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Recreational diving medicine
ARTICLE IN PRESS Current Anaesthesia & Critical Care (2008) 19, 235–246
www.elsevier.com/locate/cacc
FOCUS ON: PHYSIOLOGY
Recreational diving medicine C.J. Edge Department of Anaesthetics, The Royal Berkshire NHS Foundation Trust, London Road, Reading, RG1 5AN, UK
KEYWORDS Diving medicine; Gases; Decompression illness; Barotrauma
Summary Recreational diving medicine is a complex subject, overlapping with anaesthetics, general medicine, occupational medicine, physics, physiology and psychology. Advances in recreational diving technology mean that divers are diving in more remote areas and to deeper depths. This has implications for the recreational diving physician. & 2008 Elsevier Ltd. All rights reserved.
Introduction
Gases
Diving is a popular recreational activity and may give rise to many interesting medical problems. The definition of a dive is when a person enters water, a chamber, or any other environment and is subjected to pressure greater than 0.1 atm above local atmospheric pressure and who in order to survive in such an environment breathes in air or other breathing gases at a pressure greater than the local atmospheric pressure. The waters in and around the United Kingdom are generally cold and dark and may be strongly tidal. Such conditions generate physical, physiological and psychological problems for the diver. Diving under such conditions requires a reasonable level of medical fitness on the part of the diver. Tropical waters, increasingly the venue for many UK divers, are warmer and clearer, but may present different hazards, such as venomous marine animals and diving in areas remote from medical assistance.
Physical properties of gases
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Atmospheric pressure at sea level is 1 atm (equivalent to 101.3 kPa) and is the pressure that is experienced by all parts of the human body at sea level. Water is much denser than air (1 l of fresh water weighs 1 kg, while 1 l of air weighs 0.0012 kg). A column of water 10 m high exerts a pressure of 1 atm so that for every 10 m depth that the diver descends into the sea, his body will experience an increase in the ambient pressure of 1 atm. Thus, at a depth of 30 m for example, the diver will experience a total pressure of 4 atm (3 atm due to the pressure of the water plus 1 further atmosphere due to the pressure of the atmosphere itself).
The gas laws and gas solubility Boyle’s Law which states that at constant temperature the pressure and the volume of the gas are
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ARTICLE IN PRESS 236
C.J. Edge
inversely related: PV ¼ k, where P is the total pressure of the gas and V is the volume of the gas. k is a constant for a given gas or mixture of gases. Dalton’s Law of Partial Pressures states that the pressure exerted by a mixture of non-reacting gases is the sum of the pressures that would be exerted by the individual gases if each occupied the same volume alone: P total ¼ P1 þ P 2 þ þ P n , where Pn is the partial pressure of gas n and Ptotal is the total pressure of the gases (see Figure 1). Henry’s Law of Solubility of Gases in a Liquid states that the mass of a slightly soluble but inert gas that dissolves in a given amount of a liquid at a constant temperature is proportional to the partial pressure of that gas above the liquid. Mathematically:
the body that contain gas will be affected by pressure as indicated by Boyle’s Law. For example, the air in the lungs taken in by a breath-holding diver at the surface will shrink to one-half the original volume at a depth of 10 m, to one-third at a depth of 20 m and so on. However, scuba divers breathe gas at the ambient pressure of the surrounding water and this enables the diver to breathe with ease. Nonetheless, as the diver goes deeper, the supplied gas will become denser, and the work of breathing will become harder. In the condition where the volume of gas diminishes and further gas cannot be drawn in to occupy this space, it will either be filled by body tissues or by clothing. This state of affairs is called a ‘‘squeeze’’.
Physiological effects of increased pressure General considerations
mn ¼ cn Pn , where mn is the mass of gas n that dissolves in the liquid, cn is the solubility constant for gas n and Pn is the partial pressure of gas n above the liquid. Whilst gases are very compressible, the tissues in the body vary in their degree of compressibility. For example, in the human, nerve tissue will start to exhibit altered physiological function at a depth of approximately 150 m but bone will not be deformed until much higher pressures are reached. Cavities in
Depth
Volume
The physiological effects of changing pressure on the diver are due largely to the gases that the diver breathes. The dive may be thought of conveniently as having two stages: 1. The descent and the stay at depth. 2. The ascent.
Pressure
Partial Pressures PN2
0m 1
1 bar
10 m
1/2
2 bar
20 m
1/3
3 bar
30 m
1/4
4 bar
PO2
0.8
0.2
1.6
0.4
2.4
0.6
3.2
0.8
Figure 1 This diagram illustrates Boyle’s Law and Dalton’s Law of Partial Pressures. The fraction in the left-hand box indicates the fraction of gas left in the box, while the figures in the right-hand box give the partial pressures of nitrogen and oxygen. Note that the partial pressures in each box add to give the total pressure at a given depth.
ARTICLE IN PRESS Recreational diving medicine
The descent and the stay at depth At sea level, there is free exchange of gases between the air in the alveoli and the dissolved gases in the blood stream. As the diver descends the total pressure of the gases in the alveoli becomes greater than atmospheric and, by Henry’s law, the amount of the gases dissolved in the blood and thence in the body tissues becomes greater.
Nitrogen An increasing partial pressure of nitrogen has minimal effects on most people until a depth of about 30 m is reached. As depth is increased, divers who dive on air will experience increasing symptoms of nitrogen narcosis (the ‘‘narks’’) and, if they carry on diving deeper, they will eventually exhibit signs of narcosis.1 The initial signs are an increase in reaction time, inability to deal with a given situation and clumsiness. The cure for nitrogen narcosis is to ascend. The nitrogen is thought to act in a similar manner to an anaesthetic and may interact with, or alter the three dimensional structure of various neurotransmitter receptors.2 An alternative way to avoid nitrogen narcosis is to replace some or all of the nitrogen with a gas that is less narcotic, such as helium.
Oxygen High-pressure oxygen has several effects on the body. There is an increase in ventilation and a decrease in alveolar and arterial carbon dioxide buffering tension due to a rise in central venous carbon dioxide. This in turn is due to the reduction in carbon dioxide capacity of haemoglobin overcoming the decreased carotid body excitation. There is also a vagally mediated bradycardia and vasoconstriction of the intracranial and peripheral vessels. There is a small fall in cardiac output.3 Priestley, the discoverer of oxygen in 1775, was the first to suggest that it may be toxic. Later, in 1789, Lavoisier and Sequin4 demonstrated that oxygen at 1 atm does not alter gross oxidative metabolism but did note a damaging effect on the lungs. Paul Bert in 1878,5 showed that whilst oxygen is essential to life, it becomes lethal at high pressures. He observed that larks exposed to air at 15–20 bar developed convulsions and that the same effect could be produced by oxygen at 5 bar. This central nervous system toxicity is now known as the ‘‘Paul Bert effect’’. In 1899, J. Lorrain Smith6 described the pulmonary changes resulting from exposure to moderately
237 high oxygen partial pressures (the ‘‘Lorrain Smith effect’’) and noted that the early changes are reversible and that higher pressures shortened the time of onset. During the 1930s, evidence accumulated that high-pressure oxygen was toxic to humans. Kenneth Donald, in 1942,3 showed that there was a wide variation in the tolerance to high pressures of oxygen, both between subjects and between the same subject on different days. Underwater exposure and exercise both aggravated the problem. Central nervous system (CNS) toxicity can be seen in the diving situation when closed and semiclosed rebreather sets (see later) are used. Divers may be exposed acutely to a high partial pressure of oxygen either through equipment failure or from going too deep and thereby raising the partial pressure of oxygen in the breathing gas to an unacceptable level. It is also being seen increasingly in those sport divers using high partial pressures of oxygen (PO2) in order to decrease decompression time for a particular dive profile. The diving physician is most likely to encounter CNS toxicity when treating decompression illness in the recompression chamber using a high PO2 (typically 2.8 atm). The symptoms of CNS toxicity, can be remembered using the acronym VITBEND:
V, Visual abnormalities, such as tunnel vision. I, Irritability. Can include anxiety, confusion or fatigue. T, Twitching, usually in the lips or other facial muscles. B, Breathing. Difficulty in taking a full breath. E, Ear problems, including tinnitus and vertigo. N, Nausea, sometimes intermittent. D, Dizziness, including clumsiness and incoordination.
The most dramatic manifestation is the grand mal type convulsion. Consciousness is maintained right up to the time of the convulsion, which may strike without any warning, and which does not give rise to any electroencephalographic (EEG) changes.7 Underwater, this is a serious situation because if it occurs the diver in scuba gear may lose the mouthpiece and drown. As mentioned above, exercise and immersion in water are two conditions that can lower the threshold to CNS toxicity. A third potentiating factor has been suggested to be carbon dioxide buildup, often occurring due to the ‘‘skip’’ breathing pattern adopted by many divers in order to conserve breathing gas, in which the diver takes a
ARTICLE IN PRESS 238 breath, holds it for as long as possible, and then slowly breathes out. To reduce the problems of oxygen toxicity during dives, the US National Oceanographic and Atmospheric Administration (NOAA) has recommended that partial pressures of oxygen should not exceed 1.4 bar, with an absolute maximum of 1.6 bar.8
Carbon dioxide The normal level of carbon dioxide in the alveoli is 40 mmHg (0.055 bar). When diving the arterial and alveolar carbon dioxide tensions should be maintained at approximately 40 mmHg. The alveolar pressures of nitrogen and oxygen increase with depth and therefore the alveolar percentage of carbon dioxide decreases. However, when energy expenditure is high, the level of carbon dioxide can increase dramatically. This situation is most commonly encountered in divers using rebreather sets. It may also be seen in the recompression chamber if there is inadequate flushing of the chamber with fresh gas. The clinical features of hypercapnia are breathlessness (carbon dioxide present at about 3%), distress and dyspnoea (5–6%), rise in blood pressure and heart rate, mental confusion and lack of coordination (10%) followed by loss of consciousness and death (12–14%).9 Although carbon dioxide is a respiratory stimulant, most of its effects are related to the acidosis it produces and are neurologically depressant.
