatization of seven to ten days at an altitude of 4,500 m, severe hypoxia continues to reduce work capacity, mental efficiency and sleep quality. It would therefore be highly advantageous to reduce the degree of hypoxia in some parts of the work facility if that were feasible.

This can be done by adding oxygen to the normal air ventilation of some rooms. The value of relatively minor degrees of oxygen enrichment of the room air is remarkable. It has been shown that every 1% increase in oxygen concentration (for example from 21 to 22%) reduces the equivalent altitude by 300 m. The equivalent altitude is that which has the same inspired PO2 during air breathing as in the oxygen-enriched room. Thus at an altitude of 4,500 m, raising the oxygen concentration of a room from 21 to 26% would reduce the equivalent altitude by 1,500 m. The result would be an equivalent altitude of 3,000 m, which is easily tolerated. The oxygen would be added to the normal room ventilation and therefore would be part of the air conditioning. We all expect that a room will provide a comfortable temperature and humidity. Control of the oxygen concentration can be regarded as a further logical step in humanity’s control of our environment.

Oxygen enrichment has become feasible because of the introduction of relatively inexpensive equipment for providing large quantities of nearly pure oxygen. The most promising is the oxygen concentrator that uses a molecular sieve. Such a device preferentially adsorbs nitrogen and thus produces an oxygen-enriched gas from air. It is difficult to produce pure oxygen with this type of concentrator, but large amounts of 90% oxygen in nitrogen are readily available, and these are just as useful for this application. These devices can work continuously. In practice, two molecular sieves are used in an alternating fashion, and one is purged while the other is actively adsorbing nitrogen. The only requirement is electrical power, which is normally in abundant supply at a modern mine. As a rough indication of the cost of oxygen enrichment, a small commercial device can be bought off the shelf, and this produces 300 litres per hour of 90% oxygen. It was developed to produce oxygen for treating patients with lung disease in their homes. The device has a power requirement of 350 watts and the initial cost is about US$2,000. Such a machine is sufficient to raise the oxygen concentration in a room by 3% for one person at a minimal though acceptable level of room ventilation. Very large oxygen concentrators are also available, and they are used in the paper pulp industry. It is also possible that liquid oxygen might be economical under some circumstances.

There are several areas in a mine, for example, where oxygen enrichment might be considered. One would be the director’s office or conference room, where important decisions are being made. For example, if there is a crisis in the mine such as a serious accident, such a facility would probably result in clearer thinking than the normal hypoxic environment. There is good evidence that an altitude of 4,500 m impairs brain function (Ward, Milledge and West 1995). Another place where oxygen enrichment would be beneficial is a laboratory where quality control measurements are being carried out. A further possibility is oxygen enrichment of sleeping quarters to improve sleep quality. Double blind trials of the effectiveness of oxygen enrichment at altitudes of about 4,500 m would be easy to design and should be carried out as soon as possible.

Possible complications of oxygen enrichment should be considered. Increased fire hazard is one issue that has been raised. However, increasing the oxygen concentration by 5% at an altitude of 4,500 m produces an atmosphere which has a lower flammability than air at sea level (West 1996). It should be borne in mind that although oxygen enrichment increases the PO2, this is still much lower than the sea-level value. Flammability of an atmosphere depends on two variables (Roth 1964):

  • the partial pressure of oxygen, which is much lower in the enriched air at high altitude than at sea level
  • the quenching effect of the inert components (i.e., nitrogen) of the atmosphere.


This quenching is slightly reduced at high altitude, but the net effect is still a lower flammability. Pure or nearly pure oxygen is dangerous, of course, and the normal precautions should be taken in piping the oxygen from the oxygen concentrator to the ventilation ducting.

Loss of acclimatization to high altitude is sometimes cited as a disadvantage of oxygen enrichment. However, there is no basic difference between entering a room with an oxygen-enriched atmosphere, and descending to a lower altitude. Everybody would sleep at a lower altitude if they could, and therefore this is hardly an argument against using oxygen enrichment. It is true that frequent exposure to a lower altitude will result in less acclimatization to the higher altitude, other things being equal. However, the ultimate objective is effective working at the high altitude of the mine, and this can presumably be enhanced using oxygen enrichment.

It is sometimes suggested that altering the atmosphere in this way might increase the legal liability of the facility if some kind of hypoxia-related illness developed. Actually, the opposite view seems more reasonable. It is possible that a worker who develops, say, a myocardial infarction while working at high altitude could claim that the altitude was a contributing factor. Any procedure which reduces the hypoxic stress makes altitude-induced illnesses less likely.

Emergency Treatment

The various types of high-altitude sickness, including acute mountain sickness, high-altitude pulmonary oedema and high-altitude cerebral oedema, were discussed earlier in this chapter. Little needs to be added in the context of work at high altitude.

Anyone who develops a high-altitude illness should be allowed to rest. This may be sufficient for conditions such as acute mountain sickness. Oxygen should be given by mask if this is available. However, if the patient does not improve, or deteriorates, descent is by far the best treatment. Usually this is easily done in a large commercial facility, because transportation is always available. All the high-altitude-related illnesses usually respond rapidly to removal to lower altitude.

There may be a place in a commercial facility for a small pressurized container in which the patient can be placed, and the equivalent altitude reduced by pumping in air. In the field, this is commonly done using a strong bag. One design is known as the Gamow bag, after its inventor. However, the main advantage of the bag is its portability, and since this feature is not really essential in a commercial facility, it would probably be better to use a larger, rigid tank. This should be big enough for an attendant to be inside the facility with the patient. Of course adequate ventilation of such a container is essential. Interestingly, there is anecdotal evidence that raising the atmospheric pressure in this way is sometimes more efficacious in the treatment of high-altitude illness than giving the patient a high concentration of oxygen. It is not clear why this should be so.

Acute mountain sickness

This is usually self-limiting and the patient feels much better after a day or two. The incidence of acute mountain sickness can be reduced by taking acetazolamide (Diamox), one or two 250 mg tablets per day. These can be started before reaching high altitude or can be taken when symptoms develop. Even people with mild symptoms find that half a tablet at night often improves the quality of sleep. Aspirin or paracetamol is useful for headache. Severe acute mountain sickness can be treated with dexamethasone, 8 mg initially, followed by 4 mg every six hours. However, descent is by far the best treatment if the condition is severe.

High-altitude pulmonary oedema

This is a potentially serious complication of mountain sickness and must be treated. Again the best therapy is descent. While awaiting evacuation, or if evacuation is not possible, give oxygen or place in a high-pressure chamber. Nifedipine (a calcium channel blocker) should be given. The dose is 10 mg sublingually followed by 20 mg slow release. This results in a fall in pulmonary artery pressure and is often very effective. However, the patient should be taken down to a lower altitude.

High-altitude cerebral oedema

This is potentially a very serious complication and is an indication for immediate descent. While awaiting evacuation, or if evacuation is not possible, give oxygen or place in an increased pressure environment. Dexamethasone should be given, 8 mg initially, followed by 4 mg every six hours.

As indicated earlier, people who develop severe acute mountain sickness, high-altitude pulmonary oedema or high-altitude cerebral oedema are likely to have a recurrence if they return to high altitude. Therefore if a worker develops any of these conditions, attempts should be made to find employment at a lower altitude.



Working at high altitudes induces a variety of biological responses, as described elsewhere in this chapter. The hyperventilatory response to altitude should cause a marked increase in the total dose of hazardous substances which may be inhaled by persons occupationally exposed, as compared to people working under similar conditions at sea level. This implies that 8-hour exposure limits used as the basis of exposure standards should be reduced. In Chile, for example, the observation that silicosis progresses faster in mines at high altitudes, led to the reduction of the permitted exposure level proportional to the barometric pressure at the workplace, when expressed in terms of mg/m3. While this may be overcorrecting at intermediate altitudes, the error will be in the favour the exposed worker. The threshold limit values (TLVs), expressed in terms of parts per million (ppm), require no adjustment, however, because both the proportion of millimoles of contaminant per mole of oxygen in air and the number of moles of oxygen required by a worker remain approximately constant at different altitudes, even though the air volume containing one mole of oxygen will vary.

In order to assure that this is true, however, the method of measurement used to determine the concentration in ppm must be truly volumetric, as is the case with Orsat’s apparatus or the Bacharach Fyrite instruments. Colourimetric tubes that are calibrated to read in ppm are not true volumetric measurements because the markings on the tube are actually caused by a chemical reaction between the air contaminant and some reagent. In all chemical reactions, substances combine in proportion to the number of moles present, not in proportion to volumes. The hand-operated air pump draws a constant volume of air through the tube at any altitude. This volume at a higher altitude will contain a smaller mass of contaminant, giving a reading lower than the actual volumetric concentration in ppm (Leichnitz 1977). Readings should be corrected by multiplying the reading by the barometric pressure at sea level and dividing the result by the barometric pressure at the sampling site, using the same units (such as torr or mbar) for both pressures.

Diffusional samplers: The laws of gas diffusion indicate that the collection efficiency of diffusional samplers is independent of barometric pressure changes. Experimental work by Lindenboom and Palmes (1983) shows that other, as yet undetermined factors influence the collection of NO2 at reduced pressures. The error is approximately 3.3% at 3,300 m and 8.5% at 5,400 m equivalent altitude. More research is needed on the causes of this variation and the effect of altitude on other gases and vapours.

No information is available on the effect of altitude on portable gas detectors calibrated in ppm, which are equipped with electrochemical diffusion sensors, but it could reasonably be expected that the same correction mentioned under colourimetric tubes would apply. Obviously the best procedure would be to calibrate them at altitude with a test gas of known concentration.

The principles of operation and measurement of electronic instruments should be examined carefully to determine whether they need recalibration when employed at high altitudes.

Sampling pumps: These pumps usually are volumetric—that is, they displace a fixed volume per revolution—but they usually are the last component of the sampling train, and the actual volume of air aspirated is affected by the resistance to flow opposed by the filters, hose, flow meters and orifices that are part of the sampling train. Rotameters will indicate a lower flow rate than that actually flowing through the sampling train.

The best solution of the problem of sampling at high altitudes is to calibrate the sampling system at the sampling site, obviating the problem of corrections. A briefcase sized bubble film calibration laboratory is available from sampling pump manufacturers. This is easily carried to location and permits rapid calibration under actual working conditions. It even includes a printer which provides a permanent record of calibrations made.

TLVs and Work Schedules

TLVs have been specified for a normal 8-hour workday and a 40-hour workweek. The present tendency in work at high altitudes is to work longer hours for a number of days and then commute to the nearest town for an extended rest period, keeping the average time at work within the legal limit, which in Chile is 48 hours per week.

Departures from the normal 8-hour working schedules make it necessary to examine the possible accumulation in the body of toxic substances due to the increase in exposure and reduction of detoxification times.

Chilean occupational health regulations have recently adopted the “Brief and Scala model’’ described by Paustenbach (1985) for reducing TLVs in the case of extended working hours. At altitude, the correction for barometric pressure should also be used. This usually results in very substantial reductions of permissible exposure limits.

In the case of cumulative hazards not subject to detoxifying mechanisms, such as silica, correction for extended working hours should be directly proportional to the actual hours worked in excess of the usual 2,000 hours per year.

Physical Hazards

Noise: The sound pressure level produced by noise of a given amplitude is in direct relation to air density, as is the amount of energy transmitted. This means that the reading obtained by a sound level meter and the effect on the inner ear are reduced in the same way, so no corrections would be required.

Accidents: Hypoxia has a pronounced influence on the central nervous system, reducing response time and disrupting vision. An increase in the incidence of accidents should be expected. Above 3,000 m, the performance of persons engaged in critical tasks will benefit from supplementary oxygen.

Precautionary Note: Air Sampling 

Kenneth I. Berger and William N. Rom

The monitoring and maintenance of the occupational safety of workers requires special consideration for high altitude environments. High-altitude conditions can be expected to influence the accuracy of sampling and measuring instruments that have been calibrated for use at sea level. For example, active sampling devices rely on pumps to pull a volume of air onto a collection medium. Accurate measurement of the pump flow rate is essential in order to determine the exact volume of air drawn through the sampler and, therefore, the concentration of the contaminant. Flow calibrations are often performed at sea level. However, changes in air density with increasing altitude may alter the calibration, thereby invalidating subsequent measurements made in high altitude environments. Other factors that may influence the accuracy of sampling and measurement instruments at high altitude include changing temperature and relative humidity. An additional factor that should be considered when evaluating worker exposure to inhaled substances is the increased respiratory ventilation that occurs with acclimatization. Since ventilation is markedly increased after ascent to high altitude, workers may be exposed to excessive total doses of inhaled occupational contaminants, even though measured concentrations of the contaminant are below the threshold limit value.



Tuesday, 15 February 2011 20:15

Workplace Biohazards

Written by

The assessment of biohazards in the workplace has been concentrated on agricultural workers, health-care workers and laboratory personnel, who are at considerable risk of adverse health effects. A detailed compilation of biohazards by Dutkiewicz et al. (1988) shows how widespread the risks can be to workers in many other occupations as well (table 1).

Dutkiewicz et al. (1988) further taxonomically classified the micro-organisms and plants (table 2), as well as animals (table 3), which might possibly present biohazards in work settings.

Table 1. Occupational settings with potential exposure of workers to biological agents




Cultivating and harvesting
Breeding and tending animals

Agricultural products

Abattoirs, food packaging plants
Storage facilities: grain silos, tobacco and other processing
Processing animal hair and leather
Textile plants
Wood processing: sawmills, papermills,
cork factories

Laboratory animal care


Health care

Patient care: medical, dental

Pharmaceutical and herbal products


Personal care

Hairdressing, chiropody

Clinical and research laboratories



Production facilities

Day-care centres


Building maintenance

“Sick” buildings

Sewage and compost facilities


Industrial waste disposal systems


Source: Dutkiewicz et al. 1988.


Micro-organisms are a large and diverse group of organisms that exist as single cells or cell clusters (Brock and Madigan 1988). Microbial cells are thus distinct from the cells of animals and plants, which are unable to live alone in nature but can exist only as parts of multicellular organisms.

Very few areas on the surface of this planet do not support microbial life, because micro-organisms have an astounding range of metabolic and energy-yielding abilities and many can exist under conditions that are lethal to other life forms.

Four broad classes of micro-organisms that can interact with humans are bacteria, fungi, viruses and protozoa. They are hazardous to workers due to their wide distribution in the working environment. The most important micro-organisms of occupational hazard are listed in tables 2 and 3.

There are three major sources of such microbes:

  1. those arising from microbial decomposition of various substrates associated with particular occupations (e.g., mouldy hay leading to hypersensitivity pneumonitis)
  2. those associated with certain types of environments (e.g., bacteria in water supplies)
  3. those stemming from infective individuals harbouring a particular pathogen (e.g., tuberculosis).


Ambient air may be contaminated with or carry significant levels of a variety of potentially harmful micro-organisms (Burrell 1991). Modern buildings, especially those designed for commercial and administrative purposes, constitute a unique ecological niche with their own biochemical environment, fauna and flora (Sterling et al. 1991). The potential adverse effects on workers are described elsewhere in this Encyclopaedia.

Water has been recognized as an important vehicle for extra-intestinal infection. A variety of pathogens are acquired through occupational, recreational and even therapeutic contact with water (Pitlik et al. 1987). The nature of non-enteric water-borne disease is often determined by the ecology of aquatic pathogens. Such infections are of basically two types: superficial, involving damaged or previously intact mucosae and skin; and systemic, often serious infections that may occur in the setting of depressed immunity. A broad spectrum of aquatic organisms, including viruses, bacteria, fungi, algae and parasites may invade the host through such extra-intestinal routes as the conjunctivae, respiratory mucosae, skin and genitalia.

Although zoonotic spread of infectious disease continues to occur in laboratory animals used in biomedical research, reported outbreaks have been minimized with the advent of rigorous veterinary and husbandry procedures, the use of commercially reared animals and the institution of appropriate personnel health programmes (Fox and Lipman 1991). Maintaining animals in modern facilities with appropriate safeguards against the introduction of vermin and biological vectors is also important in preventing zoonotic disease in personnel. Nevertheless, established zoonotic agents, newly discovered micro-organisms or new animal species not previously recognized as carriers of zoonotic micro-organisms are encountered, and the potential for spread of infectious disease from animals to humans still exists.