Carbon monoxide Breathing gas must contain less than 5 parts per million (ppm) of carbon monoxide. If the breathing gas contains higher concentrations than this, then as it is compressed the partial pressure of carbon monoxide may rise to potentially lethal levels. The main source of the gas is from the exhaust fumes of the engine of an air compressor which, if not expelled well away from the inlet to the compressor, may be drawn into the diver’s air cylinder.
Long-term effects of diving under pressure Neurological changes10 and retinal changes11 have been described in divers but further work needs to be done to be sure that these changes are real. Specialised nuclear magnetic resonance imaging (MRI) scans have shown that in a few divers who have had DCI, and who have been demonstrated to have a shunt between the venous and arterial circulations (see below), have areas of high signal
C.J. Edge intensity in the cerebrum.12 However, it is unclear what these lesions represent in terms of pathology; certainly none of the divers with lesions had any demonstrable neurological symptoms. Very occasionally, sport divers may present with joint problems (especially in the shoulder and hip joints) in which part of the bone dies.13,14 This is due to exposure to compressed gases at pressures higher than atmospheric pressure over a long period of time and is known as aseptic necrosis or dysbaric osteonecrosis. The pathogenesis of dysbaric osteonecrosis is poorly understood.
The ascent from depth Decompression Unfortunately for the diver, gases that are chemically unreactive as far as the body is concerned (e.g. nitrogen, helium and neon) are sparingly soluble in blood. Even oxygen, when breathed at high partial pressures, can cause problems on ascent. When the diver ascends the gas that has dissolved in the tissues will come out of solution to form bubbles of gas in the tissues and in the blood vessels. These bubbles are then transported to the lungs where, in most cases, they are filtered out. This is the process of decompression. If the bubbles cause medical problems for the diver, then the diver is said to be suffering from decompression illness (DCI) which used to be known as caisson disease. Robert Boyle in 1690,15 was the first to investigate this phenomenon and it was he who had the idea that a rapid reduction in the atmospheric pressure could lead to the release of bubbles into the body tissues and thus cause a serious impairment in their function. Paul Bert, in a series of experiments in the late 19th century,5 showed that the more serious forms of DCI were provoked by the presence of large volumes of free gas, as opposed to dissolved gas. The composition of these bubbles was found to be largely nitrogen. Observations in caisson workers showed that if the decompression procedure was inadequate, then the blood of the workers literally frothed. This condition was called ‘‘the chokes’’ and proved to be rapidly fatal unless rapid recompression took place. If the decompression was not so provocative, then a condition known as ‘‘the staggers’’ might be seen which could lead to severe impairment of the nervous system or death. But the commonest form of DCI came to be called ‘‘the bends’’.16
ARTICLE IN PRESS Recreational diving medicine
239
At the turn of the century, Professor J.J.S. Haldane undertook a series of investigations for the purpose of producing regulations for the safe conduct of underwater work by divers.17 Experiments in the goat showed that if the goats were exposed to a raised pressure (P1) for a ‘‘prolonged period’’ (1.5–2 h) and then the pressure was rapidly dropped to a new level (P2), the goats would exhibit mild signs of DCI if P2 was about half the value of P1. If the pressure drop was less than half, then the goats would not exhibit signs of DCI. This ratio P2/P1 ¼ 0.5 was found to be generally true over a wide range of values for P1 and P2. Using this approach, mathematical analysis reveals that if the ambient pressure of a tissue is suddenly changed from P1 to P2 then the gas tensions within that tissue will increase towards P2 as shown in Figure 2. Over the next 25 years, most of the research into decompression was carried out by the US Navy, leading to the publication of the US navy decompression tables in 1956,18 which have been widely used throughout the world. These tables indicate the maximum time that the diver may spend at a certain depth with a low risk of DCI after the ascent. In 1976, the Naval Safety Center reported that the overall incidence of DCI was only 0.065% using these tables, although certain dive profiles within the tables carry a greater risk.19 Nowadays, these mathematical models have been incorporated into small computers that can be worn on the wrist by divers. This allows multi-level diving to take place rather than just allowing the diver to dive to one specified depth and then to return to the surface again. These instruments have now been accepted by the recreational diving commu-
Pressure
P2
P1
0
Time
Figure 2 Figure showing the pressure versus time curve in the tissues as the gas pressure is raised from a value P1 to P2. The time period over which the change happens is thought to depend upon different factors, such as the vascularity of the tissue, the temperature and the amount of fat present in the tissue.
nity in particular as they allow dives of greater depth and duration to be performed for the same amount of decompression time. They have the advantage that they can be interrogated by the diving doctor when a diver presents to a recompression chamber with the symptoms of DCI. This allows the doctor to ascertain the dive profiles that the diver has undertaken prior to becoming ill and enables treatment to be tailored accordingly.
The clinical symptoms and signs of DCI The symptoms and signs of DCI include the following, although the list is by no means exhaustive20:
Pruritic mottled skin rash; Vague limb discomfort (‘‘the niggles’’); Moderate or severe limb pain (‘‘the bends’’); Feelings of being abnormally tired or exhausted; Abnormalities on psychometric testing; Limb weakness or paralysis; Parasthesiae; Vertigo; Headache; Vomiting; Abdominal pain; Visual problems; Collapse, hypotension, loss of consciousness.
The symptoms and signs of DCI, when referring a patient to a recompression chamber or to a diving doctor, are now described according to onset, evolution and some estimate of inert gas load in the form of depth–time profile. The manifestations of DCI are considered to be predominantly due to a high inert gas load in the tissues. Gas may form within the tissues as a result of insufficiently rapid washout of excess dissolved inert gas during the ascent. The gas may then go on to form bubbles within the tissue and venous circulation. Once in the venous circulation, these bubbles may be detected in the right atrium and ventricle by the use of 2D Doppler echocardiography. In the vast majority of cases, these bubbles are clinically ‘‘silent’’ and are removed by the pulmonary circulation without causing any symptoms of DCI. Thus, although quantification of the bubbles is useful for elucidating the pathophysiology of DCI, it is not useful in the assessment or in the management of divers with DCI.21 Barotrauma Many tissues in the body may contain natural or unnatural collections of free gas. At one extreme
ARTICLE IN PRESS 240 there are extremely rigid containers such as blocked paranasal sinuses. At the other extreme are very compliant containers such as unobstructed lungs or patent sinuses. In the intermediate range are moderately compliant vessels such as the gastrointestinal tract and the cavity of the middle ear. The unobstructed lung has a time constant of emptying of less than 1 s22 and so it normally vents and fills with gas without difficulty during ascent and descent. If the lung is obstructed, as for example during descent on a breath-hold dive, it compresses according to Boyle’s Law, typically reaching residual volume at a depth of approximately 30 msw. Further descent causes blood to be drawn into the chest from the limbs and abdomen to compensate for further diminution of lung volume. If the lung is obstructed on ascent, e.g. by a diver unwisely holding his/her breath, the gas in the lung expands until the lung reaches its bursting pressure which is roughly 70 mmHg at about 115% of voluntary total lung capacity when it ruptures. Gas may escape from the lungs into other tissues in four ways: 1. Into the virtual space between the visceral and parietal pleura to give a pneumothorax. A particularly severe form of this condition is seen with a tension pneumothorax which must be recognised and treated rapidly if the diver is to survive. 2. Into the pulmonary venous blood from where the gas passes into the arterial circulation (arterial gas embolism, AGE) giving rise to the manifestations of DCI. 3. Into the mediastinum (pneumomediastinum) and thence into the soft tissues of the neck, giving rise to surgical emphysema. 4. Into the peritoneum to give pneumoperitoneum, although this symptom is rarely encountered. For reasons that are not understood but may be to do with posture whilst working, aviators and tunnel workers experience pneumothoraces more commonly than AGE, while the situation is reversed in divers. If the Eustachian tube is obstructed, painful bowing of the tympanic membrane into the middle ear occurs when the diver descends. Further descent will cause rupture of the tympanic membrane with entry of potentially infected water into the middle ear cavity. This can result in vertigo underwater which may cause the diver to panic and ascend rapidly to the surface. Obstructing the external meatus (which most commonly occurs by means of a tightly fitting hood) causes an outward
C.J. Edge bowing of the tympanic membrane, known as ‘‘reversed ear’’. Gas may become trapped in a tooth cavity at depth, commonly as a result of poor dental hygiene. On ascent, the expanding gas can cause severe pain in the tooth (odontalgia); in some cases the tooth has been known to shatter (odontocharexis).