Active dialogue between veterinarians and physicians regarding the potential of zoonotic disease, the species of animals that are involved, and the methods of diagnosis, is an indispensable component of a successful preventive health programme.

Table 2. Viruses, bacteria, fungi and plants: Known biohazards in the workplace



Infection zoo-



















Spiral bacteria





















Non-sporing gram-
positive rods and



























Yeast-like geophilic




Endogenous yeasts



Parasites of wheat








Other lower plants














Higher plants






Volatile oils












1 Infection-zoonosis: Causes infection or invasion usually contracted from vertebrate animals (zoonosis).
2 (e) Endotoxin.
3 (m) Mycotoxin.

Source: Dutkiewicz et al. 1988.


Some Occupational Settings with Biohazards

Medical and laboratory staff and other health-care workers, including related professions, are exposed to infection by micro-organisms if the appropriate preventive measures are not taken. Hospital workers are exposed to many biological hazards, including human immunodeficiency virus (HIV), hepatitis B, herpes viruses, rubella and tuberculosis (Hewitt 1993).

Work in the agricultural sector is associated with a wide variety of occupational hazards. Exposure to organic dust, and to airborne micro-organisms and their toxins, may lead to respiratory disorders (Zejda et al. 1993). These include chronic bronchitis, asthma, hypersensitivity pneumonitis, organic dust toxic syndrome and chronic obstructive pulmonary disease. Dutkiewicz and his colleagues (1988) studied samples of silage for the identification of potential agents causing symptoms of organic and toxic syndrome. Very high levels of total aerobic bacteria and fungi were found. Aspergillus fumigatus predominated among the fungi, whereas bacillus and gram-negative organisms (Pseudomonas, Alcaligenes, Citrobacter and Klebsiella species) and actinomycetes prevailed among the bacteria. These results show that contact with aerosolized silage carries the risk of exposure to high concentrations of micro-organisms, of which A. fumigatus and endotoxin-producing bacteria are the most probable disease agents.

Short-term exposures to certain wood dusts may result in asthma, conjunctivitis, rhinitis or allergic dermatitis. Some thermophilic micro-organisms found in wood are human pathogens, and inhalation of ascomycete spores from stored wood chips has been implicated in human illnesses (Jacjels 1985).

Examples illustrative of specific working conditions follow:

  1. The fungus Penicillium camemberti var. candidum is used in the production of some types of cheese. The high frequency of precipitating antibodies of this fungus in the workers’ blood samples, together with the clinical causes of the airway symptoms, indicate an aetiological relationship between airway symptoms and heavy exposure to this fungus (Dahl et al. 1994).
  2. Micro-organisms (bacteria and fungi) and endotoxins are potential agents of occupational hazard in a potato processing plant (Dutkiewicz 1994). The presence of precipitins to microbial antigens was significantly correlated with the occurrence of the work-related respiratory and general symptoms that were found in 45.9% of the examined workers.
  3. Museum and library personnel are exposed to moulds (e.g., Aspergillus, Pencillium) which, under certain conditions, contaminate books (Kolmodin-Hedman et al. 1986). Symptoms experienced are attacks of fever, chill, nausea and cough.
  4. Ocular infections can result from the use of industrial microscope eyepieces on multiple shifts. Staphylococcus aureus has been identified among the micro-organism cultures (Olcerst 1987).



An understanding of the principles of epidemiology and the spread of infectious disease is essential in the methods used in the control of the causing organism.

Preliminary and periodic medical examinations of workers should be carried out in order to detect biological occupational diseases. There are general principles for conducting medical examinations in order to detect adverse health effects of workplace exposure, including biological hazards. Specific procedures are to be found elsewhere in this Encyclopaedia. For example, in Sweden the Farmers’ Federation initiated a programme of preventive occupational health services for farmers (Hoglund 1990). The main goal of the Farmers’ Preventive Health Service (FPHS) is to prevent work-related injuries and illnesses and to provide clinical services to farmers for occupational medical problems.

For some infectious disease outbreaks, appropriate preventive measures may be difficult to put in place until the disease is identified. Outbreaks of the viral Crimean-Congo haemorrhagic fever (CCHF) which demonstrated this problem were reported among hospital staff in the United Arab Emirates (Dubai), Pakistan and South Africa (Van Eeden et al. 1985).

Table 3. Animals as a source of occupational hazards







Invertebrates other than arthropods

































































































1 Infection-zoonosis: Causes infection or invasion contracted from vertebrate animals.
2 Vector of pathogenic viruses, bacteria or parasites.
3 Toxic B produces toxin or venom transmitted by bite or sting.

Vertebrates: Snakes and Lizards

In hot and temperate zones, snakebites may constitute a definite hazard for certain categories of workers: agricultural workers, woodcutters, building and civil engineering workers, fishermen, mushroom gatherers, snake charmers, zoo attendants and laboratory workers employed in the preparation of antivenom serums. The vast majority of snakes are harmless to humans, although a number are capable of inflicting serious injury with their venomous bites; dangerous species are found among both the terrestrial snakes (Colubridae and Viperidae) and aquatic snakes (Hydrophiidae) (Rioux and Juminer 1983).

According to the World Health Organization (WHO 1995), snakebites are estimated to cause 30,000 deaths per year in Asia and about 1,000 deaths each in Africa and South America. More detailed statistics are available from certain countries. Over 63,000 snakebites and scorpion stings with over 300 deaths are reported yearly in Mexico. In Brazil, about 20,000 snakebites and 7,000 to 8,000 scorpion stings occur annually, with a case-fatality rate of 1.5% for snake bites and between 0.3% and 1% for scorpion stings. A study in Ouagadougou, Burkina Faso, showed 7.5 snakebites per 100,000 population in peri-urban areas and up to over 69 per 100,000 in more remote areas, where case-fatality rates reached 3%.

Snakebites are a problem also in developed parts of the world. Each year about 45,000 snakebites are reported in the United States, where the availability of health care has reduced the number of deaths to 9–15 per year. In Australia, where some of the world’s most venomous snakes exist, the annual number of snakebites is estimated at between 300 and 500, with an average of two deaths.

Environmental changes, particularly deforestation, may have caused the disappearance of many snake species in Brazil. However, the number of reported cases of snakebites did not decrease as other and sometimes more dangerous species proliferated in some of the deforested areas (WHO 1995).

Sauria (lizards)

There are only two species of venomous lizards, both members of the genus Heloderma: H. suspectum (Gila monster) and H. horridum (beaded lizard). Venom similar to that of the Viperidae penetrates wounds inflicted by the anterior curved teeth, but bites in humans are uncommon and recovery is generally rapid (Rioux and Juminer 1983).


Snakes do not usually attack humans unless they feel menaced, are disturbed or are trodden on. In regions infested with venomous snakes, workers should wear foot and leg protection and be provided with monovalent or polyvalent antivenom serum. It is recommended that persons working in a danger area at a distance of over half-an-hour’s travel from the nearest first-aid post should carry an antivenom kit containing a sterilized syringe. However, it should be explained to workers that bites even from the most venomous snakes are seldom fatal, since the amount of venom injected is usually small. Certain snake charmers achieve immunization by repeated injections of venom, but no scientific method of human immunization has yet been developed (Rioux and Juminer 1983).



International Standards and Biological Hazards

Many national occupational standards include biological hazards in their definition of harmful or toxic substances. However, in most regulatory frameworks, biological hazards are chiefly restricted to micro-organisms or infectious agents. Several US Occupational Safety and Health Administration (OSHA) regulations include provisions on biological hazards. The most specific are those concerning hepatitis B vaccine vaccination and blood-borne pathogens; biological hazards are also covered in regulations with a broader scope (e.g., those on hazard communication, the specifications for accident prevention signs and tags, and the regulation on training curriculum guidelines).

Although not the subject of specific regulations, the recognition and avoidance of hazards relating to animal, insect or plant life is addressed in other OSHA regulations concerning specific work settings—for example, the regulation on telecommunications, the one on temporary labour camps and the one on pulpwood logging (the latter including guidelines concerning snake-bite first-aid kits).

One of the most comprehensive standards regulating biological hazards in the workplace is European Directive No. 90/679. It defines biological agents as “micro-organisms, including those which have been genetically modified, cell cultures and human endoparasites, which may be able to provoke any infection, allergy or toxicity,” and classifies biological agents into four groups according to their level of risk of infection. The Directive covers the determination and assessment of risks and employers’ obligations in terms of the replacement or reduction of risks (through engineering control measures, industrial hygiene, collective and personal protection measures and so on), information (for workers, workers’ representatives and the competent authorities), health surveillance, vaccination and record-keeping. The Annexes provide detailed information on containment measures for different “containment levels” according to the nature of the activities, the assessment of risk to workers and the nature of the biological agent concerned.




Wednesday, 16 February 2011 00:28

Aquatic Animals

Written by

D. Zannini*

* Adapted from 3rd edition, Encyclopaedia of Occupational Health and Safety.

Aquatic animals dangerous to humans are to be found among practically all of the divisions (phyla). Workers may come into contact with these animals in the course of various activities including surface and underwater fishing, the installation and handling of equipment in connection with the exploitation of petroleum under the sea, underwater construction, and scientific research, and thus be exposed to health risks. Most of the dangerous species inhabit warm or temperate waters.

Characteristics and Behaviour

Porifera. The common sponge belongs to this phylum. Fishermen who handle sponges, including helmet and scuba divers, and other underwater swimmers, may contract contact dermatitis with skin irritation, vesicles or blisters. The “sponge diver’s sickness” of the Mediterranean region is caused by the tentacles of a small coelenterate (Sagartia rosea) that is a parasite of the sponge. A form of dermatitis known as “red moss” is found among North American oyster fishers resulting from contact with a scarlet sponge found on the shell of the oysters. Cases of type 4 allergy have been reported. The poison secreted by the sponge Suberitus ficus contains histamine and antibiotic substances.

Coelenterata. These are represented by many families of the class known as Hydrozoa, which includes the Millepora or coral (stinging coral, fire coral), the Physalia (Physalia physalis, sea wasp, Portuguese man-of-war), the Scyphozoa (jellyfish) and the Actiniaria (stinging anemone), all of which are found in all parts of the ocean. Common to all these animals is their ability to produce an urticaria by the injection of a strong poison that is retained in a special cell (the cnidoblast) containing a hollow thread, which explodes outwards when the tentacle is touched, and penetrates the person’s skin. The various substances contained in this structure are responsible for such symptoms as severe itching, congestion of the liver, pain, and depression of the central nervous system; these substances have been identified as thalassium, congestine, equinotoxin (which contains 5-hydroxytryptamine and tetramine) and hypnotoxin, respectively. Effects on the individual depend upon the extent of the contact made with the tentacles and hence on the number of microscopic punctures, which may amount to many thousands, up to the point where they may cause the death of the victim within a few minutes. In view of the fact that these animals are dispersed so widely throughout the world, many incidents of this nature occur but the number of fatalities is relatively small. Effects on the skin are characterized by intense itching and the formation of papules having a bright red, mottled appearance, developing into pustules and ulceration. Intense pain similar to electric shock may be felt. Other symptoms include difficulty in breathing, generalized anxiety and cardiac upset, collapse, nausea and vomiting, loss of consciousness, and primary shock.

Echinoderma. This group includes the starfishes and sea urchins, both of which possess poisonous organs (pedicellariae), but are not dangerous to humans. The spine of the sea urchin can penetrate the skin, leaving a fragment deeply imbedded; this can give rise to a secondary infection followed by pustules and persistent granuloma, which can be very troublesome if the wounds are close to tendons or ligaments. Among the sea urchins, only the Acanthaster planci seems to have a poisonous spine, which can give rise to general disturbances such as vomiting, paralysis and numbness.

Mollusca. Among the animals belonging to this phylum are the cone shells, and these can be dangerous. They live on a sandy sea-bottom and appear to have a poisonous structure consisting of a radula with needle-like teeth, which can strike at the victim if the shell is handled incautiously with the bare hand. The poison acts on the neuromuscular and central nervous systems. Penetration of the skin by the point of a tooth is followed by temporary ischaemia, cyanosis, numbness, pain, and paraesthesia as the poison spreads gradually through the body. Subsequent effects include paralysis of the voluntary muscles, lack of coordination, double vision and general confusion. Death can follow as a result of respiratory paralysis and circulatory collapse. Some 30 cases have been reported, of which 8 were fatal.

Platyhelminthes. These include the Eirythoe complanata and the Hermodice caruncolata, known as “bristle worms”. They are covered with numerous bristle-like appendages, or setae, containing a poison (nereistotoxin) with a neurotoxic and local irritant effect.

Polyzoa (Bryozoa). These are made up of a group of animals which form plant-like colonies resembling gelatinous moss, which frequently encrust rocks or shells. One variety, known as Alcyonidium, can cause an urticarious dermatitis on the arms and face of fishermen who have to clean this moss off their nets. It can also give rise to an allergic eczema.

Selachiis (Chondrichthyes). Animals belonging to this phylum include the sharks and sting-rays. The sharks live in fairly shallow water, where they search for prey and may attack people. Many varieties have one or two large, poisonous spines in front of the dorsal fin, which contain a weak poison that has not been identified; these can cause a wound giving rise to immediate and intense pain with reddening of the flesh, swelling and oedema. A far greater danger from these animals is their bite, which, because of several rows of sharp pointed teeth, causes severe laceration and tearing of the flesh leading to immediate shock, acute anaemia and drowning of the victim. The danger that sharks represent is a much-discussed subject, each variety seeming to be particularly aggressive. There seems no doubt that their behaviour is unpredictable, although it is said that they are attracted by movement and by the light colour of a swimmer, as well as by blood and by vibrations resulting from a fish or other prey that has just been caught. Sting-rays have large, flat bodies with a long tail having one or more strong spines or saws, which can be poisonous. The poison contains serotonine, 5-nucleotidase and phosphodiesterase, and can cause generalized vasoconstriction and cardio-respiratory arrest. Sting-rays live in the sandy regions of coastal waters, where they are well hidden, making it easy for bathers to step on one without seeing it. The ray reacts by bringing over its tail with the projecting spine, impaling the spike keep into the flesh of the victim. This may cause piercing wounds in a limb or even penetration of an internal organ such as the peritoneum, lung, heart or liver, particularly in the case of children. The wound can also give rise to great pain, swelling, lymphatic oedema and various general symptoms such as primary shock and cardio-circulatory collapse. Injury to an internal organ may lead to death in a few hours. Sting-ray incidents are among the most frequent, there being some 750 every year in the United States alone. They can also be dangerous for fishermen, who should immediately cut off the tail as soon as the fish is brought aboard. Various species of rays such as the torpedo and the narcine possess electric organs on their back, which, when stimulated by touch alone, can produce electric shocks ranging from 8 up to 220 volts; this may be enough to stun and temporarily disable the victim, but recovery is usually without complications.

Osteichthyes. Many fishes of this phylum have dorsal, pectoral, caudal and anal spines which are connected with a poison system and whose primary purpose is defence. If the fish is disturbed or stepped upon or handled by a fisherman, it will erect the spines, which can pierce the skin and inject the poison. Not infrequently they will attack a diver seeking fish, or if they are disturbed by accidental contact. Numerous incidents of this kind are reported because of the widespread distribution of fish of this phylum, which includes the catfish, which are also found in fresh water (South America, West Africa and the Great Lakes), the scorpion fish (Scorpaenidae), the weever fish (Trachinus), the toadfish, the surgeon fish and others. Wounds from these fishes are generally painful, particularly in the case of the catfish and the weever fish, causing reddening or pallor, swelling, cyanosis, numbness, lymphatic oedema and haemorrhagic suffusion in the surrounding flesh. There is a possibility of gangrene or phlegmonous infection and peripheral neuritis on the same side as the wound. Other symptoms include faintness, nausea, collapse, primary shock, asthma and loss of consciousness. They all represent a serious danger for underwater workers. A neurotoxic and haemotoxic poison has been identified in the catfish, and in the case of the weever fish a number of substances have been isolated such as 5-hydroxytryptamine, histamine and catecholamine. Some catfishes and stargazers that live in fresh water, as well as the electric eel (Electrophorus), have electric organs (see under Selachii above).