Treatment of DCI The most common problem with the treatment of DCI is lack of recognition of the symptoms and signs either by the colleagues of the diver or by the medical profession. For example, neurological problems in the peripheral nervous system may go unnoticed by the physician if not specifically sought as the diver may well be too anxious and confused due to symptoms of DCI in the cerebrum to tell the physician that there are problems with the feeling in his arms or legs, or that he is unable to pass urine. The treatment of DCI is by recompression in a recompression chamber.23 For less severe cases of DCI, the earlier that recompression is started after the onset of symptoms and signs of DCI, the better the result, but successful therapy has commenced as long as several days after the initial symptoms of DCI had presented.24 In the most severe cases, it has been argued that there is no ‘‘time to treatment’’ effect.25 Algorithms are published showing the depths, times and treatment gases that are used depending on the presentation and evolution of signs and symptoms of DCI in the diver. An example of such an algorithm is given in Figure 3. In addition, fluid should be administered either orally or intravenously depending upon the conscious state of the diver, as in some cases of DCI the diver is found to be very dehydrated. The use of non-steroidal anti-inflammatory agents is more controversial.26 Currently steroids and lidocaine are not in use for the routine treatment of DCI. DCI may develop some hours after the diver has finished diving. Surveys of divers have shown that about 50% of cases of DCI will exhibit signs and symptoms within 1 h of surfacing, while 90% will present within 6 h of surfacing.27 In a few cases, the time interval has been of the order of days. A diver could be thought to be drunk or under the influence of drugs when he presents to the GP’s surgery or police station. If in doubt as to whether the diver is suffering from DCI then advice should be sought from diving medical experts.
ARTICLE IN PRESS Recreational diving medicine
241 DIAGNOSIS OF ACUTE DECOMPRESSION ILLNESS
COMPRESS TO 18m ON O2
Assess the patient after 20 mins
Neurological Symptoms or Signs?
YES
Symptoms relieved after 10 mins at 18m?
NO
YES
NO Compress to 50m on AIR or 32.5/67.5 O2/N2 if available
YES
Consult a Diving Medical Specialist
Is the patient deteriorating ?
NO
Consult a Diving Medical Specialist
NO
Compress to 18m on O2
USE TABLE 62
Have symptoms and signs resolved after 3 O2 periods?
YES
Consult a Diving YES Medical Specialist
DECOMPRESS ON TABLE 61
Have ANY symptoms resumed?
NO
YES
Patient free of symptoms after 25 mins at 50m?
Have symptoms and signs resolved?
EXTEND TABLE 62
NO
YES
NO
Patient continuing to deteriorate?
NO
Remain at 50m for a total of 2 hrs.
Are there any significant signs?
YES
NO
DECOMPRESS USING TABLE 62
YES Consult a Diving YES Medical Specialist
Consult a Diving Medical Specialist
Have any symptoms worsened or returned?
NO DECOMPRESS USING TABLE 63
COMPRESS TO DEPTH OF RELIEF (MAX 70m) AND USE TABLE 65
DECOMPRESS USING TABLE 64
Consider recompression to 18m and transfer to Table 64 or extending Table 62
COMPLETE TABLE 62
COMPLETE TABLE 61
Figure 3 Example algorithm for the treatment of DCI (from Francis TJR, Smith DJ, Sykes JJW. The prevention and management of diving accidents. Report no. R92004. Institute of Naval Medicine, Alverstoke, Gosport, 1992).
Risk factors for, and prevention of, DCI Despite the use of decompression tables or computers, cases of DCI still occur, especially in sport
divers. Sometimes these cases are due to missed decompression stops or because the diver has ascended too rapidly from depth. Occasionally, divers get DCI when they have stayed well within
ARTICLE IN PRESS 242 the times specified by the decompression tables. Some of these cases can be shown to have a patent foramen ovale (PFO) which, when the right atrial pressure exceeds the left atrial pressure, will allow bubbles from the venous circulation to bypass the pulmonary circulation and enter directly into the arterial circulation.28 Often these cases will present with a skin rash and neurological symptoms within a few minutes of reaching the surface after a dive. Sometimes it is possible to elicit a history of migraine with aura from the subject. Divers who have exhibited these signs and symptoms and who have been shown to have a PFO should not be passed as fit to dive unless the PFO can be closed by interventional cardiological techniques using a prosthetic surgical device, or the diver is prepared to dive very conservatively to depths less than 15 m. Other risk factors for DCI are thought to be age, poor physical fitness, cigarette smoking, dehydration, carbon dioxide retention and possibly obesity.20 Divers who are being placed under pressure frequently can become acclimatised to a particular pressure, but this acclimatisation quickly wears off over 2–3 days if the diver has time off. When giving advice to divers about the risks of DCI, it should be remembered that many recreational divers are flying to the dive sites. In a few circumstances, the diver may be forced to travel by land at high altitude in order to gain access to the dive site. Both flying and high altitude travel are associated with a reduction in atmospheric pressure and inert gas bubbles are therefore likely to form more readily if such travel is undertaken shortly after a dive. A good general rule is to avoid flying or high altitude travel for at least 24 h after diving.
Diving equipment Recreational gas delivery systems SCUBA apparatus Self-Contained Underwater Breathing Apparatus (SCUBA) equipment is carried by the recreational diver and enables the diver to be independent of the surface. In open circuit scuba, gas (most commonly air) is delivered to the diver at the ambient pressure of the surrounding water from a cylinder carried on the back by means of a demand valve. This consists of a first stage to reduce the cylinder pressure to a lower, intermediate pressure and a second stage to further reduce the gas
C.J. Edge pressure to that of the surrounding water. Once the diver has taken a breath of the gas, it is then vented into the water. At depths greater than 50 m, nitrogen narcosis and the effort involved in breathing the dense air prevents the diver from working effectively. For such dives, the nitrogen is replaced by helium which is not considered to be narcotic, even at depths of 600 m. However, if compression to depth using helium/oxygen mixtures (‘‘heliox’’) is carried out too rapidly, then high pressure nervous syndrome29 may be experienced by the diver. This syndrome is characterised by decrements in motor and intellectual performance, accompanied by dizziness, nausea, vomiting and a marked tremor of the hands, arms and torso. The incidence of the syndrome can be decreased by slowing the rate of compression to depth and by adding to the helium/oxygen mixture a small amount of an anaesthetic gas, most commonly nitrogen. This helium/oxygen/nitrogen mixture is now known as ‘‘trimix’’. For many years, dives using trimix and heliox were undertaken only by divers working offshore in the oil and gas industry. Since the early 1970s however, recreational and scientific divers have started to use heliox and, more commonly, trimix to dive to greater depths. Thus, wrecks such as the ‘‘Andrea Doria’’ (85 m deep) and the ‘‘Lusitania’’ (93 m deep) have been dived using scuba gear and trimix. Such dives, without the backup and facilities that are available to commercial organisations in the oil and gas industry, are more hazardous than those usually undertaken by a standard recreational diver.
Rebreathers In open circuit scuba, every breath taken contains about 21% oxygen, but only 4–5% of this is metabolically consumed. The rest is exhaled along with the unused inert gases and the carbon dioxide produced by the body. A better method would be to use a system which allows the exhaled gas to be cleansed of carbon dioxide and replenished with fresh gas for further consumption, as is commonly seen in modern anaesthetic machines. This is the basis of a rebreather. This concept is not new; the first rebreather was produced in 1878 by Henry Fleuss and the idea was extensively developed during the first and second world wars by the military. During the 1960s and 1970s, the scientific community started to use rebreathers and since the 1990s, the recreational diver has been able to buy production-model rebreathers.
ARTICLE IN PRESS Recreational diving medicine Rebreathers come in two basic forms: 1. Semi-closed circuit, in which the gas the diver is breathing is recycled through a scrubber to remove the carbon dioxide and then a fixed amount of fresh gas is added to maintain a constant oxygen pressure. Such a unit will occasionally need to vent excess gas as the amount of inert gas builds up, and therefore wastes a small amount of the gas supply. These devices are relatively cheap because they are purely mechanical. Oxygen partial pressure can be monitored using a sensor but the device will continue to operate even if the sensor fails. Such units are becoming more popular with scientific, media and recreational divers. 2. Closed circuit, in which the gas that the diver breathes is recycled through a scrubber to remove the carbon dioxide and the percentage of oxygen in this mix is detected using an oxygen sensor. The correct amount of oxygen can then be injected into the mix to give the correct partial pressure of oxygen for the diver to breathe. These units are very expensive, requiring microprocessors to function efficiently. The electronic instrumentation occasionally fails, which may have disastrous consequences for the diver underwater. Against this, they do make the best use of the available gas and if maintained properly, they can be used for very deep dives.
243
Other equipment Buoyancy aids Buoyancy control can be maintained either by adjusting the volume of air in the dry suit (if the diver is wearing one), or by adjusting the amount of air in a buoyancy compensator (BC) which is worn over the wet suit or dry suit in the manner of a waistcoat. Gas can be injected into the BC directly from the first stage of the demand valve.
Mask and fins Recreational divers commonly wear a facemask which encloses the eyes and nose, thus enabling the diver to equilibrate the pressure in the middle ears and Eustachian tubes with the ambient pressure of the surrounding water. Additionally, the lenses in the mask may be optically corrected to avoid the use of spectacles or contact lenses in the water. The bulky diving equipment slows progress in the water very considerably and so fins are a necessary accessory for the diver to allow adequate propulsion in the water.
Light sources Most recreational divers carry a torch of some form underwater. Red light penetrates the shortest distance underwater, blue light the farthest. A torch may thus reveal the true colours of an object underwater; it may also be used for signalling purposes.