Hydrophiidae. This group (sea snakes) is to be found mostly in the seas around Indonesia and Malaysia; some 50 species have been reported, including Pelaniis platurus, Enhydrina schistosa and Hydrus platurus. The venom of these snakes is very similar to that of the cobra, but is 20 to 50 times as poisonous; it is made up of a basic protein of low molecular weight (erubotoxin) which affects the neuromuscular junction blocking the acetylcholine and provoking myolysis. Fortunately sea snakes are generally docile and bite only when stepped on, squeezed or dealt a hard blow; furthermore, they inject little or no venom from their teeth. Fishermen are among those most exposed to this hazard and account for 90% of all reported incidents, which result either from stepping on the snake on the sea bottom or from encountering them among their catch. Snakes are probably responsible for thousands of the occupational accidents attributed to aquatic animals, but few of these are serious, while only a small percentage of the serious accidents turn out to be fatal. Symptoms are mostly slight and not painful. Effects are usually felt within two hours, starting with muscular pain, difficulty with neck movement, lack of dexterity, and trismus, and sometimes including nausea and vomiting. Within a few hours myoglobinuria (the presence of complex proteins in urine) will be seen. Death can ensue from paralysis of the respiratory muscles, from renal insufficiency due to tubular necrosis, or from cardiac arrest due to hyperkalaemia.


Every effort should be made to avoid all contact with the spines of these animals when they are being handled, unless strong gloves are worn, and the greatest care should be taken when wading or walking on a sandy sea bottom. The wet suit worn by skin divers offers protection against the jellyfish and the various Coelenterata as well as against snakebite. The more dangerous and aggressive animals should not be molested, and zones where there are jellyfish should be avoided, as they are difficult to see. If a sea snake is caught on a line, the line should be cut and the snake allowed to go. If sharks are encountered, there are a number of principles that should be observed. People should keep their feet and legs out of the water, and the boat should be gently brought to shore and kept still; a swimmer should not stay in the water with a dying fish or with one that is bleeding; a shark’s attention should not be attracted by the use of bright colours, jewellery, or by making a noise or explosion, by showing a bright light, or by waving the hands towards it. A diver should never dive alone.



Wednesday, 16 February 2011 00:30

Terrestrial Venomous Animals

Written by

J.A. Rioux and B. Juminer*

*Adapted from 3rd edition, Encyclopaedia of Occupational Health and Safety.

Annually millions of scorpion stings and anaphylactic reactions to insect stings may occur worldwide, causing tens of thousands of deaths in humans each year. Between 30,000 and 45,000 cases of scorpion stings are reported annually in Tunisia, causing between 35 and 100 deaths, mostly among children. Envenomation (toxic effects) is an occupational hazard for populations involved in agriculture and forestry in these regions.

Among the animals that can inflict injury on humans by the action of their venom are invertebrates, such as Arachnida (spiders, scorpions and sun spiders), Acarina (ticks and mites), Chilopoda (centipedes) and Hexapoda (bees, wasps, butterflies, and midges).


Arachnida (spiders—Aranea)

All species are venomous, but in practice only a few types produce injury in humans. Spider poisoning may be of two types:

  1. Cutaneous poisoning, in which the bite is followed after a few hours by oedema centred around a cyanotic mark, and then by a blister; extensive local necrosis may ensue, and healing may be slow and difficult in cases of bites from spiders of the Lycosa genus (e.g., the tarantula).
  2. Nerve poisoning due to the exclusively neurotoxic venom of the mygales (Latrodectus ctenus), which produces serious injury, with early onset, tetany, tremors, paralysis of the extremities and, possibly, fatal shock; this type of poisoning is relatively common amongst forestry and agricultural workers and is particularly severe in children: in the Amazonas, the venom of the “black widow” spider (Latrodectus mactans) is used for poison arrows.


Prevention. In areas where there is a danger of venomous spiders, sleeping accommodation should be provided with mosquito nets and workers should be equipped with footwear and working clothes that give adequate protection.

Scorpions (Scorpionida)

These arachnids have a sharp poison claw on the end of the abdomen with which they can inflict a painful sting, the seriousness of which varies according to the species, the amount of venom injected and the season (the most dangerous season being at the end of the scorpions’ hibernation period). In the Mediterranean region, South America and Mexico, the scorpion is responsible for more deaths than poisonous snakes. Many species are nocturnal and are less aggressive during the day. The most dangerous species (Buthidae) are found in arid and tropical regions; their venom is neurotropic and highly toxic. In all cases, the scorpion sting immediately produces intense local signs (acute pain, inflammation) followed by general manifestations such as tendency to fainting, salivation, sneezing, lachrymation and diarrhoea. The course in young children is often fatal. The most dangerous species are found amongst the genera Androctonus (sub-Saharan Africa), Centrurus (Mexico) and Tituus (Brazil). The scorpion will not spontaneously attack humans, and stings only when it considers itself endangered, as when trapped in a dark corner or when boots or clothes in which it has taken refuge are shaken or put on. Scorpions are highly sensitive to halogenated pesticides (e.g., DDT).

Sun spiders (Solpugida)

This order of arachnid is found chiefly in steppe and sub-desert zones such as the Sahara, Andes, Asia Minor, Mexico and Texas, and is non-venomous; nevertheless, sun spiders are extremely aggressive, may be as large as 10 cm across and have a fearsome appearance. In exceptional cases, the wounds they inflict may prove serious due to their multiplicity. Solpugids are nocturnal predators and may attack a sleeping individual.

Ticks and mites (Acarina)

Ticks are blood-sucking arachnids at all stages of their life cycle, and the “saliva” they inject through their feeding organs may have a toxic effect. Poisoning may be severe, although mainly in children (tick paralysis), and may be accompanied by reflex suppression. In exceptional cases death may ensue due to bulbar paralysis (in particular where a tick has attached itself to the scalp). Mites are haematophagic only at the larval stage, and their bite produces pruritic inflammation of the skin. The incidence of mite bites is high in tropical regions.

Treatment. Ticks should be detached after they are anaesthetized with a drop of benzene, ethyl ether or xylene. Prevention is based on the use of organophosphorus pesticide pest repellents.

Centipedes (Chilopoda)

Centipedes differ from millipedes (Diplopoda) in that they have only one pair of legs per body segment and that the appendages of the first body segment are poison fangs. The most dangerous species are encountered in the Philippines. Centipede venom has only a localized effect (painful oedema).

Treatment. Bites should be treated with topical applications of dilute ammonia, permanganate or hypochlorite lotions. Antihistamines may also be administered.

Insects (Hexapoda)

Insects may inject venom via the mouthparts (Simuliidae—black flies, Culicidae—mosquitoes, Phlebotomus—sandflies) or via the sting (bees, wasps, hornets, carnivorous ants). They may cause rash with their hairs (caterpillars, butterflies), or they may produce blisters by their haemolymph (Cantharidae—blister flies and Staphylinidae—rove beetles). Black fly bites produce necrotic lesions, sometimes with general disorders; mosquito bites produce diffuse pruriginous lesions. The stings of Hymenoptera (bees, etc.) produce intense local pain with erythema, oedema and, sometimes, necrosis. General accidents may result from sensitization or multiplicity of stings (shivering, nausea, dyspnoea, chilling of the extremities). Stings on the face or the tongue are particularly serious and may cause death by asphyxiation due to glottal oedema. Caterpillars and butterflies may cause generalized pruriginous skin lesions of an urticarial or oedematous type (Quincke’s oedema), sometimes accompanied by conjunctivitis. Superimposed infection is not infrequent. The venom from blister flies produces vesicular or bullous skin lesions (Poederus). There is also the danger of visceral complications (toxic nephritis). Certain insects such as Hymenoptera and caterpillars are found in all parts of the world; other suborders are more localized, however. Dangerous butterflies are found mainly in Guyana and the Central African Republic; blister flies are found in Japan, South America and Kenya; black flies live in the intertropical regions and in central Europe; sandflies are found in the Middle East.

Prevention. First level prevention includes mosquito nets and repellent and/or insecticide application. Workers who are severely exposed to insect bites can be desensitized in cases of allergy by the administration of increasingly large doses of insect body extract.



Wednesday, 16 February 2011 00:33

Clinical Features of Snakebite

Written by

David A. Warrell*

* Adapted from The Oxford Textbook of Medicine, edited by DJ Weatherall, JGG Ledingham and DA Warrell (2nd edition, 1987), pp. 6.66-6.77. By permission of Oxford University Press.