Thermal insulation A diver must be kept warm whilst underwater. Wet suits, which are a close fit, trap a layer of water between the suit and the diver which acts as thermal insulation. The suit is made out of foamed neoprene and the insulation is derived from the gas trapped within the closed cells of the material. They are cheap and allow the diver to urinate without loss of insulation effectiveness. However, at depth, the suit material compresses and insulation is lost. They also offer little protection to the diver in polluted water. Dry suits keep the diver dry by being waterproof, having seals at the neck and wrists and retaining an insulating layer of air between the diver and the suit. As the diver descends, the air in the suit becomes compressed, but this can be avoided by injecting gas into the suit to maintain the volume. These suits have the disadvantage that if punctured, insulation is lost. Additionally, hygienic urination can be difficult and this may cause problems if the dive is prolonged.
The role of the doctor Any medical carried out for the purposes of determining whether a person is fit to dive must be carried out by a doctor who, as in all medical specialities, has specialist knowledge of the subject (e.g. has attended a diving medical examiner course) and who is a diver. It must be remembered that a diver is responsible not only for his/her safety but also that of his/her buddy and any surface support. Any medical condition that may interfere with diver safety should be considered with care before allowing a person to dive. Space does not allow a complete list of all the medical conditions that may affect a diver to be given here but some useful references are given below. Discussion will be confined to a few of the most common problems present in the potential diving population.
ARTICLE IN PRESS 244
Asthma In the developed world, asthma is an increasing problem. In the UK, approximately 12% of the population have symptoms at some time that may be attributable to asthma. There is a risk that a mild asthma attack whilst diving may seriously impair the ability of a diver to swim against a current or to return to safety. A more severe attack may lead to gas trapping underwater with the possibility of barotrauma occurring. These scenarios may put both the diver and his/her buddy at risk. The current advice in the UK is that people with asthma induced by stress, exercise, or cold should not dive30 Those with allergen-induced asthma may dive provided their asthma is not too severe (stage 1 or stage 2 in the British Thoracic Society guidelines31) and that they take a puff of a b2-agonist approximately 30 min before every dive as a prophylactic measure against bronchoconstriction. Such asthmatic divers also should not dive within 48 h of any attack of wheezing, no matter how slight this may be.
Hypertension Well-controlled idiopathic hypertension (blood pressure less than 140/90 mmHg) in a potential diver should not cause problems, unless the diver is on a b-blocker. Such drugs may limit the exercise capability of the diver when undertaking hard exercise, e.g. swimming against a current. The use of b-blockers when diving is therefore contraindicated.
Diabetes mellitus Recent studies have shown that well-controlled diabetic persons may be permitted to dive provided that they have none of the long-term complications of diabetes.32,33 It is essential that the older person with type II diabetes is evaluated carefully for such complications as renal, neurological and cardiac problems are more common in this population and may not be picked up in a routine medical examination.
C.J. Edge in women who are not taking the oral contraceptive pill during the first week of the menstrual cycle.34 The physiological mechanism for this is unclear and further research is necessary before any firm conclusions may be drawn. There are no hard data on the effects of DCI on the foetus and papers published showing such effects in the human are either anecdotal cases or have serious methodological flaws. Women who dive whilst they are unknowingly pregnant understandably become very anxious about the possible adverse effects that this may have had on their unborn child. The diver must be referred to a physician who has specialist knowledge of diving medicine and an interest in this area for further consultation.
Psychological and psychiatric disease Current thinking in the UK is that no diver should be permitted to dive whilst currently taking, or in the last 3 months have taken medication for any psychological or psychiatric condition. This includes antidepressant medication, medication for panic attacks, and medication for Attention Deficit Hyperactivity Disorder (ADHD).
Epilepsy The issue of allowing persons with epilepsy to scuba dive is controversial.35 Issues that have been raised by those against allowing persons with epilepsy to dive include the possible interaction of high partial pressures of nitrogen with the sedative effects of anti-epileptic medications, and the epileptogenic properties of high partial pressures of oxygen, either when diving or in the hyperbaric chamber.36 Those who argue in favour of allowing persons with epilepsy to dive often compare the current ban with that on persons with diabetes before 1991. However, it is not yet possible to predict when a person with epilepsy will have a seizure, and therefore the opinion of all the recreational diving medical bodies is that no person with epilepsy should be allowed to dive until they have been off all medication and fit-free for a period of 5 years.
The effect of the menstrual cycle and pregnancy
Children and diving
Some preliminary data are available that would appear to show an increase in the incidence of DCI
Children of age 12 years and above are permitted to dive in the UK. Sometimes younger children will
ARTICLE IN PRESS Recreational diving medicine express their desire to dive through their parents, but it is important to explain to both parties that such children are unlikely to have the physical and mental maturity to deal with problems that may arise underwater, particularly if it involves the lifting of an adult to the surface followed by towing that adult to a place of safety. Cases of DCI have arisen in children, mainly through panic ascents to the surface, and severe permanent injuries have been the result.37
245
17. 18. 19.
20.
21.
References 1. Cousteau JY. The silent world. London: Hazell Watson and Viney; 1954. 2. Franks NP, Lieb WR. Molecular and cellular mechanisms of general anaesthesia. Nature 1994;367(6464):607–14. 3. Donald KW. Oxygen and the diver. Worcester: Harley Swan; 1992. 4. Lavoisier AL, Seguin A. Premier memoire sur la respiration des animaux. Hist Acad Sci Paris 1789;185:566–84. 5. Bert P. La Pression Barometrique: Recherches de Physiologie Experimentale, 1878. Translated by Hitchcock MA, Hitchcock FA. Published as: Barometric pressure: researches in experimental physiology. Columbus, OH: College Book Company. Reprinted 1978 by Undersea Medical Society, Bethesda, MD. 6. Smith JL. The pathological effects due to increase of oxygen tension in the air breathed. J Physiol 1899;24(1): 19–35. 7. Lambertsen CJ. The effects of oxygen at high partial pressure. In: Fenn WO, Rahn H, editors. Handbook of physiology, section 3: respiration. Washington, DC: American Physiological Society; 1965. p. 1027–46. 8. Joiner JT, editor. NOAA diving manual. 4th ed. Flagstaff, AZ: Best Publishing Company; 2001. 9. Lanphier EH. Carbon dioxide poisoning. In: Waite CL, editor. Case histories of diving and hyperbaric accidents. Bethesda, MD: Undersea and Hyperbaric Medical Society; 1988. 10. Todnem K, Nyland H, Kambestad BK, Aarli JA. Influence of occupational diving upon the nervous system: an epidemiological study. Br J Ind Med 1990;47(10):708–14. 11. Polkinghorne PJ, Sehmi K, Cross MR, Minassian D, Bird AC. Ocular fundus lesions in divers. Lancet 1988;2(8625): 1381–3. 12. Gerriets T, Tetzlaff K, Hutzelmann A, Liceni T, Kopiske G, Struck N, et al. Association between right-to-left shunts and brain lesions in sport divers. Aviat Space Environ Med 2003; 74(10):1058–60. 13. Laden GD, Grout P. Aseptic bone necrosis in an amateur scuba diver. Br J Sports Med 2004;38(5):E19. 14. Wilmshurst P, Ross K. Dysbaric osteonecrosis of the shoulder in a sport scuba diver. Br J Sports Med 1998;32(4): 344–5. 15. Boyle R. New pneumatical experiments about respiration. Philos Trans 1670;5:2011–58. 16. Jaminet A. Physical effects of compressed air and of the causes of pathological symptoms produced on man, by increased atmospheric pressure employed for the sinking of piers in the construction of the Illinois and St. Louis Bridge
22.
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28.
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31.
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33.
34.
35.
over the Mississippi River at St. Louis, Missouri. St. Louis: R & TA Enious; 1871. Boycott AE, Damant GC, Haldane JS. Prevention of compressed air illness. J Hyg Lond 1908;8:342–443. Des Granges M. Standard air decompression table. USN, EDU report 5-57. Washington, DC: Naval Gun Factory; 1956. Beckman EL. Recommendations for improved air decompression schedules for commercial diving. Sea grant technical report UNIHI-SEA GRANT-TR-76-02, 1976. Walker R. Decompression sickness: clinical. In: Edmonds C, Lowry C, Pennefather J, Walker R, editors. Diving and subaquatic medicine. 4th ed. London: Arnold; 2002. Nishi RY, Brubakk AO, Eftedal OS. Bubble detection. In: Brubakk AO, Neuman TS, editors. Bennett and Elliott’s physiology and medicine of diving. 5th ed. London: Elsevier Science; 2003. Francis TJ, Denison DM. Pulmonary barotrauma. In: Lundgren CE, Miller JN, editors. The lung at depth. New York: Marcel Dekker; 1999. Moon RE, Gorman DF. Treatment of the decompression disorders. In: Brubakk AO, Neuman TS, editors. Bennett and Elliott’s physiology and medicine of diving. 5th ed. London: Elsevier Science; 2003. Dovenbarger JA, Corson K, Moon RE, Bennett PB. A review of 33 dive accidents with a delay to treatment of 4 days or greater. Undersea Biomed Res 1990;17(Suppl.): 169. Ball R. Effect of severity, time to recompression with oxygen, and re-treatment on outcome in forty-nine cases of spinal cord decompression sickness. Undersea Hyperb Med 1993;20(2):133–45. Bennett M, Mitchell S, Dominguez A. Adjunctive treatment of decompression illness with a non-steroidal anti-inflammatory drug (tenoxicam) reduces compression requirement. Undersea Hyperb Med 2003;30(3):195–205. Elliott DH, Kindwall EP. Manifestations of the decompression disorders. In: Bennett PB, Elliott DH, editors. The physiology and medicine of diving. 3rd ed. London: Bailliere Tindall; 1982. Wilmshurst P, Bryson P. Relationship between the clinical features of neurological decompression illness and its causes. Clin Sci (Lond) 2000;99(1):65–75. Bennett PB. The high pressure nervous syndrome in man. In: Bennett PB, Elliott DH, editors. The physiology and medicine of diving. 3rd ed. London: Bailliere Tindall; 1982. Godden D, Currie G, Denison D, et al. British Thoracic Society guidelines on respiratory aspects of fitness for diving. Thorax 2003;58:3–13. British Thoracic Society Guideline on the Management of Asthma. Available at: /www.enterpriseportal2.co.uk/filestore/bts/asthmaupdatenov05.pdfS [accessed 5.09.07]. Edge CJ, St Leger Dowse M, Bryson P. Scuba diving with diabetes mellitus—the UK experience 1991–2001. Undersea Hyperb Med 2005;32(1):27–37. Dear Gde L, Pollock NW, Uguccioni DM, Dovenbarger J, Feinglos MN, Moon RE. Plasma glucose responses in recreational divers with insulin-requiring diabetes. Undersea Hyperb Med 2004;31(3):291–301. Lee V, St Leger Dowse M, Edge C, Gunby A, Bryson P. Decompression sickness in women: a possible relationship with the menstrual cycle. Aviat Space Environ Med 2003; 74(11):1177–82. Almeida Mdo R, Bell GS, Sander JW. Epilepsy and recreational scuba diving: an absolute contraindication or can there be exceptions? A call for discussion. Epilepsia 2007; 48(5):851–8.
ARTICLE IN PRESS 246 36. Greer HD, Massey EW. Neurologic consequences of diving. In: Bove AA, editor. Bove and Davis’ diving medicine. 4th ed. Philadelphia, PA: Saunders; 2004. 37. Tsung JW, Chou KJ, Martinez C, Tyrrell J, Touger M. An adolescent scuba diver with 2 episodes of diving-related
C.J. Edge injuries requiring hyperbaric oxygen recompression therapy: a case report with medical considerations for child and adolescent scuba divers. Pediatr Emerg Care 2005;21(10): 681–6.
www.elsevier.com/locate/cacc
FOCUS ON: PHYSIOLOGY
Recreational diving medicine C.J. Edge Department of Anaesthetics, The Royal Berkshire NHS Foundation Trust, London Road, Reading, RG1 5AN, UK
KEYWORDS Diving medicine; Gases; Decompression illness; Barotrauma
Summary Recreational diving medicine is a complex subject, overlapping with anaesthetics, general medicine, occupational medicine, physics, physiology and psychology. Advances in recreational diving technology mean that divers are diving in more remote areas and to deeper depths. This has implications for the recreational diving physician. & 2008 Elsevier Ltd. All rights reserved.
Introduction
Gases
Diving is a popular recreational activity and may give rise to many interesting medical problems. The definition of a dive is when a person enters water, a chamber, or any other environment and is subjected to pressure greater than 0.1 atm above local atmospheric pressure and who in order to survive in such an environment breathes in air or other breathing gases at a pressure greater than the local atmospheric pressure. The waters in and around the United Kingdom are generally cold and dark and may be strongly tidal. Such conditions generate physical, physiological and psychological problems for the diver. Diving under such conditions requires a reasonable level of medical fitness on the part of the diver. Tropical waters, increasingly the venue for many UK divers, are warmer and clearer, but may present different hazards, such as venomous marine animals and diving in areas remote from medical assistance.
Physical properties of gases
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Atmospheric pressure at sea level is 1 atm (equivalent to 101.3 kPa) and is the pressure that is experienced by all parts of the human body at sea level. Water is much denser than air (1 l of fresh water weighs 1 kg, while 1 l of air weighs 0.0012 kg). A column of water 10 m high exerts a pressure of 1 atm so that for every 10 m depth that the diver descends into the sea, his body will experience an increase in the ambient pressure of 1 atm. Thus, at a depth of 30 m for example, the diver will experience a total pressure of 4 atm (3 atm due to the pressure of the water plus 1 further atmosphere due to the pressure of the atmosphere itself).
The gas laws and gas solubility Boyle’s Law which states that at constant temperature the pressure and the volume of the gas are
0953-7112/$ - see front matter & 2008 Elsevier Ltd. All rights reserved. doi:10.1016/j.cacc.2008.06.001
ARTICLE IN PRESS 236
C.J. Edge
inversely related: PV ¼ k, where P is the total pressure of the gas and V is the volume of the gas. k is a constant for a given gas or mixture of gases. Dalton’s Law of Partial Pressures states that the pressure exerted by a mixture of non-reacting gases is the sum of the pressures that would be exerted by the individual gases if each occupied the same volume alone: P total ¼ P1 þ P 2 þ þ P n , where Pn is the partial pressure of gas n and Ptotal is the total pressure of the gases (see Figure 1). Henry’s Law of Solubility of Gases in a Liquid states that the mass of a slightly soluble but inert gas that dissolves in a given amount of a liquid at a constant temperature is proportional to the partial pressure of that gas above the liquid. Mathematically:
the body that contain gas will be affected by pressure as indicated by Boyle’s Law. For example, the air in the lungs taken in by a breath-holding diver at the surface will shrink to one-half the original volume at a depth of 10 m, to one-third at a depth of 20 m and so on. However, scuba divers breathe gas at the ambient pressure of the surrounding water and this enables the diver to breathe with ease. Nonetheless, as the diver goes deeper, the supplied gas will become denser, and the work of breathing will become harder. In the condition where the volume of gas diminishes and further gas cannot be drawn in to occupy this space, it will either be filled by body tissues or by clothing. This state of affairs is called a ‘‘squeeze’’.
Physiological effects of increased pressure General considerations
mn ¼ cn Pn , where mn is the mass of gas n that dissolves in the liquid, cn is the solubility constant for gas n and Pn is the partial pressure of gas n above the liquid. Whilst gases are very compressible, the tissues in the body vary in their degree of compressibility. For example, in the human, nerve tissue will start to exhibit altered physiological function at a depth of approximately 150 m but bone will not be deformed until much higher pressures are reached. Cavities in
Depth
Volume
The physiological effects of changing pressure on the diver are due largely to the gases that the diver breathes. The dive may be thought of conveniently as having two stages: 1. The descent and the stay at depth. 2. The ascent.
Pressure
Partial Pressures PN2
0m 1
1 bar
10 m
1/2
2 bar
20 m
1/3
3 bar
30 m
1/4
4 bar
PO2
0.8
0.2
1.6
0.4
2.4
0.6
3.2
0.8
Figure 1 This diagram illustrates Boyle’s Law and Dalton’s Law of Partial Pressures. The fraction in the left-hand box indicates the fraction of gas left in the box, while the figures in the right-hand box give the partial pressures of nitrogen and oxygen. Note that the partial pressures in each box add to give the total pressure at a given depth.
ARTICLE IN PRESS Recreational diving medicine
The descent and the stay at depth At sea level, there is free exchange of gases between the air in the alveoli and the dissolved gases in the blood stream. As the diver descends the total pressure of the gases in the alveoli becomes greater than atmospheric and, by Henry’s law, the amount of the gases dissolved in the blood and thence in the body tissues becomes greater.
Nitrogen An increasing partial pressure of nitrogen has minimal effects on most people until a depth of about 30 m is reached. As depth is increased, divers who dive on air will experience increasing symptoms of nitrogen narcosis (the ‘‘narks’’) and, if they carry on diving deeper, they will eventually exhibit signs of narcosis.1 The initial signs are an increase in reaction time, inability to deal with a given situation and clumsiness. The cure for nitrogen narcosis is to ascend. The nitrogen is thought to act in a similar manner to an anaesthetic and may interact with, or alter the three dimensional structure of various neurotransmitter receptors.2 An alternative way to avoid nitrogen narcosis is to replace some or all of the nitrogen with a gas that is less narcotic, such as helium.
Oxygen High-pressure oxygen has several effects on the body. There is an increase in ventilation and a decrease in alveolar and arterial carbon dioxide buffering tension due to a rise in central venous carbon dioxide. This in turn is due to the reduction in carbon dioxide capacity of haemoglobin overcoming the decreased carotid body excitation. There is also a vagally mediated bradycardia and vasoconstriction of the intracranial and peripheral vessels. There is a small fall in cardiac output.3 Priestley, the discoverer of oxygen in 1775, was the first to suggest that it may be toxic. Later, in 1789, Lavoisier and Sequin4 demonstrated that oxygen at 1 atm does not alter gross oxidative metabolism but did note a damaging effect on the lungs. Paul Bert in 1878,5 showed that whilst oxygen is essential to life, it becomes lethal at high pressures. He observed that larks exposed to air at 15–20 bar developed convulsions and that the same effect could be produced by oxygen at 5 bar. This central nervous system toxicity is now known as the ‘‘Paul Bert effect’’. In 1899, J. Lorrain Smith6 described the pulmonary changes resulting from exposure to moderately
237 high oxygen partial pressures (the ‘‘Lorrain Smith effect’’) and noted that the early changes are reversible and that higher pressures shortened the time of onset. During the 1930s, evidence accumulated that high-pressure oxygen was toxic to humans. Kenneth Donald, in 1942,3 showed that there was a wide variation in the tolerance to high pressures of oxygen, both between subjects and between the same subject on different days. Underwater exposure and exercise both aggravated the problem. Central nervous system (CNS) toxicity can be seen in the diving situation when closed and semiclosed rebreather sets (see later) are used. Divers may be exposed acutely to a high partial pressure of oxygen either through equipment failure or from going too deep and thereby raising the partial pressure of oxygen in the breathing gas to an unacceptable level. It is also being seen increasingly in those sport divers using high partial pressures of oxygen (PO2) in order to decrease decompression time for a particular dive profile. The diving physician is most likely to encounter CNS toxicity when treating decompression illness in the recompression chamber using a high PO2 (typically 2.8 atm). The symptoms of CNS toxicity, can be remembered using the acronym VITBEND:
V, Visual abnormalities, such as tunnel vision. I, Irritability. Can include anxiety, confusion or fatigue. T, Twitching, usually in the lips or other facial muscles. B, Breathing. Difficulty in taking a full breath. E, Ear problems, including tinnitus and vertigo. N, Nausea, sometimes intermittent. D, Dizziness, including clumsiness and incoordination.