Clinical Features

A proportion of patients bitten by venomous snakes (<10% to >60%), depending on the species, will develop minimal or no signs of toxic symptoms (envenoming) despite having puncture marks which indicate that the snake’s fangs have penetrated the skin.

Fear and effects of treatment, as well as the snake’s venom, contribute to the symptoms and signs. Even patients who are not envenomed may feel flushed, dizzy and breathless, with constriction of the chest, palpitations, sweating and acroparaesthesiae. Tight tourniquets may produce congested and ischaemic limbs; local incisions at the site of the bite may cause bleeding and sensory loss; and herbal medicines often induce vomiting.

The earliest symptoms directly attributable to the bite are local pain and bleeding from the fang punctures, followed by pain, tenderness, swelling and bruising extending up the limb, lymphangitis and tender enlargement of regional lymph nodes. Early syncope, vomiting, colic, diarrhoea, angio-oedema and wheezing may occur in patients bitten by European Vipera, Daboia russelii, Bothrops sp, Australian Elapids and Atractaspis engaddensis. Nausea and vomiting are common symptoms of severe envenoming.

Types of bites

Colubridae (back-fanged snakes such as Dispholidus typus, Thelotornis sp, Rhabdophis sp, Philodryas sp)

There is local swelling, bleeding from the fang marks and sometimes (Rhabophis tigrinus) fainting. Later vomiting, colicky abdominal pain and headache, and widespread systemic bleeding with extensive ecchymoses (bruising), incoagulable blood, intravascular haemolysis and kidney failure may develop. Envenoming may develop slowly over several days.

Atractaspididae (burrowing asps, Natal black snake)

Local effects include pain, swelling, blistering, necrosis and tender enlargement of local lymph nodes. Violent gastro-intestinal symptoms (nausea, vomiting and diarrhoea), anaphylaxis (dyspnoea, respiratory failure, shock) and ECG changes (a-v block, ST, T-wave changes) have been described in patients envenomed by A. engaddensis.

Elapidae (cobras, kraits, mambas, coral snakesand Australian venomous snakes)

Bites by kraits, mambas, coral snakes and some cobras (e.g., Naja haje and N. nivea) produce minimal local effects, whereas bites by African spitting cobras (N. nigricollis, N. mossambica, etc.) and Asian cobras (N. naja, N. kaouthia, N. sumatrana, etc.) cause tender local swelling which may be extensive, blistering and superficial necrosis.

Early symptoms of neurotoxicity before there are objective neurological signs include vomiting, “heaviness” of the eyelids, blurred vision, fasciculations, paraesthesiae around the mouth, hyperacusis, headache, dizziness, vertigo, hypersalivation, congested conjunctivae and “gooseflesh”. Paralysis starts as ptosis and external ophthalmoplegia appearing as early as 15 minutes after the bite, but sometimes delayed for ten hours or more. Later the face, palate, jaws, tongue, vocal cords, neck muscles and muscles of deglutition become progressively paralysed. Respiratory failure may be precipitated by upper airway obstruction at this stage, or later after paralysis of intercostal muscles, diaphragm and accessory muscles of respiration. Neurotoxic effects are completely reversible, either acutely in response to antivenom or anticholinesterases (e.g., following bites by Asian cobras, some Latin American coral snakes—Micrurus, and Australian death adders—Acanthophis) or they may wear off spontaneously in one to seven days.

Envenoming by Australian snakes causes early vomiting, headache and syncopal attacks, neurotoxicity, haemostatic disturbances and, with some species, ECG changes, generalized rhabdomyolysis and kidney failure. Painful enlargement of regional lymph nodes suggests impending systemic envenoming, but local signs are usually absent or mild except after bites by Pseudechis sp.

Venom ophthalmia caused by “spitting” elapids

Patients “spat” at by spitting elapids experience intense pain in the eye, conjunctivitis, blepharospasm, palpebral oedema and leucorrhoea. Corneal erosions are detectable in more than half the patients spat at by N. nigricollis. Rarely, venom is absorbed into the anterior chamber, causing hypopyon and anterior uveitis. Secondary infection of corneal abrasions may lead to permanent blinding opacities or panophthalmitis.

Viperidae (vipers, adders, rattlesnakes, lance-headed vipers, moccasins and pit vipers)

Local envenoming is relatively severe. Swelling may become detectable within 15 minutes but is sometimes delayed for several hours. It spreads rapidly and may involve the whole limb and adjacent trunk. There is associated pain and tenderness in regional lymph nodes. Bruising, blistering and necrosis may appear during the next few days. Necrosis is particularly frequent and severe following bites by some rattlesnakes, lance-headed vipers (genus Bothrops), Asian pit vipers and African vipers (genera Echis and Bitis). When the envenomed tissue is contained in a tight fascial compartment such as the pulp space of the fingers or toes or the anterior tibial compartment, ischaemia may result. If there is no swelling two hours after a viper bite it is usually safe to assume that there has been no envenoming. However, fatal envenoming by a few species can occur in the absence of local signs (e.g., Crotalus durissus terrificus, C. scutulatus and Burmese Russell’s viper).

Blood pressure abnormalities are a consistent feature of envenoming by Viperidae. Persistent bleeding from fang puncture wounds, venepuncture or injection sites, other new and partially healed wounds and post partum, suggests that the blood is incoagulable. Spontaneous systemic haemorrhage is most often detected in the gums, but may also be seen as epistaxis, haematemesis, cutaneous ecchymoses, haemoptysis, subconjunctival, retroperitoneal and intracranial haemorrhages. Patients envenomed by the Burmese Russell’s viper may bleed into the anterior pituitary gland (Sheehan’s syndrome).

Hypotension and shock are common in patients bitten by some of the North American rattlesnakes (e.g., C. adamanteus, C. atrox and C. scutulatus), Bothrops, Daboia and Vipera species (e.g., V. palaestinae and V. berus). The central venous pressure is usually low and the pulse rate rapid, suggesting hypovolaemia, for which the usual cause is extravasation of fluid into the bitten limb. Patients envenomed by Burmese Russell’s vipers show evidence of generally increased vascular permeability. Direct involvement of the heart muscle is suggested by an abnormal ECG or cardiac arrhythmia. Patients envenomed by some species of the genera Vipera and Bothrops may experience transient recurrent fainting attacks associated with features of an autopharmacological or anaphylactic reaction such as vomiting, sweating, colic, diarrhoea, shock and angio-oedema, appearing as early as five minutes or as late as many hours after the bite.

Renal (kidney) failure is the major cause of death in patients envenomed by Russell’s vipers who may become oliguric within a few hours of the bite and have loin pain suggesting renal ischaemia. Renal failure is also a feature of envenoming by Bothrops species and C. d. terrificus.

Neurotoxicity, resembling that seen in patients bitten by Elapidae, is seen after bites by C. d. terrificus, Gloydius blomhoffii, Bitis atropos and Sri Lankan D. russelii pulchella. There may be evidence of generalized rhabdomyolysis. Progression to respiratory or generalized paralysis is unusual.

Laboratory Investigations

The peripheral neutrophil count is raised to 20,000 cells per microlitre or more in severely envenomed patients. Initial haemo-concentration, resulting from extravasation of plasma (Crotalus species and Burmese D. russelii), is followed by anaemia caused by bleeding or, more rarely, haemolysis. Thrombocytopenia is common following bites by pit vipers (e.g., C. rhodostoma, Crotalus viridis helleri) and some Viperidae (e.g., Bitis arietans and D. russelii), but is unusual after bites by Echis species. A useful test for venom-induced defibrin(ogen)ation is the simple whole blood clotting test. A few millilitres of venous blood is placed in a new, clean, dry, glass test tube, left undisturbed for 20 minutes at ambient temperature, and then tipped to see if it has clotted or not. Incoagulable blood indicates systemic envenoming and may be diagnostic of a particular species (for example Echis species in Africa). Patients with generalized rhabdomyolysis show a steep rise in serum creatine kinase, myoglobin and potassium. Black or brown urine suggests generalized rhabdomyolysis or intravascular haemolysis. Concentrations of serum enzymes such as creatine phosphokinase and aspartate aminotransferase are moderately raised in patients with severe local envenoming, probably because of local muscle damage at the site of the bite. Urine should be examined for blood/haemoglobin, myoglobin and protein and for microscopic haematuria and red cell casts.


First aid

Patients should be moved to the nearest medical facility as quickly and comfortably as possible, avoiding movement of the bitten limb, which should be immobilized with a splint or sling.

Most traditional first-aid methods are potentially harmful and should not be used. Local incisions and suction may introduce infection, damage tissues and cause persistent bleeding, and are unlikely to remove much venom from the wound. The vacuum extractor method is of unproven benefit in human patients and could damage soft tissues. Potassium permanganate and cryotherapy potentiate local necrosis. Electric shock is potentially dangerous and has not proved beneficial. Tourniquets and compression bands can cause gangrene, fibrinolysis, peripheral nerve palsies and increased local envenoming in the occluded limb.

The pressure immobilization method involves firm but not tight bandaging of the entire bitten limb with a crepe bandage 4-5 m long by 10 cm wide starting over the site of the bite and incorporating a splint. In animals, this method was effective in preventing systemic uptake of Australian elapid and other venoms, but in humans it has not been subjected to clinical trials. Pressure immobilization is recommended for bites by snakes with neurotoxic venoms (e.g., Elapidae, Hydrophiidae) but not when local swelling and necrosis may be a problem (e.g., Viperidae).

Pursuing, capturing or killing the snake should not be encouraged, but if the snake has been killed already it should be taken with the patient to hospital. It must not be touched with bare hands, as reflex bites may occur even after the snake is apparently dead.

Patients being transported to hospital should be laid on their side to prevent aspiration of vomit. Persistent vomiting is treated with chlorpromazine by intravenous injection (25 to 50 mg for adults, 1 mg/kg body weight for children). Syncope, shock, angio-oedema and other anaphylactic (autopharmacological) symptoms are treated with 0.1% adrenaline by subcutaneous injection (0.5 ml for adults, 0.01 ml/kg body weight for children), and an antihistamine such as chlorpheniramine maleate is given by slow intravenous injection (10 mg for adults, 0.2 mg/kg body weight for children). Patients with incoagulable blood develop large haematomas after intramuscular and subcutaneous injections; the intravenous route should be used whenever possible. Respiratory distress and cyanosis are treated by establishing an airway, giving oxygen and, if necessary, assisted ventilation. If the patient is unconscious and no femoral or carotid pulses can be detected, cardiopulmonary resuscitation (CPR) should be started immediately.

Hospital treatment

Clinical assessment

In most cases of snakebite there are uncertainties about the species responsible and the quantity and composition of venom injected. Ideally, therefore, patients should be admitted to hospital for at least 24 hours of observation. Local swelling is usually detectable within 15 minutes of significant pit viper envenoming and within two hours of envenoming by most other snakes. Bites by kraits (Bungarus), coral snakes (Micrurus, Micruroides), some other elapids and sea snakes may cause no local envenoming. Fang marks are sometimes invisible. Pain and tender enlargement of lymph nodes draining the bitten area is an early sign of envenoming by Viperidae, some Elapidae and Australasian elapids. All the patient’s tooth sockets should be examined meticulously, as this is usually the first site at which spontaneous bleeding can be detected clinically; other common sites are nose, eyes (conjunctivae), skin and gastro-intestinal tract. Bleeding from venipuncture sites and other wounds implies incoagulable blood. Hypotension and shock are important signs of hypovolaemia or cardiotoxicity, seen particularly in patients bitten by North American rattlesnakes and some Viperinae (e.g., V berus, D russelii, V palaestinae). Ptosis (e.g., drooping of the eyelid) is the earliest sign of neurotoxic envenoming. Respiratory muscle power should be assessed objectively—for example, by measuring vital capacity. Trismus, generalized muscle tenderness and brownish-black urine suggests rhabdomyolysis (Hydrophiidae). If a procoagulant venom is suspected, coagulability of whole blood should be checked at the bedside using the 20-minute whole blood clotting test.

Blood pressure, pulse rate, respiratory rate, level of consciousness, presence/absence of ptosis, extent of local swelling and any new symptoms must be recorded at frequent intervals.

Antivenom treatment

The most important decision is whether or not to give antivenom, as this is the only specific antidote. There is now convincing evidence that in patients with severe envenoming, the benefits of this treatment far outweigh the risk of antivenom reactions (see below).

General indications for antivenom

Antivenom is indicated if there are signs of systemic envenoming such as:

  1. haemostatic abnormalities such as spontaneous systemic bleeding, incoagulable blood or profound thrombocytopenia (<50/l x 10-9)
  2. neurotoxicity
  3. hypotension and shock, abnormal ECG or other evidence of cardiovascular dysfunction
  4. impaired consciousness of any cause
  5. generalized rhabdomyolysis.


Supporting evidence of severe envenoming is a neutrophil leucocytosis, elevated serum enzymes such as creatine kinase and aminotransferases, haemoconcentration, severe anaemia, myoglobinuria, haemoglobinuria, methaemoglobinuria, hypoxaemia or acidosis.

In the absence of systemic envenoming, local swelling involving more than half the bitten limb, extensive blistering or bruising, bites on digits and rapid progression of swelling are indications for antivenom, especially in patients bitten by species whose venoms are known to cause local necrosis (e.g., Viperidae, Asian cobras and African spitting cobras).

Special indications for antivenom

Some developed countries have the financial and technical resources for a wider range of indications:

United States and Canada: After bites by the most dangerous rattlesnakes (C. atrox, C. adamanteus, C. viridis, C. horridus and C. scutulatus) early antivenom therapy is recommended before systemic envenoming is evident. Rapid spread of local swelling is considered to be an indication for antivenom, as is immediate pain or any other symptom or sign of envenoming after bites by coral snakes (Micruroides euryxanthus and Micrurus fulvius).

Australia: Antivenom is recommended for patients with proved or suspected snakebite if there are tender regional lymph nodes or other evidence of systemic spread of venom, and in anyone effectively bitten by an identified highly venomous species.

Europe: (Adder: Vipera berus and other European Vipera): Antivenom is indicated to prevent morbidity and reduce the length of convalescence in patients with moderately severe envenoming as well as to save the lives of severely envenomed patients. Indications are:

  1. fall in blood pressure (systolic to less than 80 mmHg, or by more than 50 mmHg from the normal or admission value) with or without signs of shock
  2. other signs of systemic envenoming (see above), including spontaneous bleeding, coagulopathy, pulmonary oedema or haemorrhage (shown by chest radiograph), ECG abnormalities and a definite peripheral leucocytosis (more than 15,000/ μl) and elevated serum creatine kinase
  3. severe local envenoming—swelling of more than half the bitten limb developing within 48 hours of the bite—even in the absence of systemic envenoming
  4. in adults, swelling extending beyond the wrist after bites on the hand or beyond the ankle after bites on the foot within four hours of the bite.


Patients bitten by European Vipera who show any evidence of envenoming should be admitted to hospital for observation for at least 24 hours. Antivenom should be given whenever there is evidence of systemic envenoming—(1) or (2) above—even if its appearance is delayed for several days after the bite.

Prediction of antivenom reactions

It is important to realize that most antivenom reactions are not caused by acquired Type I, IgE-mediated hypersensitivity but by complement activation by IgG aggregates or Fc fragments. Skin and conjunctival tests do not predict early (anaphylactic) or late (serum sickness type) antivenom reactions but delay treatment and may sensitize the patient. They should not be used.

Contraindications to antivenom

Patients with a history of reactions to equine antiserum suffer an increased incidence and severity of reactions when given equine antivenom. Atopic subjects have no increased risk of reactions, but if they develop a reaction it is likely to be severe. In such cases, reactions may be prevented or ameliorated by pretreatment with subcutaneous adrenaline, antihistamine and hydrocortisone, or by continuous intravenous infusion of adrenaline during antivenom administration. Rapid desensitization is not recommended.

Selection and administration of antivenom

Antivenom should be given only if its stated range of specificity includes the species responsible for the bite. Opaque solutions should be discarded, as precipitation of protein indicates loss of activity and increased risk of reactions. Monospecific (monovalent) antivenom is ideal if the biting species is known. Polyspecific (polyvalent) antivenoms are used in many countries because it is difficult to identify the snake responsible. Polyspecific antivenoms may be just as effective as monospecific ones but contain less specific venom-neutralizing activity per unit weight of immunoglobulin. Apart from the venoms used for immunizing the animal in which the antivenom has been produced, other venoms may be covered by paraspecific neutralization (e.g., Hydrophiidae venoms by tiger snake—Notechis scutatus—antivenom).