The most dramatic manifestation is the grand mal type convulsion. Consciousness is maintained right up to the time of the convulsion, which may strike without any warning, and which does not give rise to any electroencephalographic (EEG) changes.7 Underwater, this is a serious situation because if it occurs the diver in scuba gear may lose the mouthpiece and drown. As mentioned above, exercise and immersion in water are two conditions that can lower the threshold to CNS toxicity. A third potentiating factor has been suggested to be carbon dioxide buildup, often occurring due to the ‘‘skip’’ breathing pattern adopted by many divers in order to conserve breathing gas, in which the diver takes a
ARTICLE IN PRESS 238 breath, holds it for as long as possible, and then slowly breathes out. To reduce the problems of oxygen toxicity during dives, the US National Oceanographic and Atmospheric Administration (NOAA) has recommended that partial pressures of oxygen should not exceed 1.4 bar, with an absolute maximum of 1.6 bar.8
Carbon dioxide The normal level of carbon dioxide in the alveoli is 40 mmHg (0.055 bar). When diving the arterial and alveolar carbon dioxide tensions should be maintained at approximately 40 mmHg. The alveolar pressures of nitrogen and oxygen increase with depth and therefore the alveolar percentage of carbon dioxide decreases. However, when energy expenditure is high, the level of carbon dioxide can increase dramatically. This situation is most commonly encountered in divers using rebreather sets. It may also be seen in the recompression chamber if there is inadequate flushing of the chamber with fresh gas. The clinical features of hypercapnia are breathlessness (carbon dioxide present at about 3%), distress and dyspnoea (5–6%), rise in blood pressure and heart rate, mental confusion and lack of coordination (10%) followed by loss of consciousness and death (12–14%).9 Although carbon dioxide is a respiratory stimulant, most of its effects are related to the acidosis it produces and are neurologically depressant.
Carbon monoxide Breathing gas must contain less than 5 parts per million (ppm) of carbon monoxide. If the breathing gas contains higher concentrations than this, then as it is compressed the partial pressure of carbon monoxide may rise to potentially lethal levels. The main source of the gas is from the exhaust fumes of the engine of an air compressor which, if not expelled well away from the inlet to the compressor, may be drawn into the diver’s air cylinder.
Long-term effects of diving under pressure Neurological changes10 and retinal changes11 have been described in divers but further work needs to be done to be sure that these changes are real. Specialised nuclear magnetic resonance imaging (MRI) scans have shown that in a few divers who have had DCI, and who have been demonstrated to have a shunt between the venous and arterial circulations (see below), have areas of high signal
C.J. Edge intensity in the cerebrum.12 However, it is unclear what these lesions represent in terms of pathology; certainly none of the divers with lesions had any demonstrable neurological symptoms. Very occasionally, sport divers may present with joint problems (especially in the shoulder and hip joints) in which part of the bone dies.13,14 This is due to exposure to compressed gases at pressures higher than atmospheric pressure over a long period of time and is known as aseptic necrosis or dysbaric osteonecrosis. The pathogenesis of dysbaric osteonecrosis is poorly understood.
The ascent from depth Decompression Unfortunately for the diver, gases that are chemically unreactive as far as the body is concerned (e.g. nitrogen, helium and neon) are sparingly soluble in blood. Even oxygen, when breathed at high partial pressures, can cause problems on ascent. When the diver ascends the gas that has dissolved in the tissues will come out of solution to form bubbles of gas in the tissues and in the blood vessels. These bubbles are then transported to the lungs where, in most cases, they are filtered out. This is the process of decompression. If the bubbles cause medical problems for the diver, then the diver is said to be suffering from decompression illness (DCI) which used to be known as caisson disease. Robert Boyle in 1690,15 was the first to investigate this phenomenon and it was he who had the idea that a rapid reduction in the atmospheric pressure could lead to the release of bubbles into the body tissues and thus cause a serious impairment in their function. Paul Bert, in a series of experiments in the late 19th century,5 showed that the more serious forms of DCI were provoked by the presence of large volumes of free gas, as opposed to dissolved gas. The composition of these bubbles was found to be largely nitrogen. Observations in caisson workers showed that if the decompression procedure was inadequate, then the blood of the workers literally frothed. This condition was called ‘‘the chokes’’ and proved to be rapidly fatal unless rapid recompression took place. If the decompression was not so provocative, then a condition known as ‘‘the staggers’’ might be seen which could lead to severe impairment of the nervous system or death. But the commonest form of DCI came to be called ‘‘the bends’’.16
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239
At the turn of the century, Professor J.J.S. Haldane undertook a series of investigations for the purpose of producing regulations for the safe conduct of underwater work by divers.17 Experiments in the goat showed that if the goats were exposed to a raised pressure (P1) for a ‘‘prolonged period’’ (1.5–2 h) and then the pressure was rapidly dropped to a new level (P2), the goats would exhibit mild signs of DCI if P2 was about half the value of P1. If the pressure drop was less than half, then the goats would not exhibit signs of DCI. This ratio P2/P1 ¼ 0.5 was found to be generally true over a wide range of values for P1 and P2. Using this approach, mathematical analysis reveals that if the ambient pressure of a tissue is suddenly changed from P1 to P2 then the gas tensions within that tissue will increase towards P2 as shown in Figure 2. Over the next 25 years, most of the research into decompression was carried out by the US Navy, leading to the publication of the US navy decompression tables in 1956,18 which have been widely used throughout the world. These tables indicate the maximum time that the diver may spend at a certain depth with a low risk of DCI after the ascent. In 1976, the Naval Safety Center reported that the overall incidence of DCI was only 0.065% using these tables, although certain dive profiles within the tables carry a greater risk.19 Nowadays, these mathematical models have been incorporated into small computers that can be worn on the wrist by divers. This allows multi-level diving to take place rather than just allowing the diver to dive to one specified depth and then to return to the surface again. These instruments have now been accepted by the recreational diving commu-
Pressure
P2
P1
0
Time
Figure 2 Figure showing the pressure versus time curve in the tissues as the gas pressure is raised from a value P1 to P2. The time period over which the change happens is thought to depend upon different factors, such as the vascularity of the tissue, the temperature and the amount of fat present in the tissue.
nity in particular as they allow dives of greater depth and duration to be performed for the same amount of decompression time. They have the advantage that they can be interrogated by the diving doctor when a diver presents to a recompression chamber with the symptoms of DCI. This allows the doctor to ascertain the dive profiles that the diver has undertaken prior to becoming ill and enables treatment to be tailored accordingly.
The clinical symptoms and signs of DCI The symptoms and signs of DCI include the following, although the list is by no means exhaustive20:
Pruritic mottled skin rash; Vague limb discomfort (‘‘the niggles’’); Moderate or severe limb pain (‘‘the bends’’); Feelings of being abnormally tired or exhausted; Abnormalities on psychometric testing; Limb weakness or paralysis; Parasthesiae; Vertigo; Headache; Vomiting; Abdominal pain; Visual problems; Collapse, hypotension, loss of consciousness.
The symptoms and signs of DCI, when referring a patient to a recompression chamber or to a diving doctor, are now described according to onset, evolution and some estimate of inert gas load in the form of depth–time profile. The manifestations of DCI are considered to be predominantly due to a high inert gas load in the tissues. Gas may form within the tissues as a result of insufficiently rapid washout of excess dissolved inert gas during the ascent. The gas may then go on to form bubbles within the tissue and venous circulation. Once in the venous circulation, these bubbles may be detected in the right atrium and ventricle by the use of 2D Doppler echocardiography. In the vast majority of cases, these bubbles are clinically ‘‘silent’’ and are removed by the pulmonary circulation without causing any symptoms of DCI. Thus, although quantification of the bubbles is useful for elucidating the pathophysiology of DCI, it is not useful in the assessment or in the management of divers with DCI.21 Barotrauma Many tissues in the body may contain natural or unnatural collections of free gas. At one extreme
ARTICLE IN PRESS 240 there are extremely rigid containers such as blocked paranasal sinuses. At the other extreme are very compliant containers such as unobstructed lungs or patent sinuses. In the intermediate range are moderately compliant vessels such as the gastrointestinal tract and the cavity of the middle ear. The unobstructed lung has a time constant of emptying of less than 1 s22 and so it normally vents and fills with gas without difficulty during ascent and descent. If the lung is obstructed, as for example during descent on a breath-hold dive, it compresses according to Boyle’s Law, typically reaching residual volume at a depth of approximately 30 msw. Further descent causes blood to be drawn into the chest from the limbs and abdomen to compensate for further diminution of lung volume. If the lung is obstructed on ascent, e.g. by a diver unwisely holding his/her breath, the gas in the lung expands until the lung reaches its bursting pressure which is roughly 70 mmHg at about 115% of voluntary total lung capacity when it ruptures. Gas may escape from the lungs into other tissues in four ways: 1. Into the virtual space between the visceral and parietal pleura to give a pneumothorax. A particularly severe form of this condition is seen with a tension pneumothorax which must be recognised and treated rapidly if the diver is to survive. 2. Into the pulmonary venous blood from where the gas passes into the arterial circulation (arterial gas embolism, AGE) giving rise to the manifestations of DCI. 3. Into the mediastinum (pneumomediastinum) and thence into the soft tissues of the neck, giving rise to surgical emphysema. 4. Into the peritoneum to give pneumoperitoneum, although this symptom is rarely encountered. For reasons that are not understood but may be to do with posture whilst working, aviators and tunnel workers experience pneumothoraces more commonly than AGE, while the situation is reversed in divers. If the Eustachian tube is obstructed, painful bowing of the tympanic membrane into the middle ear occurs when the diver descends. Further descent will cause rupture of the tympanic membrane with entry of potentially infected water into the middle ear cavity. This can result in vertigo underwater which may cause the diver to panic and ascend rapidly to the surface. Obstructing the external meatus (which most commonly occurs by means of a tightly fitting hood) causes an outward
C.J. Edge bowing of the tympanic membrane, known as ‘‘reversed ear’’. Gas may become trapped in a tooth cavity at depth, commonly as a result of poor dental hygiene. On ascent, the expanding gas can cause severe pain in the tooth (odontalgia); in some cases the tooth has been known to shatter (odontocharexis).
Treatment of DCI The most common problem with the treatment of DCI is lack of recognition of the symptoms and signs either by the colleagues of the diver or by the medical profession. For example, neurological problems in the peripheral nervous system may go unnoticed by the physician if not specifically sought as the diver may well be too anxious and confused due to symptoms of DCI in the cerebrum to tell the physician that there are problems with the feeling in his arms or legs, or that he is unable to pass urine. The treatment of DCI is by recompression in a recompression chamber.23 For less severe cases of DCI, the earlier that recompression is started after the onset of symptoms and signs of DCI, the better the result, but successful therapy has commenced as long as several days after the initial symptoms of DCI had presented.24 In the most severe cases, it has been argued that there is no ‘‘time to treatment’’ effect.25 Algorithms are published showing the depths, times and treatment gases that are used depending on the presentation and evolution of signs and symptoms of DCI in the diver. An example of such an algorithm is given in Figure 3. In addition, fluid should be administered either orally or intravenously depending upon the conscious state of the diver, as in some cases of DCI the diver is found to be very dehydrated. The use of non-steroidal anti-inflammatory agents is more controversial.26 Currently steroids and lidocaine are not in use for the routine treatment of DCI. DCI may develop some hours after the diver has finished diving. Surveys of divers have shown that about 50% of cases of DCI will exhibit signs and symptoms within 1 h of surfacing, while 90% will present within 6 h of surfacing.27 In a few cases, the time interval has been of the order of days. A diver could be thought to be drunk or under the influence of drugs when he presents to the GP’s surgery or police station. If in doubt as to whether the diver is suffering from DCI then advice should be sought from diving medical experts.
ARTICLE IN PRESS Recreational diving medicine
241 DIAGNOSIS OF ACUTE DECOMPRESSION ILLNESS
COMPRESS TO 18m ON O2
Assess the patient after 20 mins
Neurological Symptoms or Signs?
YES
Symptoms relieved after 10 mins at 18m?
NO
YES
NO Compress to 50m on AIR or 32.5/67.5 O2/N2 if available
YES
Consult a Diving Medical Specialist
Is the patient deteriorating ?
NO
Consult a Diving Medical Specialist
NO
Compress to 18m on O2
USE TABLE 62
Have symptoms and signs resolved after 3 O2 periods?
YES
Consult a Diving YES Medical Specialist
DECOMPRESS ON TABLE 61
Have ANY symptoms resumed?
NO
YES
Patient free of symptoms after 25 mins at 50m?
Have symptoms and signs resolved?
EXTEND TABLE 62
NO
YES
NO
Patient continuing to deteriorate?
NO
Remain at 50m for a total of 2 hrs.
Are there any significant signs?
YES
NO
DECOMPRESS USING TABLE 62
YES Consult a Diving YES Medical Specialist
Consult a Diving Medical Specialist
Have any symptoms worsened or returned?
NO DECOMPRESS USING TABLE 63
COMPRESS TO DEPTH OF RELIEF (MAX 70m) AND USE TABLE 65
DECOMPRESS USING TABLE 64
Consider recompression to 18m and transfer to Table 64 or extending Table 62
COMPLETE TABLE 62
COMPLETE TABLE 61
Figure 3 Example algorithm for the treatment of DCI (from Francis TJR, Smith DJ, Sykes JJW. The prevention and management of diving accidents. Report no. R92004. Institute of Naval Medicine, Alverstoke, Gosport, 1992).
Risk factors for, and prevention of, DCI Despite the use of decompression tables or computers, cases of DCI still occur, especially in sport
divers. Sometimes these cases are due to missed decompression stops or because the diver has ascended too rapidly from depth. Occasionally, divers get DCI when they have stayed well within
ARTICLE IN PRESS 242 the times specified by the decompression tables. Some of these cases can be shown to have a patent foramen ovale (PFO) which, when the right atrial pressure exceeds the left atrial pressure, will allow bubbles from the venous circulation to bypass the pulmonary circulation and enter directly into the arterial circulation.28 Often these cases will present with a skin rash and neurological symptoms within a few minutes of reaching the surface after a dive. Sometimes it is possible to elicit a history of migraine with aura from the subject. Divers who have exhibited these signs and symptoms and who have been shown to have a PFO should not be passed as fit to dive unless the PFO can be closed by interventional cardiological techniques using a prosthetic surgical device, or the diver is prepared to dive very conservatively to depths less than 15 m. Other risk factors for DCI are thought to be age, poor physical fitness, cigarette smoking, dehydration, carbon dioxide retention and possibly obesity.20 Divers who are being placed under pressure frequently can become acclimatised to a particular pressure, but this acclimatisation quickly wears off over 2–3 days if the diver has time off. When giving advice to divers about the risks of DCI, it should be remembered that many recreational divers are flying to the dive sites. In a few circumstances, the diver may be forced to travel by land at high altitude in order to gain access to the dive site. Both flying and high altitude travel are associated with a reduction in atmospheric pressure and inert gas bubbles are therefore likely to form more readily if such travel is undertaken shortly after a dive. A good general rule is to avoid flying or high altitude travel for at least 24 h after diving.
Diving equipment Recreational gas delivery systems SCUBA apparatus Self-Contained Underwater Breathing Apparatus (SCUBA) equipment is carried by the recreational diver and enables the diver to be independent of the surface. In open circuit scuba, gas (most commonly air) is delivered to the diver at the ambient pressure of the surrounding water from a cylinder carried on the back by means of a demand valve. This consists of a first stage to reduce the cylinder pressure to a lower, intermediate pressure and a second stage to further reduce the gas
C.J. Edge pressure to that of the surrounding water. Once the diver has taken a breath of the gas, it is then vented into the water. At depths greater than 50 m, nitrogen narcosis and the effort involved in breathing the dense air prevents the diver from working effectively. For such dives, the nitrogen is replaced by helium which is not considered to be narcotic, even at depths of 600 m. However, if compression to depth using helium/oxygen mixtures (‘‘heliox’’) is carried out too rapidly, then high pressure nervous syndrome29 may be experienced by the diver. This syndrome is characterised by decrements in motor and intellectual performance, accompanied by dizziness, nausea, vomiting and a marked tremor of the hands, arms and torso. The incidence of the syndrome can be decreased by slowing the rate of compression to depth and by adding to the helium/oxygen mixture a small amount of an anaesthetic gas, most commonly nitrogen. This helium/oxygen/nitrogen mixture is now known as ‘‘trimix’’. For many years, dives using trimix and heliox were undertaken only by divers working offshore in the oil and gas industry. Since the early 1970s however, recreational and scientific divers have started to use heliox and, more commonly, trimix to dive to greater depths. Thus, wrecks such as the ‘‘Andrea Doria’’ (85 m deep) and the ‘‘Lusitania’’ (93 m deep) have been dived using scuba gear and trimix. Such dives, without the backup and facilities that are available to commercial organisations in the oil and gas industry, are more hazardous than those usually undertaken by a standard recreational diver.
Rebreathers In open circuit scuba, every breath taken contains about 21% oxygen, but only 4–5% of this is metabolically consumed. The rest is exhaled along with the unused inert gases and the carbon dioxide produced by the body. A better method would be to use a system which allows the exhaled gas to be cleansed of carbon dioxide and replenished with fresh gas for further consumption, as is commonly seen in modern anaesthetic machines. This is the basis of a rebreather. This concept is not new; the first rebreather was produced in 1878 by Henry Fleuss and the idea was extensively developed during the first and second world wars by the military. During the 1960s and 1970s, the scientific community started to use rebreathers and since the 1990s, the recreational diver has been able to buy production-model rebreathers.