Antivenom treatment is indicated as long as signs of systemic envenoming persist (i.e., for several days) but ideally it should be given as soon as these signs appear. The intravenous route is the most effective. Infusion of antivenom diluted in approximately 5 ml of isotonic fluid/kg body weight is easier to control than intravenous “push” injection of undiluted antivenom given at the rate of about 4 ml/min, but there is no difference in the incidence or severity of antivenom reactions in patients treated by these two methods.

Dose of antivenom

Manufacturers’ recommendations are based on mouse protection tests and may be misleading. Clinical trials are needed to establish appropriate starting doses of major antivenoms. In most countries the dose of antivenom is empirical. Children must be given the same dose as adults.

Response to antivenom

Marked symptomatic improvement may be seen soon after antivenom has been injected. In shocked patients, the blood pressure may rise and consciousness return (C. rhodostoma, V. berus, Bitis arietans). Neurotoxic signs may improve within 30 minutes (Acanthophis sp, N. kaouthia), but this usually takes several hours. Spontaneous systemic bleeding usually stops within 15 to 30 minutes, and blood coagulability is restored within six hours of antivenom, provided that a neutralizing dose has been given. More antivenom should be given if severe signs of envenoming persist after one to two hours or if blood coagulability is not restored within about six hours. Systemic envenoming may recur hours or days after an initially good response to antivenom. This is explained by continuing absorption of venom from the injection site and the clearance of antivenom from the bloodstream. The apparent serum half-lives of equine F(ab’)2 antivenoms in envenomed patients range from 26 to 95 hours. Envenomed patients should therefore be assessed daily for at least three or four days.

Antivenom reactions

  • Early (anaphylactic) reactions develop within 10 to 180 minutes of starting antivenom in 3 to 84% of patients. The incidence increases with dose and decreases when more highly refined antivenom is used and administration is by intramuscular rather than intravenous injection. The symptoms are itching, urticaria, cough, nausea, vomiting, other manifestations of autonomic nervous system stimulation, fever, tachycardia, bronchospasm and shock. Very few of these reactions can be attributed to acquired Type I IgE-mediated hypersensitivity.
  • Pyrogenic reactions result from contamination of the antivenom with endotoxins. Fever, rigors, vasodilatation and a fall in blood pressure develop one to two hours after treatment. In children, febrile convulsions may be precipitated.
  • Late reactions of serum sickness (immune complex) type may develop 5 to 24 (mean 7) days after antivenom. The incidence of those reactions and the speed of their development increases with the dose of antivenom. Clinical features include fever, itching, urticaria, arthralgia (including the temporomandibular joint), lymphadenopathy, periarticular swellings, mononeuritis multiplex, albuminuria and, rarely, encephalopathy.


Treatment of antivenom reactions

Adrenaline (epinephrine) is the effective treatment for early reactions; 0.5 to 1.0 ml of 0.1% (1 in 1000, 1 mg/ml) is given by subcutaneous injection to adults (children 0.01 ml/kg) at the first signs of a reaction. The dose may be repeated if the reaction is not controlled. An antihistamine H1 antagonist, such as chlorpheniramine maleate (10 mg for adults, 0.2 mg/kg for children) should be given by intravenous injection to combat the effects of histamine release during the reaction. Pyrogenic reactions are treated by cooling the patient and giving antipyretics (paracetamol). Late reactions respond to an oral antihistamine such as chlorpheniramine (2 mg every six hours for adults, 0.25 mg/kg/day in divided doses for children) or to oral prednisolone (5 mg every six hours for five to seven days for adults, 0.7 mg/kg/day in divided doses for children).

Supportive treatment

Neurotoxic envenoming

Bulbar and respiratory paralysis may lead to death from aspiration, airway obstruction or respiratory failure. A clear airway must be maintained and, if respiratory distress develops, a cuffed endotracheal tube should be inserted or tracheostomy performed. Anticholinesterases have a variable but potentially useful effect in patients with neurotoxic envenoming, especially when post-synaptic neurotoxins are involved. The “Tensilon test” should be done in all cases of severe neurotoxic envenoming as with suspected myasthenia gravis. Atropine sulphate (0.6 mg for adults, 50 μg/kg body weight for children) is given by intravenous injection (to block muscarinic effects of acetylcholine) followed by an intravenous injection of edrophonium chloride (10 mg for adults, 0.25 mg/kg for children). Patients who respond convincingly can be maintained on neostigmine methyl sulphate (50 to 100 μg/kg body weight) and atropine, every four hours or by continuous infusion.

Hypotension and shock

If the jugular or central venous pressure is low or there is other clinical evidence of hypovolaemia or exsanguination, a plasma expander, preferably fresh whole blood or fresh frozen plasma, should be infused. If there is persistent or profound hypotension or evidence of increased capillary permeability (e.g., facial and conjunctival oedema, serous effusions, haemoconcentration, hypoalbuminaemia) a selective vasoconstrictor such as dopamine (starting dose 2.5 to 5 μg/kg body weight/min by infusion into a central vein) should be used.

Oliguria and renal failure

Urine output, serum creatinine, urea and electrolytes should be measured each day in patients with severe envenoming and in those bitten by species known to cause renal failure (e.g., Drusselii, C. d. terrificus, Bothrops species, sea snakes). If urine output drops below 400 ml in 24 hours, urethral and central venous catheters should be inserted. If urine flow fails to increase after cautious rehydration and diuretics (e.g., frusemide up to 1000 mg by intravenous infusion), dopamine (2.5 μg/kg body weight/min by intravenous infusion) should be tried and the patient placed on strict fluid balance. If these measures are ineffective, peritoneal or haemodialysis or haemofiltration are usually required.

Local infection at the site of the bite

Bites by some species (e.g., Bothrops sp, C. rhodostoma) seem particularly likely to be complicated by local infections caused by bacteria in the snake’s venom or on its fangs. These should be prevented with penicillin, chloramphenicol or erythromycin and a booster dose of tetanus toxoid, especially if the wound has been incised or tampered with in any way. An aminoglycoside such as gentamicin and metronidazole should be added if there is evidence of local necrosis.

Management of local envenoming

Bullae can be drained with a fine needle. The bitten limb should be nursed in the most comfortable position. Once definite signs of necrosis have appeared (blackened anaesthetic area with putrid odour or signs of sloughing), surgical debridement, immediate split skin grafting and broad-spectrum antimicrobial cover are indicated. Increased pressure within tight fascial compartments such as the digital pulp spaces and anterior tibial compartment may cause ischaemic damage. This complication is most likely after bites by North American rattlesnakes such as C. adamanteus, Calloselasma rhodostoma, Trimeresurus flavoviridis, Bothrops sp and Bitis arietans. The signs are excessive pain, weakness of the compartmental muscles and pain when they are passively stretched, hypaesthesia of areas of skin supplied by nerves running through the compartment, and obvious tenseness of the compartment. Detection of arterial pulses (e.g., by Doppler ultrasound) does not exclude intracompartmental ischaemia. Intracompartmental pressures exceeding 45 mm Hg are associated with a high risk of ischaemic necrosis. In these circumstances, fasciotomy may be considered but must not be attempted until blood coagulability and a platelet count of more than 50,000/ μl have been restored. Early adequate antivenom treatment will prevent the development of intracompartmental syndromes in most cases.

Haemostatic disturbances

Once specific antivenom has been given to neutralize venom procoagulants, restoration of coagulability and platelet function may be accelerated by giving fresh whole blood, fresh frozen plasma, cryoprecipitates (containing fibrinogen, factor VIII, fibronectin and some factors V and XIII) or platelet concentrates. Heparin must not be used. Corticosterioids have no place in the treatment of envenoming.

Treatment of snake venom ophthalmia

When cobra venom is “spat” into the eyes, first aid consists of irrigation with generous volumes of water or any other bland liquid which is available. Adrenaline drops (0.1 per cent) may relieve the pain. Unless a corneal abrasion can be excluded by fluorescein staining or slit lamp examination, treatment should be the same as for any corneal injury: a topical antimicrobial such as tetracycline or chloramphenicol should be applied. Instillation of diluted antivenom is not currently recommended.