ARTICLE IN PRESS Recreational diving medicine Rebreathers come in two basic forms: 1. Semi-closed circuit, in which the gas the diver is breathing is recycled through a scrubber to remove the carbon dioxide and then a fixed amount of fresh gas is added to maintain a constant oxygen pressure. Such a unit will occasionally need to vent excess gas as the amount of inert gas builds up, and therefore wastes a small amount of the gas supply. These devices are relatively cheap because they are purely mechanical. Oxygen partial pressure can be monitored using a sensor but the device will continue to operate even if the sensor fails. Such units are becoming more popular with scientific, media and recreational divers. 2. Closed circuit, in which the gas that the diver breathes is recycled through a scrubber to remove the carbon dioxide and the percentage of oxygen in this mix is detected using an oxygen sensor. The correct amount of oxygen can then be injected into the mix to give the correct partial pressure of oxygen for the diver to breathe. These units are very expensive, requiring microprocessors to function efficiently. The electronic instrumentation occasionally fails, which may have disastrous consequences for the diver underwater. Against this, they do make the best use of the available gas and if maintained properly, they can be used for very deep dives.
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Other equipment Buoyancy aids Buoyancy control can be maintained either by adjusting the volume of air in the dry suit (if the diver is wearing one), or by adjusting the amount of air in a buoyancy compensator (BC) which is worn over the wet suit or dry suit in the manner of a waistcoat. Gas can be injected into the BC directly from the first stage of the demand valve.
Mask and fins Recreational divers commonly wear a facemask which encloses the eyes and nose, thus enabling the diver to equilibrate the pressure in the middle ears and Eustachian tubes with the ambient pressure of the surrounding water. Additionally, the lenses in the mask may be optically corrected to avoid the use of spectacles or contact lenses in the water. The bulky diving equipment slows progress in the water very considerably and so fins are a necessary accessory for the diver to allow adequate propulsion in the water.
Light sources Most recreational divers carry a torch of some form underwater. Red light penetrates the shortest distance underwater, blue light the farthest. A torch may thus reveal the true colours of an object underwater; it may also be used for signalling purposes.
Thermal insulation A diver must be kept warm whilst underwater. Wet suits, which are a close fit, trap a layer of water between the suit and the diver which acts as thermal insulation. The suit is made out of foamed neoprene and the insulation is derived from the gas trapped within the closed cells of the material. They are cheap and allow the diver to urinate without loss of insulation effectiveness. However, at depth, the suit material compresses and insulation is lost. They also offer little protection to the diver in polluted water. Dry suits keep the diver dry by being waterproof, having seals at the neck and wrists and retaining an insulating layer of air between the diver and the suit. As the diver descends, the air in the suit becomes compressed, but this can be avoided by injecting gas into the suit to maintain the volume. These suits have the disadvantage that if punctured, insulation is lost. Additionally, hygienic urination can be difficult and this may cause problems if the dive is prolonged.
The role of the doctor Any medical carried out for the purposes of determining whether a person is fit to dive must be carried out by a doctor who, as in all medical specialities, has specialist knowledge of the subject (e.g. has attended a diving medical examiner course) and who is a diver. It must be remembered that a diver is responsible not only for his/her safety but also that of his/her buddy and any surface support. Any medical condition that may interfere with diver safety should be considered with care before allowing a person to dive. Space does not allow a complete list of all the medical conditions that may affect a diver to be given here but some useful references are given below. Discussion will be confined to a few of the most common problems present in the potential diving population.
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Asthma In the developed world, asthma is an increasing problem. In the UK, approximately 12% of the population have symptoms at some time that may be attributable to asthma. There is a risk that a mild asthma attack whilst diving may seriously impair the ability of a diver to swim against a current or to return to safety. A more severe attack may lead to gas trapping underwater with the possibility of barotrauma occurring. These scenarios may put both the diver and his/her buddy at risk. The current advice in the UK is that people with asthma induced by stress, exercise, or cold should not dive30 Those with allergen-induced asthma may dive provided their asthma is not too severe (stage 1 or stage 2 in the British Thoracic Society guidelines31) and that they take a puff of a b2-agonist approximately 30 min before every dive as a prophylactic measure against bronchoconstriction. Such asthmatic divers also should not dive within 48 h of any attack of wheezing, no matter how slight this may be.
Hypertension Well-controlled idiopathic hypertension (blood pressure less than 140/90 mmHg) in a potential diver should not cause problems, unless the diver is on a b-blocker. Such drugs may limit the exercise capability of the diver when undertaking hard exercise, e.g. swimming against a current. The use of b-blockers when diving is therefore contraindicated.
Diabetes mellitus Recent studies have shown that well-controlled diabetic persons may be permitted to dive provided that they have none of the long-term complications of diabetes.32,33 It is essential that the older person with type II diabetes is evaluated carefully for such complications as renal, neurological and cardiac problems are more common in this population and may not be picked up in a routine medical examination.
C.J. Edge in women who are not taking the oral contraceptive pill during the first week of the menstrual cycle.34 The physiological mechanism for this is unclear and further research is necessary before any firm conclusions may be drawn. There are no hard data on the effects of DCI on the foetus and papers published showing such effects in the human are either anecdotal cases or have serious methodological flaws. Women who dive whilst they are unknowingly pregnant understandably become very anxious about the possible adverse effects that this may have had on their unborn child. The diver must be referred to a physician who has specialist knowledge of diving medicine and an interest in this area for further consultation.
Psychological and psychiatric disease Current thinking in the UK is that no diver should be permitted to dive whilst currently taking, or in the last 3 months have taken medication for any psychological or psychiatric condition. This includes antidepressant medication, medication for panic attacks, and medication for Attention Deficit Hyperactivity Disorder (ADHD).
Epilepsy The issue of allowing persons with epilepsy to scuba dive is controversial.35 Issues that have been raised by those against allowing persons with epilepsy to dive include the possible interaction of high partial pressures of nitrogen with the sedative effects of anti-epileptic medications, and the epileptogenic properties of high partial pressures of oxygen, either when diving or in the hyperbaric chamber.36 Those who argue in favour of allowing persons with epilepsy to dive often compare the current ban with that on persons with diabetes before 1991. However, it is not yet possible to predict when a person with epilepsy will have a seizure, and therefore the opinion of all the recreational diving medical bodies is that no person with epilepsy should be allowed to dive until they have been off all medication and fit-free for a period of 5 years.
The effect of the menstrual cycle and pregnancy
Children and diving
Some preliminary data are available that would appear to show an increase in the incidence of DCI
Children of age 12 years and above are permitted to dive in the UK. Sometimes younger children will
ARTICLE IN PRESS Recreational diving medicine express their desire to dive through their parents, but it is important to explain to both parties that such children are unlikely to have the physical and mental maturity to deal with problems that may arise underwater, particularly if it involves the lifting of an adult to the surface followed by towing that adult to a place of safety. Cases of DCI have arisen in children, mainly through panic ascents to the surface, and severe permanent injuries have been the result.37
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References 1. Cousteau JY. The silent world. London: Hazell Watson and Viney; 1954. 2. Franks NP, Lieb WR. Molecular and cellular mechanisms of general anaesthesia. Nature 1994;367(6464):607–14. 3. Donald KW. Oxygen and the diver. Worcester: Harley Swan; 1992. 4. Lavoisier AL, Seguin A. Premier memoire sur la respiration des animaux. Hist Acad Sci Paris 1789;185:566–84. 5. Bert P. La Pression Barometrique: Recherches de Physiologie Experimentale, 1878. Translated by Hitchcock MA, Hitchcock FA. Published as: Barometric pressure: researches in experimental physiology. Columbus, OH: College Book Company. Reprinted 1978 by Undersea Medical Society, Bethesda, MD. 6. Smith JL. The pathological effects due to increase of oxygen tension in the air breathed. J Physiol 1899;24(1): 19–35. 7. Lambertsen CJ. The effects of oxygen at high partial pressure. In: Fenn WO, Rahn H, editors. Handbook of physiology, section 3: respiration. Washington, DC: American Physiological Society; 1965. p. 1027–46. 8. Joiner JT, editor. NOAA diving manual. 4th ed. Flagstaff, AZ: Best Publishing Company; 2001. 9. Lanphier EH. Carbon dioxide poisoning. In: Waite CL, editor. Case histories of diving and hyperbaric accidents. Bethesda, MD: Undersea and Hyperbaric Medical Society; 1988. 10. Todnem K, Nyland H, Kambestad BK, Aarli JA. Influence of occupational diving upon the nervous system: an epidemiological study. Br J Ind Med 1990;47(10):708–14. 11. Polkinghorne PJ, Sehmi K, Cross MR, Minassian D, Bird AC. Ocular fundus lesions in divers. Lancet 1988;2(8625): 1381–3. 12. Gerriets T, Tetzlaff K, Hutzelmann A, Liceni T, Kopiske G, Struck N, et al. Association between right-to-left shunts and brain lesions in sport divers. Aviat Space Environ Med 2003; 74(10):1058–60. 13. Laden GD, Grout P. Aseptic bone necrosis in an amateur scuba diver. Br J Sports Med 2004;38(5):E19. 14. Wilmshurst P, Ross K. Dysbaric osteonecrosis of the shoulder in a sport scuba diver. Br J Sports Med 1998;32(4): 344–5. 15. Boyle R. New pneumatical experiments about respiration. Philos Trans 1670;5:2011–58. 16. Jaminet A. Physical effects of compressed air and of the causes of pathological symptoms produced on man, by increased atmospheric pressure employed for the sinking of piers in the construction of the Illinois and St. Louis Bridge
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